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Why is there a seeming dichotomy between mobility and photosynthesis?

Why is there a seeming dichotomy between mobility and photosynthesis?


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At least among more complex organisms, I cannot think of any examples of highly mobile species (like animals) that also incorporate photosynthesis. Perhaps there are examples that I'm unaware of, but even so it seems to be exceedingly rare.

Is there some good reason for this, or is it a mere chance of evolution?

I could speculate, perhaps, in that photosynthesis just doesn't provide enough energy for the relatively high metabolism of mobile species; but even then, there seems there should be a "sweet spot" where some level of mobility would still be "worth it" for a photosynthesizing species, rather than the strict dichotomy that seems to be observable, so I naïvely find that explanation somewhat dissatisfactory. There just seems to be little reason for animals to not practice photosynthesis, if only to be able to eat less than they need to without it.


The difference in energy requirements of a motile species make photosynthesis an unsuitable form of primary energy generation for them.

Since plants are sessile, their energy consumption rates are lower. Plants have approximate respiration:photosynthesis rates of 0.35-0.9, as can be seen in this table (click to enlarge):

Once the energy consumption rates exceed 1, the organisms will, by definition, no longer be full autotrophs, as they will need to obtain their energy from alternative sources. Therefore, the relative low energy content of sunlight makes it impossible for motile animals, which have a larger energy requirement, to survive fully via photosynthesis.


Why be mobile? To follow the sun?

Plants are mobile. Their seeds are. We have plants living on other plants.

Once they have a spot on the sun though moving does not necessarily improve your situation, being stationary and defending your territory though does. (Growing taller, deeper roots, wider crowns)


There is at least one species of highly mobile animal that can photosynthesize, depending on your definition of "highly mobile":

Sea Sheep? This Adorable Sea Slug Eats So Much Algae It Can Photosynthesize

The catch is that this animal does not produce its own chloroplast.


There are unicellular eukaryotes that photosynthesize and are very mobile. Many are in the phylum Chlorophyta. This one mentioned below is used for research and protein production, and can live on eating organic compounds in the dark. In the lab you dont need to stir small containers growing them - they move themselves to the light.

https://en.wikipedia.org/wiki/Chlamydomonas_reinhardtii


Materials and pathways of the organic carbon cycle through time

The cycle of organic carbon through the atmosphere, oceans, continents and mantle reservoirs is a hallmark of Earth. Over geological time, chemical exchanges between those reservoirs have produced a diversity of reduced carbon materials that differ in their molecular structures and reactivity. This reactive complexity challenges the canonical dichotomy between the surface and deep, short-term and long-term organic carbon cycle. Old and refractory carbon materials are not confined to the lithosphere but are ubiquitous in the surface environment, and the lithosphere hosts various forms of reduced carbon that can be very reactive. The biological and geological pathways that drive the organic carbon cycle have changed through time from a synthesis of these changes, it emerges that although a biosphere is required to produce organic carbon, mortality is required to ensure its export to the lithosphere, and graphitization is essential for its long-term stabilization in the solid Earth. Among the by-products of the organic carbon cycle are the accumulation of a massive lithospheric reservoir of organic carbon, the accumulation of dioxygen in the atmosphere and the rise of a terrestrial biosphere. Besides driving surface weathering reactions, free dioxygen has allowed the evolution of new metabolic pathways to produce and respire organic carbon. From the evolution of photosynthesis until the expansion of biomineralization in the Phanerozoic, inorganic controls on the organic carbon cycle have diversified, tightening the connection between the biosphere and geosphere.


Introduction

- 1 -

Language is not life it gives life orders.
Life does not speak it listens and waits.
— Gilles Deleuze and Felix Guattari A Thousand Plateaus. (1987: 76)

After the age of the machinic, the bios reenters the zeitgeist. Cybernetics and hacker culture in the 80s, the ‘network society’ in the 90s, the dot-com bubble around 2000 and the ‘long tail’ of the metadata of Web 2.0 marked the evolution of the digital phylum. In the last decade, a different conurbation of forces—climate change and energy crisis, ‘pop genetics’ and protests against GMOs, bioterrorism hysteria and bioethical crusades—started to sediment a new episteme concerned with the living. This affected the technological discourse too. If, according to Michel Foucault, modern biopolitics was about the management of populations and corporeal discipline, then since WWII a new interest has emerged around the microscopic scale of the bios—around the cell as the unit of life. Cultural mediators have been gathering in the interstice of this shift, developing the missing theoretical tissue between digital code and genetic code, between media art and a new controversial bioart.

Two main questions arise concerning this cultural shift. First: To what extent can biological models be employed to describe the mediascape as a new sort of ecosystem? To what extent, for example, can the metaphor of ‘media ecology’ be grounded in a properly biological paradigm? This question has relevance for political debate too, as biomimetic figures inspired by digital networks begin to be applied to new political concepts: see, for instance, the figure of the swarm applied to the postmodern notion of the multitude (Hardt and Negri, 2004, and also Parikka, 2008 Thacker, 2004). Conversely, a second question addresses the biological from the point of view of the digital. If ‘code’ is the universal semiotic form that is common to human language, computers and DNA, to what extent can cybernetic and digital models be applied to the biological? The history of bioinformatics started shortly after the discovery of DNA in the 1950s, accommodating quite a strict reductionism between ‘digital code’ and ‘genetic code.’ What are the consequences of a computer-based understanding of cellular reproduction for the sphere of ecology and biodiversity?

Schematically, the question is how to apply the forms of the bios to the techne? And conversely, how to apply the forms of the techne to the bios? In answer to the first question this essay tests the homogeneity of the biomimetic continuum, which supposes the mediascape as an extension of the biological realm (like in the notion of the machinic formulated in Deleuze and Guattari, 1987). Responding to the second question, this essay analyses the biodigital continuum, which takes binary code as a universal grammar from the Turing Machine to DNA, and then reduces the bios to a computable logos. Or, as Kelly (2002) puts it in his logocentric manifesto ‘God is the Machine’: computation can describe all things, all things can compute, all computation is one. The general purpose of this essay is to clarify the notion of ‘media ecology’ from the perspective of these two continua which consciously or unconsciously trouble its definition.

Sliding along the different typologies of the continuum that cut across the physical, biological, technological and cognitive domains (hyle, bios, techne, logos in Greek archetypes), this essay starts by positing the cell as the unit of life as opposed to the code as the unit of life. Reversing the dominant paradigm of the ‘genetic code’ is considered a necessary move in opening the biopolitical field of the cell, to ground a visceral materialism and eventually to outline, a new ‘ecology of biotechnologies.’

The first part of the article presents a basic ‘bestiary of the invisible’ to demonstrate paradigms of (microscopic) life which do not follow genetic logocentrism. Through authors such as Freud, Serres and Margulis, a new energetic diagram of the cell is advanced, calling for a general metabolics of organic life in opposition to the dominant partisan genetics. Trying to debunk the fatal opposition between code and energy, the second part of the article introduces DNA as an extension of the cellular body. Deleuze’s notion of the fold is employed to recognise ‘genetic code’ as a folding of organic matter in on itself with no intervention of any external grammar. This incestuous relation between linguistics and genetics is traced back to Erwin Schrödinger’s seminal book What is Life? precisely, Schrödinger’s notion of negative entropy is finally taken up as a key concept to clarify the four different regimes of entropy that compose the physical, biological, technological, and cognitive domains.

Inspired by the post-structuralist paradigm of Deleuze and Guattari, this essay nevertheless advances a critique of their notion of the machinic continuum. Against the enthusiasm of new media scholars and activists, the mineral, organic, technological and informational domains cannot be so smoothly compared, translated and coupled with each other as they belong to different entropic regimes. Only the recognition of the frictions and accumulations of energy surpluses occurring between these different ontological strata will make possible the imagining of a new ecology of machines.


Why does a biological underpinning to gender identity matter?

Biological essentialism (or biological determinism), is the idea that behaviours, interests or abilities are biologically pre-determined, rather than shaped by society. In an essentialist interpretation, innate differences between men and women result in ‘natural’ gender divisions – with men inherently (innately) better at decision making and women better at nurturing.

Feminists, Freudians, and queer theorists have all challenged biological essentialism. Second wave feminists argued that gender-based inequalities and differences were not natural, and were instead socially constructed. Girls are not inherently worse than boys at physics (due to having pink and fluffy brains) but rather, are often denied the opportunities offered to boys. Social constructivists demonstrated the many ways in which observed gender differences between men and women are socially engineered. Some went a step further, arguing that gender is purely a learned behaviour or a performance.

Brains are complex, and social constructivists, like the popular science writer Cordelia Fine, have rightly debunked the simplified and shoddy science that underpins essentialist claims that men are from Mars with their manly brains, and women are from Venus, with feminine brains.

Gender identity and the neurology of ‘trans brains’

Where then does gender identity fit in?

Some scientists have conducted neurological imaging studies on trans people, exploring whether there are specific, sexually dimorphic areas of the brain in which trans people differ from their assigned sex (the sex they were presumed to have at birth).

Published research findings, often with low sample sizes, have been interpreted as indicating that trans women have a brain more similar to a cis (not trans) woman’s brain than to a cis man’s brain. Such findings have been publicised in newspaper headlines as proof of the existence of trans people.

Such scientific studies, and their shallow interpretation and presentation in the media, have received strong criticism from a wide number of transgender commentators. There are a range of extremely valid reasons for criticism:

  • The suggestion that one specific variable can define ‘transness’ is reductive and overlooks the ways in which society, culture and experience impact on every individual including on the structure of the brain.
  • The reliance on any study as legitimacy for human rights is extremely dangerous – if the study results are later rejected, what happens to these rights?
  • The idea that any brain can be easily classified as male or female is simplistic and overly binary.
  • The suggestion (made by inaccurate media representation of the studies) that one specific variable can be used as a diagnostic test for transness also fills people with fear that any such test could be used by gatekeepers to judge who is accepted as trans and who can be denied support and denied rights. Any such diagnostic test would be entirely at odds with autonomy, with respecting people’s lived experience, with self-identification and dignity.

These reasons for fearing how science will be politically used, or for criticising simplified interpretations of scientific data, make total sense and have historical antecedents – I understand the fear and upset.

Rejection of biology

However, such comments very often seem to take one step further, rejecting not only biological essentialism and the unhelpful simplified, ‘soundbite’ biology loved by the media, but also moving into a sweeping rejection of any mention of a link between biology and gender identity. A culture in which the very mention of biology is discouraged.

This is where as a cisgender (not trans) parent of a transgender child I feel uneasy. I’ll attempt here to explore this from my cis parent’s perspective.

Pathologisation of diversity

For many decades, psychologists and psychiatrists have been aware of trans children expressing distinct gender identities at an early age – 2 or 3 years old.

Across the twentieth century mainstream medical convention, with some exceptions, rejected out of hand any possibility of a biological underpinning to gender identity. The consensus then was that a trans gender identity was a delusion, a mental illness that could, and should, be ‘cured’.

For young trans children, misogynist male psychologists and psychiatrists, frequently working in the field of sexology, focused their attention on the mother.

Therapy and treatment for young trans children focused on presumed maternal abuse or maternal failings.

Does it even matter why trans adults are trans?

When I hear people say ‘does it even matter why people are trans’ – when I hear people dismiss as offensive and unnecessary any consideration of any biological influence on gender identity, I have an emotional response. I also see this reaction in some other parents of trans children (though certainly not in all).

The denial of any possibility of a ‘biological underpinning to gender identity’ is historically tied up with the denial of the existence of younger trans children. The erasure of the existence of younger trans children has caused untold suffering.

As a parent of a trans child who is loving life, it makes me think of the trans children from decades past (and present in too many places in the world) who were traumatised and institutionally abused by medical systems designed to prevent or convert their gender identity. Neither the genitals = sex = gender approach of simplified biology, nor the feminist ‘gender is a social construct’ mantra, left any space for younger children to be trans. Trans children did not fit with either theory so therefore could not exist.

Impact of denial on families

Denial of the possibility of some young children being trans makes me think of the consequences of this denial. It makes me think of the mums who were coerced into distancing themselves from their trans daughters, based on some unsubstantiated theory that an overly close mother-‘son’ bond might lead to a child ‘misidentifying’ as female. How unbelievably cruel to do that to a family.

Shon Faye, whose work I greatly admire, recently wrote that she disagrees with anyone who suggests gender identity is innate and that it should not matter why people are trans. CN Lester, another writer whose work, and excellent book, I’ve learnt a lot from, critiqued the reporting of the research study under discussion and recommended reading work by Cordelia Fine, author of ‘Delusions of Gender’.

This particular recommendation makes me want to cry.

Delusions of gender as a book has real merits in its debunking of simplified biology, in its understanding that gender-based inequalities are not natural, and that men are not inherently better at parking. So far so commendable.

However, Cordelia Fine replaces the simplified biology of biological essentialism not with nuanced and complex biology, but a nod to social constructivism. Her work is routinely used by those who argue that gender is merely a ‘performance’ and that trans identities do not exist, except perhaps as a non-conforming person’s misguided response to gender norms.

The view that gender is purely a construct and therefore not ‘real’ is pervasive and extremely dangerous. Adherents of this view may well tolerate trans adults – with a patronising assumption that trans adults made a ‘choice’ to ‘change gender’ as a response to their non-conformity. But whilst adherents of social constructivism may begrudgingly tolerate the existence of trans adults to some degree, they allow no such tolerance for younger trans children.

The gender as purely a social construct contingent see social influence and gender stereotyping as the only reason for trans identities. They see no valid reason for the existence of young trans children.

Some of the more fringe, actively transphobic, elements of this group, throw their hate and bile at parents of trans children, accusing us of child abuse, demanding that the state take our children away, demanding that children be protected from ‘transing’.

The recommendation to read Cordelia Fine hit a particular nerve as ‘Delusions of Gender’ had a direct impact on my family. We had a family friend who was unable ‘ideologically’ to accept the possibility of the existence of a trans child. They rejected our child and through that rejection, our family entirely. In a parting gesture, they pleaded for us to read ‘Delusions of Gender’. This very book had been the germ of our now former friend’s belief that any trans identity is a delusion, and that pandering to childhood delusion is parental abuse.

Through my shock and upset, I was struck at the time by the unbelievable arrogance. The recommendation that instead of loving my daughter, I should ‘read up on Fine’ and learn that gender isn’t real. This was not to be the first such recommendation.

Fine’s work is populist and best selling, and over the years I’ve had countless similar comments from ‘well meaning’ individuals. It is not that I am ignorant or closed minded, far from it, I’d hazard I know more of Fine’s exploration of gender than those dabblers. I have read, considered, understood the theoretical position being proffered. The same cannot however be said of the Fine pushers. Their position is based on an assumption (from those who have no first hand experience of trans children) that trans children do not, indeed cannot, exist.

The recommendation to read Cordelia Fine is also, depressingly, front and centre in the advice that the UK Children’s Gender Service’s website provides for parents of trans kids. No space here for a clear and much needed message that ‘some kids are trans – get over it, try to be kind’. Instead they present a false dichotomy between simplified biological essentialism reduced to mention of “a boy’s brain in a girl’s body” and “academic psychologist Dr Cordelia Fine” and “gender as a social construct”, with differences based on experiences rather than biology. Parents wondering whether to accept and love their trans child are instead advised to read about the delusion of gender.

When parents and their children reach the children’s gender service in the UK, if they are allocated one of several apparently deeply transphobic clinicians (clinicians who hold so much power over trans children and families), they may then endure literally years of probing and questioning on parental views on gender, as the clinicians probe for the ‘root cause’ of gender diversity.

The social constructivist view also makes me think of the school teachers and class parents and wider community who argue that a child is too young to make a ‘choice’ to be trans and should wait until adolescence or adulthood. Who don’t see the harm of denying a child a happy childhood.

It makes me think of the people who look at us with suspicion, hostility, scrutiny, when I mention I have a trans child. Of the parents who steer their child away from ours, in case being trans is socially contagious.

It makes me think of the people who are no longer in our family’s life, who are unable to see a trans child as anything other than ‘social conditioning gone wrong’.

It makes me think of the people online and in person who target parents of trans children and accuse them of child abuse for loving their child. It makes me think of the haters who want trans children erased from our schools and communities. Who want trans children to be marginalised, made invisible, kept apart from other children.

The existence of trans children poses a challenge both to the simplified biology of biological essentialism and to social constructivism (the idea that gender is merely a performance).

Who cares whether or not biology has any role?

Many people argue that it should not matter whether being trans is partly influenced by biology or fully shaped by culture, society and upbringing. They argue that acceptance will not come through identifying a ‘cause’ for transness, but through people getting to know trans people.

I imagine and hope that acceptance will gradually emerge for trans adults. I think things are slowly moving forward.

What about trans children though? How do we ensure that gains in acceptance and visibility and legislative rights do not leave out trans children, the most vulnerable, those without a voice.

Too many advocates for the rights of trans adults are silent on the topic of young trans children. Many have no understanding or awareness that trans children exist. Others, consider trans children too controversial, too divisive to stick up for.

Trans children are nearly completely invisible. And whilst there remains a default assumption that gender identity is shaped not at all by biology but purely by culture and upbringing, then there will remain a reluctance to support younger transgender children.

Those who believe that gender is purely a performance, who believe that trans identities are socially constructed, do not believe in the existence of young trans children.

The erasure of trans children allows haters to paint themselves as crusaders saving children from being socially influenced or indoctrinated into being trans.

With no openness to the possibility of a trans child being part of natural diversity, they look for a reason. With young children it is blame the parents. With older children it is social contagion. In the first scenario they advocate removing children from abusive parents. With the second scenario they ask that trans identities never be mentioned, embraced or supported at school. For parents who are afraid and unsure how to react to a trans child, they advise conversion therapy.

Another way

Yet, as soon as people open their minds to the idea that there might be a (complex, messy, unattributable) biological underpinning to trans identities, that trans children exist, and have in fact, always existed, the whole deck of cards upon which the transphobes build their hate comes crashing down.

This opening of minds is possible. This opening of minds and shifting of world view happened to me.

Growing up as a gender non-conforming feminist, tired of sexist societal restrictions and expectations, I was instinctively drawn to a social constructivist view point. I had never met a trans person, but had subconscious, lazy, uneducated assumptions about trans people being enthralled to gender stereotypes. I have former friends who are still tied to this world view.

My world view was shaken when I had the good fortune to have a child who opened my eyes. An assigned male child who was insistent, consistent and persistent that she was a girl from the youngest age.

Learning to reset my assumptions

At first, I really struggled to accept my child as a girl. I told her she was wrong. Mistaken.

I did not believe it was possible for a young child to be trans.

I was certain that this child was too young to understand or reject gender norms or sexism or heteronormativity. I knew they were not making a choice, and certainly weren’t being influenced to be trans (she had never come across any representation of a trans person and I was unconsciously transphobic). She wasn’t even gender non-conforming in her interests. A suggestion I sometimes hear (from people who have barely met a trans person) that she was repressing internalised homophobia in infancy is absurd.

She had a persistent, consistent, insistent knowledge that she was a girl that withstood all forms of persuasion.

Like hundreds of parents all around the world who have experienced the same, I had to learn to reset my assumptions about gender identity. I learnt to love and accept my child for who she is. I have never looked back. She is happy and thriving.

I see how people who emphasise ‘gender as a social construct’ utilise that simplistic maxim to make my daughter’s life impossible. How they use it to argue against her rights. How they use it to accuse parents of abuse.

I see how people who claim genitals = sex = gender similarly use simplified biological essentialism to argue that my child is defined and invalidated by parts of her anatomy.

Neither the simplified biology of essentialism, nor simplistic social constructivism, leaves space for my daughter to exist.

Is there an alternative paradigm?

Holistic views of gender

I recently had a short email exchange with Julia Serano and she kindly shared a chapter she wrote on this topic back in 2013 (Excluded: Making Feminist and Queer Movements More Inclusive – chapter 13: Homogenizing Versus Holistic Views of Gender and Sexuality). What follows is what I took away from her chapter, adapted into my own words – I recommend reading her chapter first hand.

In this chapter, Julia critiques the failings of both simplified biology, (gender determinism) and social constructivism, which she terms gender artifactualism.

She outlines how biological essentialists and biological determinists, (often genital obsessed religious conservatist non-scientists), misrepresent and misunderstand biology and science. They present a simplistic last century school child’s version of human biology, assuming that a simple gene or hormone or chromosome works unilaterally triggering a domino rally of binary outcomes.

She also outlines the failings in social constructivism. For decades children’s gender services were dominated by social constructivists who believed that children could not really be trans and that such children could be engineered into accepting their assigned gender. Yet these efforts failed. Medical consensus is now absolutely clear that conversion therapy is unethical and ineffective – conversion therapy did not change a person’s gender identity, merely produced shame, self-hate and depression. Julia notes that gender identities are often ‘profound, deeply felt and resistant to change’. She notes that some people have a fluid gender identity, and that some people do experience a shift in their identity over time, but that such shifts do not result from external pressure and are ‘almost always inexplicable, unexpected’.

She advocates rejection of both simplified biology (biological determinism) and social constructivism (gender artifactualism). In its place she presents a holistic model of gender.

This holistic model of gender acknowledges that biology is complicated. Human biology is not the simplistic yes/no on/off approach that non-scientists and biological essentialists like to pretend. Real biology is complex, multi-faceted, interactive. Just because some people misuse (simplified) biology, does not mean biology itself is essentialist, deterministic, reductionist or sexist.

Julia notes that ‘the human genome has 20,000-25,000 genes. Any given gene or hormone is affected by countless different interacting factors. Because genes and other biological factors act within intricate networks, any given factor will push a system in a particular direction, but will not single-handedly determine a particular outcome’.

Julia argues that ‘while our brains are shaped by learning and socialisation, they are not infinitely plastic ie they are not blank slates. Some traits have a strong intrinsic component’. She notes that though ‘socialisation has a significant impact on brains and behaviours’ it ‘cannot fully override certain intrinsic inclinations’.

She makes a comparison with left-handedness, which is observed in utero before any socialisation. Even with societal pressure to conform to right-handedness some individuals maintain a preference for using their left-hand.

A holistic model of gender allows space for a biological underpinning to gender identity. A holistic model of gender considers the complex interactions between biology, society, experience.

Biological underpinning to gender identity

A wide number of scientific studies have concluded that there is a durable biological underpinning to gender identity.

This supports what other parents with experience like mine have been saying for decades from their lived experience. This backs up what some trans adults remember from their earliest childhood memories.

There is increasing evidence of trans children who have clear gender identities at a very young age. This evidence of young trans children is present in diverse countries and cultures across the world.

The growing scientific consensus of a biological underpinning to gender identity led to the global endocrine society publishing a position statement last year:

“The medical consensus in the late 20th century was that transgender and gender incongruent individuals suffered a mental health disorder termed “gender identity disorder.” Gender identity was considered malleable and subject to external influences. Today, however, this attitude is no longer considered valid. Considerable scientific evidence has emerged demonstrating a durable biological element underlying gender identity. Individuals may make choices due to other factors in their lives, but there do not seem to be external forces that genuinely cause individuals to change gender identity.”

(for the full position statement and more on the studies see here)

I welcome this consensus. I view it with hope that it will help open eyes and minds and hearts to the existence of trans children like my daughter.

I would happily share this scientific consensus on a biological underpinning to gender identity with a wider audience – I see in it hope of greater acceptance and support for trans children.

However I note that since the publication of this evidence based position statement from the medical establishment, I cannot recall having seen this printed in the media or even referenced in the few articles commissioned by trans authors. Indeed quite the opposite – more often there is a strong resistance to any mention of biology.

Do we have to reject biology?

I understand the scepticism around how biology can be misused, but surely that does not mean this should be rejected outright?

Whilst supporters of trans rights shy away from biology and science, it allows transphobic groups to present themselves as champions of science and rationality. Claims that couldn’t be farther from the truth.

Transphobes focus on gender as performance, as fake, as a delusion. Whilst a huge part of what we call gender is socially constructed, my child’s gender identity is not a choice, is not a delusion, is not a product of societal or parental persuasion.

Transphobic groups like to focus on what they simplistically call biological sex. They describe biological sex as a simple binary reality, with gender identity operating on some parallel dimension outside of biology. My daughter is 100% biological. She does not have a magic gender identity spirit disconnected to her biological body. Her biology is no less real or valid than the biology of cis girls. It is not essentialist to claim that her identity is an integral aspect of her biological reality. The true essentialists are those trying to present a simplified and fraudulent version of biological science, utilising distorted, cherry picked and biased pseudo-science to support a transphobic position.

Acknowledging biology without essentialism

The argument that we should avoid science in case it is essentialist or in case it is used against trans rights is a false logic.

  • It is possible to acknowledge the biological underpinnings of gender identity whilst acknowledging that a person’s felt and expressed gender identity is a complex interplay of biology, culture, socialisation and experience.
  • It is possible to acknowledge the biological underpinnings of gender identity whilst simultaneously recognising that identity is neither fixed, nor binary.
  • It is possible to acknowledge the biological underpinnings of gender identity whilst arguing very strongly against diagnostic testing for ‘transness’ or biological gate-keeping and identity policing.
  • It is possible to acknowledge the biological underpinnings of gender identity whilst maintaining that the only way to know someone’s gender identity is to ask them, and that a right to self-identification is a basic part of dignity

My daughter is real and valid and deserving of rights, equality, respect and dignity regardless of our current understanding of science.

But science already has plenty of evidence that trans children exist and that there is a biological underpinning to gender identity and I see no reason not to talk about this. Having a trans child (or being a trans child) does not mean rejecting science.

We should embrace science

My daughter is growing up with a love of science. A thirst for knowledge. I’ll teach her all the science I know, on microbiology, on chemical reactions, on photosynthesis, on plate tectonics. On neurology, on genes, on hormones and gender identity. On sample sizes, on causality, on peer review, on rigour, on interpretation and data manipulation.

Biology is rich and complex and we have so much still to learn. If she carries on with a love of science she will learn things far beyond my knowledge. Science (high quality science) is full of wonder and excitement and discovery.

We should not be afraid of saying loud and proud that we support science. We should be clear that those attempting to attack or dismiss transgender children and adults not only lack empathy and kindness, they also lack sophisticated understanding of science, of biology, of complexity.


Life’s little oscillations

Living things must deal with a universe that is both regular and ever-changing: No day exactly mirrors the last, yet the sun and moon still appear at their appointed hours.

Cells contain their own seeming chaos, with countless molecules cooperating to produce subtle responses and behaviors. And in recent decades, a great deal of focus has specifically centered on the periodic patterns that underlie many cellular processes.

Oscillations &mdash such as a pendulum&rsquos swing or a ball&rsquos bouncing on the end of a spring &mdash are among the simplest and most common phenomena in physics, but researchers have come to appreciate their ubiquity in the biological world, too. Concentrations of molecules rise and fall, genes alternate between on and off, and circadian clocks keep time almost as well as human-made machinery. Together, these biochemical fluctuations are crucial for a blizzard of biological needs: timing daily activities, orchestrating cell division and movement, even mapping out parts of an embryo as it grows. Cells would be unable to function without them.

Such patterns were harder to spot in years past because scientists analyzed whole populations of cells at a time and looked at averages, says synthetic and systems biologist Michael Elowitz of Caltech in Pasadena. But biochemists can now tag molecules in individual cells with fluorescent biomarkers and film their ebbs and flows. &ldquoMore and more people started to look at individual cells over time and discovered that some of the most important systems in biology are not static &mdash they&rsquore really dynamic,&rdquo Elowitz says.

Some biochemical oscillations are simple: A few proteins or other organic chemicals go through a repeating pattern. Others are so complex that scientists have yet to map out their pathways. But their pervasiveness has drawn a great deal of attention from those seeking insight into biochemical behavior and researchers like Elowitz who hope to apply such knowledge by engineering novel functions into cells.

&ldquoAll of these are self-organized,&rdquo says theoretical physicist Karsten Kruse of the University of Geneva in Switzerland, who coauthored an article about oscillations in the Annual Review of Condensed Matter Physics. &ldquoIf you add the right components together, then they don&rsquot have a choice &mdash they must produce these oscillations.&rdquo

Here&rsquos a look at some of the most well-studied and intriguing biochemical oscillations that emerge from the complexity of the cell to produce order.

Circadian rhythms in cyanobacteria

Daily activity cycles are important for survival in our 24-hour world. In 2017, the Nobel Prize in Physiology or Medicine went to researchers who unraveled the details underlying these rhythms in higher creatures. In contrast, single-celled organisms, such as light-harvesting blue-green algae or cyanobacteria, were once thought too simple and fast-dividing to harbor such clocks.

But keeping track of the sun is obviously important for organisms whose livelihood depends on light. Today researchers know that these life forms also have intrinsic circadian rhythms &mdash and know a lot about how they function. Molecular geneticist Susan Golden of the University of California, San Diego, has helped to decode the molecular machinery regulating time in the cyanobacterium Synechococcus elongatus, and coauthored a description of the clock in the Annual Review of Genetics. The story goes like this:

The cyanobacterial circadian rhythm relies on an oscillation among three proteins: the enormous KaiC, which consists of two six-sided, doughnut-like rings stacked atop one another its helper, the butterfly-shaped KaiA and the component KaiB, which is usually inert but can spontaneously change to a rare, active form.

As the sun rises, wiggly molecular chains extending from the top of KaiC&rsquos upper stack grab hold of little KaiA. Once bound, KaiA induces the immense KaiC to accept phosphate groups. Over the course of the day, more and more phosphate is added to KaiC&rsquos top ring, stiffening it and causing its lower doughnut to deform.

By sunset, the lower ring has been so squished that it exposes a hidden binding site along its bottom. The rare active form of KaiB can now stick to this site, changing KaiC&rsquos structure so it lets go of KaiA. As the night progresses, KaiC slowly gives up phosphates, eventually returning to its original state and releasing KaiB. The cycle takes about 24 hours.

And how does this oscillation cause rhythms in the cell&rsquos biochemical activities? By cyclically activating a key gene-regulating protein named RpaA. RpaA switches on (or off) around 100 genes in S. elongatus. These genes, in turn, direct the cell&rsquos metabolism and physiology &mdash telling it, for instance, when it&rsquos time to photosynthesize or burn sugar stores. Since RpaA activity peaks at dusk, the bevy of activities occur with daily cycles.<*

Division in E. coli

Bacteria divide to reproduce, but an off-center partition will cause lopsided daughter cells, potentially leaving descendants understocked with the materials they need to survive. Not surprisingly, then, many microbes use molecular systems to split perfectly in half.

Perhaps the best understood is a team of three globule-shaped proteins called MinC, MinD and MinE that create waves of fluctuations in Escherichia coli.

The key component is MinC &mdash in high concentrations, it blocks a protein that kicks off the process of division. But MinC doesn&rsquot work solo. On its own, it will diffuse throughout an E. coli cell and stop division from happening anywhere at all. So MinC relies on MinD and MinE to tell it where to go.

MinD binds to the membrane at one end of the cell, painting the interior with clusters of itself. That attracts huge collections of MinC that come in and bind to MinD &mdash blocking the molecular machinery that initiates division from setting up shop at that location.

Next comes the work of MinE. Lots of MinEs are attracted to the MinDs and they force MinD to undergo a small change. The result: MinDs and MinCs are kicked off the membrane. They move on to search for a place devoid of MinEs &mdash like the other side of the bacterium &mdash where they can bind once again to the cell membrane.

Then it happens all over: MinEs chase and kick off the MinD-MinC complexes again. Wherever MinD tries to stick to the wall, it gets booted out, and MinC along with it. The process generates a pulsation of Min proteins that moves back and forth between the cellular antipodes over the course of a minute.

Why does this cause the cell to divide right in the center? Because MinC spends the least time in the middle of the cell &mdash giving the division machinery an opportunity to assemble there.

This wouldn&rsquot be the case if E. coli&rsquos sizing were different. By constructing synthetic rod-shaped compartments of different lengths and widths and introducing concentrations of MinD and MinE into them, biophysicist Petra Schwille of the Max Planck Institute of Biochemistry in Munich, Germany, and colleagues created beautiful videos of the molecules&rsquo fluctuations. They showed that longer or shorter cells would allow the division site to be at other locations.

Vertebrate segmentation

In the seventeenth century, Italian physiologist Marcello Malpighi used an early microscope to study developing chicken embryos and observe the formation of their spinal columns. More than 300 years later, modern researchers are still puzzling over the incredibly complex process that forms each vertebra and segment of the body. One key component: a clock-like oscillation that travels down the developing embryo.

&ldquoIt&rsquos easiest to think about it as an oscillator that gets displaced in space with a certain speed and direction,&rdquo says developmental biologist Olivier Pourquié of Harvard Medical School in Boston. Each time the embryo reaches a certain phase in the oscillation, it stamps out a segment. Then it goes through the cycle again, producing a second segment. And so on. &ldquoBut because the oscillator moves, it will stamp the segment at a different position,&rdquo Pourquié says. &ldquoIn this way, you can generate a sequential series of segments&rdquo along the length of a gradually extending body.

In embryos of vertebrates like fish, chickens, mice and humans, the future head is one of the first structures to appear. Later, bumpy segments called somites emerge, one by one, below the head, eventually giving rise to the spine, rib cage, skeletal muscles, cartilage and skin of the back. These ball-like pairs of somites are generated from tissue below the head when that tissue receives cues from two separate systems &mdash called the wavefront and the clock &mdash at the same time.

First, the wavefront. It involves two molecules, fibroblast growth factor (FGF) and Wnt, each of which forms a gradient, with their highest levels farthest from the head: a place near the tail that is constantly moving away as the embryo elongates. (An inhibitory substance called retinoic acid, produced by already formed somites, helps to keep FGF-Wnt activity toward the rear.) The two molecules set off a complex series of steps and act to inhibit somite formation. Somites appear right around the spots where they are least abundant.

Second, the clock component. That&rsquos governed by a third molecule &mdash called Notch &mdash and the signaling pathway it sets off. Notch causes cells to oscillate between active, &ldquopermissive&rdquo states and inactive, &ldquorestrictive&rdquo states at a characteristic rate that varies from species to species. If the cells happen to be in a permissive state at a spot where the Wnt-FGF gradient has sufficiently weakened, a cascade of genetic activity tells cells in that region to gather into somites.

And as the body elongates and the tail moves farther from the head, the Wnt-FGF wavefront will move in a posterior direction, stamping out a line of somite segments with each tick of the Notch clock. (Read more about segment formation in this article in Knowable Magazine&rsquos special report on Building Bodies.)

Waving motion

Just like their multicellular kin, single-celled creatures need to move in order to hunt, escape predators or seek out light and nutrients. But getting around when you don&rsquot have limbs can be a tough task. So cells that need to move, be they free-living or part of a multicelled creature, rely on various types of molecules to do the job. In certain cases, the action of these molecules can induce wave-like ripples on the cell&rsquos surface, which the cell uses to skate forward.

Actin, a protein found broadly in nature, is key. The molecule, a major component of the mesh-like cytoskeleton, is involved in a slew of operations: mobility, contraction as cells divide, changes in cell shape and internal transport.

Along with colleagues, computational biologist Alex Mogilner of New York University in New York City has investigated how actin can drive waves that allow certain types of fish cells known as keratocytes to crawl around. Keratocytes are responsible for producing collagen and other connective proteins, moving to sites of injury and inflammation to assist in healing. They have often been used as model systems to study cell locomotion.

Normally, cells get around by protruding long, limb-like extensions and tottering forward like tiny, exotic aliens. But when they enter an especially sticky environment, their strategy changes and they no longer extend thin limbs, instead skimming forward using short ruffling motions of their cell membranes.

Beneath the membrane of a keratocyte, actin proteins are constantly assembling and disassembling into long filaments. In a highly adhesive environment, the cell membrane will sometimes stick to the external material, which tugs on the membrane as the cell tries to move. This tugging creates a small pocket right beneath the membrane that actin filaments can expand into.

An enzyme called vasodilator-stimulated phosphoprotein (VASP) will often be hanging around beneath the membrane, too. VASP binds to the actin and stimulates it to form even longer filaments and branches. If both VASP and actin are present in high enough concentrations, a cascade of actin filament-lengthening can begin. &ldquoWhen it starts, it&rsquos like a fire starting,&rdquo says Mogilner.

The elongating filaments push on the tight cell membrane, producing a bump that gives the actin chains room to grow even more, and bind more VASP. Tension in the membrane causes it to sway like an audience doing &ldquothe wave,&rdquo sending the cell skating in the wave&rsquos direction. The actin filaments beneath the membrane grow sideways as well as forward, helping to push the wave along. At the original spot where the wave began, the actin filaments will have used up all the available VASP, preventing further lengthening. The sticky external environment adhering to the taut membrane also dampens the wave at the origin spot.

&ldquoIn a way, VASP proteins are like trees, actin filaments are like fire, and adhesions and membrane are like water: At the back of the wave, trees are all burnt and drenched in water, and the fire stops,&rdquo says Mogilner. But at parts of the membrane far from the wave&rsquos origin, high concentrations of actin and free VASP will still exist, often leading to a new wave that begins where the previous one was extinguished.

It&rsquos still unclear just how keratocytes choose what direction to move in. Presumably, says Mogilner, the leading edge of a cell is oriented toward some external cue, like a chemical gradient from some food. Also poorly understood are the benefits of this particular mobility tactic. &ldquoIn some cases, it&rsquos not obvious why waves are better than other mechanisms,&rdquo says Kruse, whose work on cytoskeleton dynamics focuses on theoretical descriptions of cell movement and division.

Some researchers have suggested that the wave-like motion might help cells get around small obstacles that they would otherwise run into head-on. Or maybe it&rsquos prudent for them not to overextend their limb-like protrusions in certain environments.

A synthetic cellular circuit

When Caltech&rsquos Elowitz was in graduate school at Princeton University in the 1990s, he often got frustrated by diagrams showing the inferred interactions of genes and proteins, with their many unknowns and arrows going every which way. &ldquoI just became convinced that if we really want to understand these things we need to be able to build them ourselves,&rdquo he says.

Along with his advisor, Stanislas Leibler, he created a synthetic genetic oscillator in order to show that a simple biological system could be programmed and built from scratch. Called the repressilator, it consists of a tiny loop of DNA with three genes on it. They carry instructions for making three proteins called repressors, each of which binds to the next gene and turns it off.

And here&rsquos where it got fun. In their construction, the first gene produced a repressor protein, LacI, which would shut off the second gene, called tetR, whose product would shut off the third gene, cI, whose product would shut off the first gene.

&ldquoIt&rsquos like a game of rock, scissors, paper,&rdquo says Elowitz. &ldquoThe first repressor turns off the second one, the second turns off the third one, and the third turns off the first one.&rdquo Once the first gene is turned off, the second gene can turn on, and thus turn off the third gene. And then the first gene can turn on again &mdash and on and on.

To watch the circuit run, Elowitz included a fourth gene that would cause E. coli to light up bright green &mdash but only when it was turned on by one of the three repressors. Placed inside E. coli, the repressilator causes the microbe and its descendants to flash green fluorescent light with a period of around 150 minutes.

Beyond simply showing that such circuits could be created, the research provided insight into the noise of biological systems. E. coli did not turn out to be a perfect little deterministic machine, says Elowitz. When loaded with the repressilator, some daughter cells flashed more strongly or weakly than others, suggesting that there is a great deal of variability inherent in their biochemical workings.

Studies have continued on the system and, in 2016, a team at Harvard University and the University of Cambridge significantly improved the precision of the circuit, allowing much larger numbers of daughter cells to flash in sync.

The field of synthetic biology has grown rapidly in the two decades since Elowitz&rsquos early work, and now offers a plethora of interesting applications, including novel proteins and enzymes for medicine, biological sensors and even cells that perform calculations like living computers. Being able to fine-tune biochemical oscillations &mdash with far more exquisite precision than can be found in natural systems &mdash will be crucial to building future synthetic biological products, says Elowitz.

&ldquoOut of physics, we have electronics and electrical engineering,&rdquo he says. &ldquoWe&rsquore just beginning to learn these principles of genetic circuit design, and I think we&rsquore at an interesting moment.&rdquo

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews.


Xenodesignerly Ways of Knowing

While it is impossible, as a human, to fully adopt an other-ed perspective, there are ways of getting closer to it. This can be useful in order to include a variety of perspectives in the design process, but it can also create interesting design outcomes. Such outcomes can be products or interactions that invite an audience into the perspective of the other, becoming a tool for exploring it. While speculative realism’s impact on fine art has been critiqued for having led to a rejection of the role of human experience, 18 xenodesign does not dismiss the human perspective, but seeks to reposition it as one among many.

Subjectivity and tacit knowledge are a part of this as elements of design’s specific ways of knowing. 19 Knowledge in design is not only describable and rationalizable, but also inherent in the objects of design: a subjectivity and intuition similar to that brought forward within xeno theories, when discussing the not-fully-knowable.

The following three approaches are intended as starting points toward exploring what xenodesign might mean in practice.


Why is there a seeming dichotomy between mobility and photosynthesis? - Biology

The mutualism between plants and arbuscular mycorrhizal fungi shows several market characteristics, including partner choice and adjustments to supply and demand.

Nutrient exchanges via communally formed arbuscules reduce trading costs the same way the formation of firms reduces ‘transaction costs’ on human markets.

Plants may discriminate among individual arbuscules, which are associated with subsets of the many nuclei found in a single fungus.

Subsets of polymorphic nuclei acting in unison are like co-ooperatives (‘co-ops’), institutions midway between independently acting traders and firms, that help traders coordinate their trading strategies and reduce competition among themselves.

Future models of the evolution of mycorrhizal mutualisms should concurrently incorporate their market-, firm-, and co-op-like characteristics.

The nutrient exchange mutualism between arbuscular mycorrhizal fungi (AMFs) and their host plants qualifies as a biological market, but several complications have hindered its appropriate use. First, fungal ‘trading agents’ are hard to identify because AMFs are potentially heterokaryotic, that is, they may contain large numbers of polymorphic nuclei. This means it is difficult to define and study a fungal ‘individual’ acting as an independent agent with a specific trading strategy. Second, because nutrient exchanges occur via communal structures (arbuscules), this temporarily reduces outbidding competition and transaction costs and hence resembles exchanges among divisions of firms, rather than traditional trade on markets. We discuss how fungal nuclei may coordinate their trading strategies, but nevertheless retain some independence, similar to human co-operatives (co-ops).


I wrote a brief essay on the nature of qualia, an issue I've been thinking about a lot lately. Read it and give me your opinions!

The Nature and Human Impact of Qualia

Qualia have captured the imagination of philosophy of mind for generations, with a substantial body of scholarly literature devoted to exclusive analysis of this subject. What are these mysterious phenomena both internal and external to mind, which create the appearance of our world while being simultaneously informed by environments, both inside and outside of particularized matter as we know it intuitively? Why do qualia differ between species and human individuals, even when surroundings are nearly identical, and looking at the opposite side of the coin, why are qualia similar enough that many billions of organisms can perceive, conceive, predict each other’s behaviors, intentions, even overall mental states despite differing conditions of their biochemistries and physiologies? Some phenomenon extremely basic to the structure of mind as such must exist, embodied in all these hugely variant lifeforms as a foundational dynamic of cognition, yet at the same time so subtly and diversely intricate that no two moments of mental experience can ever be regarded as exactly the same, even for the intensely self-observant human psyche.

A verified understanding of qualia pends much further research, but we can make some initial speculations based on current science. In particular, the application of quantum physics to biology sheds light on intriguing phenomena. Scientists have identified entanglement in photosynthetic reaction centers within which light-activated electrons of multiple chlorophyll pigments are actually more like a single perturbing quanta field than a particle transport chain, with energization transmitted to centrally located reaction center molecules responsible for initiating biochemical pathways that drive much of cellular metabolism in plants, stimulation that can take place from any direction and while diffuse electron wavicle structure is in any orientation. We can liken this type of quanta phenomenon to a subatomic body of water, where translation of light into kinetic energy at any point in the electron field generates a holistic ripple effect that never fails to evince statistical signs of reaction center activation in nearly identical proportion to UV exposure, total energy yield from any quantity or orientation of ultraviolet photons.

Though experimental proof is still lacking, the key functional role of ‘entanglement systems’ or hybrid electron waves spanning multiple molecules to a biological process as basic as photosynthesis makes it seem probable that this type of phenomenon is one of the core components of physiology, a pillar of life’s chemistry. From this provisional assumption, and it cannot be emphasized enough that it is wholly an assumption, we can consider possible wider implications.

First of all, we know that photons of different wavelengths have additive properties when combined: any two primary colors synthesize to produce a secondary color, all visible wavelengths together produce white light, and so on. Like photons, electrons also have a wavelike nature and no doubt additive properties within single atoms or small collections of molecules, which are probably minute enough to evade detection by the naked eye, and most likely decompose quickly in an inorganic environment due to decoherence from thermodynamic “noise” of kinetic entropy characterizing large aggregates of agitated mass.

However, in a physiological context, mass is much less subjected to entropic effects of kinetic motion, being stabilized as emergent structurality in biochemical pathways and additional types of molecular systems, so that these additive properties of electron wavelength may possibly be sustained for a prolonged period. Not only this, but electrons can hypothetically be entangled in multiple ways at once, creating a superposition in which additive properties of numerous entanglement structures are simultaneously congregated into larger entanglement structures, systems within systems that we might want to distinguish from the relatively simplistic situation inhering in photosynthesis, a categorically different phenomenon of hybridized ‘coherence field’. If coherence fields are found to be supported by the molecular assemblages of cellular biochemistry in the nervous system, especially likely to be discovered in the brain, their extremely complex additive properties may be what we know as ‘qualia’. In this scenario, qualia are not merely an immateriality supervenient on atoms, but instead a kind of exceedingly complex “color” or electromagnetically quantum resonance, material states intrinsic to tangible structure of the physical world.

The question then is how what we know as our conscious self-awareness can emerge from this basic qualia phenomenon. How do qualia give rise to the qualitative “experience” of a perceiver? A possible explanation is that biochemical and physiological structures exist, particularly in the brain, for synchronizing these sustained coherence fields, analogous to the clock mechanism of a CPU, so that qualia are metaorganized into a large array of experiential modules, parts of which compose the self-aware mind. Activity of these compound modules may manifest as the standing brain waves detected by EEG (electroencephalogram).

Based on the anatomy of macroscopic organisms, it seems that some level of constraint is imposed on the ability of these coherence fields alone to adequately manage behavior. Limitations probably arise from the division of labor necessary for strong, efficient mobility in an environment influenced by gravitation, with systems that must be devoted more exclusively to gas exchange (respiration) and distribution (circulation), excretion, access to nutritional sources, defense from predation, and so on, which precludes ubiquitous presence of standing waves and clock mechanisms in many tissues.

Nervous systems resolve this structural complication as a highly effective means of integrating far-flung parts of the body by extremely rapid electron coherence and tunneling in more or less dense webs of nerve cells, theoretically comparable to the electrical conductance of electronic devices, which allows organisms to simply grow bigger without prohibitive sacrifice of motility and general responsiveness to demands of ecosystems. Extreme density of nerve cells in the brain strongly hints that either some kind of upper limit exists to the possible size or synchronization of functional coherence fields in organic tissues, requiring a further mechanism of physiological connectivity, or molecular organization of nerve cells is key for somehow amplifying coherence field effects, perhaps in conjunction with the chemistry of glial cells. The vast variety of different kinds of neurons and glia in the brain may be an indication of why there are such widely varying classes of qualia - visual, aural, olfactory, gustatory, tactile, and so on - a gigantic miscellany in possibilities for additive resonance.

These insights point to some very definite theoretical conclusions. Qualia themselves, as a basic facet of matter, may be more fundamental than the modular experiencing we term ‘mind’. A bacterium or bacteria colony for instance could participate in an emergent phenomenon of qualia as a result of its molecular assemblages, even to the extent of remote analogy with the essence of human awareness, without a metaorganization sufficient to yield the kind of agency we call ‘self’. It may also be possible to induce sustained coherence fields as qualialike states in inorganic matter by some unknown mechanism, so that awareness and perhaps self-awareness are not confined to carbon-based material forms. Additional unintuitive phenomena of the quantum scale such as retroactive causality in photon entanglement indicate that entangled systems, hypothesized coherence fields and probably substance in general exceed the boundaries of spatiotemporality, a nonlocality transcending particular places and times that organic processes and perceptual mechanisms conceivably have access to. Ongoing synthesis of progressing experimental science with introspective psychology can possibly bring much more clarity to qualia as we investigate the nature of our own experiencing bodies, those of additional species, and their interactions with the environment, contextualizing these multifarious dynamics in theoretical constructs.

If qualia and emergent experiential modules of the mind are this deeply rooted in the very essence of matter, it shows human existence in a new light, not entirely unintuitive, but certainly not scientifically conventional either. Qualitative perception may have a multibillion year history, and qualia may be as ancient as the universe itself. Even the slightest signs of what would become large-scale civilization by contrast, with its institutions for inculcating high-level reasoning as the foundation of a prediction-based social economy, appeared on this planet only ten thousand years ago. From a historical perspective, qualitative perception is an unfathomably vast tapestry, while rationality in civic systems is like a single pixel. Nevertheless, reasoning has completely transformed ecosystems globally and given humans unprecedented influence on terrestrial life’s destiny. Humans are an intelligent species, but considering the colossal forces of nature that oppose this sliver of an opportunity for deeply reflective pauses we have attained, it is evident we must never take planned society for granted. The security of humanity’s civilized future demands that everyone make commitments towards advancing the precarious culture of rationality whenever possible, a personal conviction to distribute and put into practice conceptual tools that built, maintain and augment our humble edifice of sanity amongst the leviathan psychoactive essence of the material universe.

Science inclines in modern times to think of the human being as machinelike, a mechanistic system of coordinated parts analogous to our technological gadgetry. In the Information Age, this has transitioned towards viewing consciousness as a massively complex device of computation. The mind certainly calculates and predicts its surroundings, so in this respect it can be interpreted as performing many of the same functions as a computer, but even if conscious experience does someday turn out to operate according to fixed mathematical laws that resemble human engineering, its mechanisms must far surpass any theoretical idea we have remotely entertained. Scientific revolutions we can barely imagine are no doubt possible, but we can stagnate from excessive attachment to precedential theories, or even make civilization inhospitable for human actualization by overreifying, assigning names and concepts to phenomena without a culture that provides for successive improvements in comprehension and related practices. We must achieve balance between dedicated thought and entrepreneuring flexibility so that reason remains one of our primary psychical instruments rather than becoming our oppressive structural master.


Origin of animal multicellularity: precursors, causes, consequences—the choanoflagellate/sponge transition, neurogenesis and the Cambrian explosion

Evolving multicellularity is easy, especially in phototrophs and osmotrophs whose multicells feed like unicells. Evolving animals was much harder and unique probably only one pathway via benthic ‘zoophytes’ with pelagic ciliated larvae allowed trophic continuity from phagocytic protozoa to gut-endowed animals. Choanoflagellate protozoa produced sponges. Converting sponge flask cells mediating larval settling to synaptically controlled nematocysts arguably made Cnidaria. I replace Haeckel's gastraea theory by a sponge/coelenterate/bilaterian pathway: Placozoa, hydrozoan diploblasty and ctenophores were secondary stem anthozoan developmental mutations arguably independently generated coelomate bilateria and ctenophores. I emphasize animal origin's conceptual aspects (selective, developmental) related to feeding modes, cell structure, phylogeny of related protozoa, sequence evidence, ecology and palaeontology. Epithelia and connective tissue could evolve only by compensating for dramatically lower feeding efficiency that differentiation into non-choanocytes entails. Consequentially, larger bodies enabled filtering more water for bacterial food and harbouring photosynthetic bacteria, together adding more food than cell differentiation sacrificed. A hypothetical presponge of sessile triploblastic sheets (connective tissue sandwiched between two choanocyte epithelia) evolved oogamy through selection for larger dispersive ciliated larvae to accelerate benthic trophic competence and overgrowing protozoan competitors. Extinct Vendozoa might be elaborations of this organismal grade with choanocyte-bearing epithelia, before poriferan water channels and cnidarian gut/nematocysts/synapses evolved.

This article is part of the themed issue ‘Evo-devo in the genomics era, and the origins of morphological diversity’.

1. Introduction: unicells to multicells (and vice versa)

Unicells vastly outnumber multicells and are far more important for the biosphere in biogeochemical recycling. Bacteria and protists greatly exceed vertebrates in different kinds of organism too. Lamarck thought unicells so evolutionarily recent that they had not yet had time to inexorably become multicellular. Not so they existed billions of years longer than complex multicells and may outlive them. There are hordes of excellent unicellular niches multicellularity is often selectively disadvantageous. Yeasts evolved multiply from multicellular filamentous ancestors Myxozoa are parasitic unicells that evolved from animals with nervous systems (early-branching Cnidaria), losing epithelia, connective tissue, nerves and 70% of genes as useless, only their multicellular spores keeping nematocysts [1]. So how and why do some lineages become multicellular? Evolving multicellularity is mechanistically extremely simple. Every unicell group has a cellular and mutational potential to do so given a selective advantage.

Multicellularity evolves in two ways. Naked cells, as in animals and slime moulds, evolve glue to stick together. Walled cells modify wall biogenesis to inhibit the final split that normally makes separate unicells, so daughters remain joined. The ease of blocking that split allowed almost every group of bacteria, fungi and plants (and many chromists) to evolve multicellular walled filaments, more rarely two-dimensional sheets, most rarely three-dimensional tissues. Tissues require more geometric control of daughter wall orientation, as in embryophyte green plants and chromist brown algae both can grow longer than blue whales. Evolving tissues is selectively harmful to many walled multicells whose filaments are best for reproductive success. Almost all multicells retain unicellular phases (eggs, sperm, zygotes), so adhesion is temporally controlled and developmentally reversible—except for purely clonal vegetatively propagating plants or ‘colonial’ invertebrates (evolutionarily transient) the only organisms that are never unicellular.

Merely joining daughter cells together suffices to create efficient multicellular phototrophs or osmotrophic saprotrophs because their essential trophic features remain intracellular. A bacterial or protist phototroph can easily become multicellular while maintaining the same way of feeding and identical cell functions. An algal filament feeds (on light, H2O, CO2 and minerals) just as does a single cell so does a saprotrophic bacterial or fungal filament. However, a phagotrophic amoeba could not aggregate into a multicellular body and still locomote and feed the same way. Nor could most other protozoa. Many amoebae have become multicellular, but only temporarily for spore dispersal, not feeding. Aggregative multicellularity has produced multispore fruiting bodies numerous times in fundamentally different protist lineages (dictyostelids in Amoebozoa, Guttulinopsis in Cercozoa, in Ciliophora [2]), so is evolutionarily easy. That is because their multicellular phases are non-trophic they evolved purely for efficient aerial spore dispersal, free of conflict between need to feed and to aggregate spores still function as unicells. Thus, Dictyostelium [3] is irrelevant for properly understanding animal multicellularity origins.

2. Uniqueness of animal multicellularity

If evolving multicellularity is mechanistically so easy for bacteria and protists, then why did animals evolve only once? Primarily, because it is selectively immensely harder for organisms that feed by swallowing others or bits of them (a purely eukaryotic propensity) to switch from intracellular phagocytosis, as in amoebae or ciliates, to eating with a multicellular mouth and gut, whose cells have novel functions and structures absent in their unicellular ancestors. Animal feeding is effective only if novel cell types cooperate at a higher organizational level most give up the ability to feed or reproduce, huge selective disadvantages not easily overcome.

In 1866, James-Clark discovered choanoflagellate protozoa and their feeding on bacteria trapped by a collar surrounding their undulating cilium that generates the water current that draws them towards it. He noted that sponge collar cells (choanocytes) have the same structure and feeding method, correctly suggesting that sponges evolved from a choanoflagellate [4]. Often sponges were thought unrelated to other animals, being classified in Protista by Haeckel and Protozoa by Kent [5]. Schulze [6] argued that sponge spermatogenesis allied them with eumetazoa, but doubted the homology of choanocytes and choanoflagellates. For over a century, opinion ebbed and flowed between these contradictory views, until sequence trees proved that sponges are related to other animals and choanoflagellates are the closest protozoan relatives of animals [1,7–9]. Ultrastructurally, collars of both consist of a circlet of microvilli crosslinked by a mucus mesh into an extremely effective bacterial filter trapped bacteria are moved down to the cell body for phagocytosis [10]. Unaggregated microvilli are present generally on the cell body choanoflagellate microvilli exemplify a broader class of narrrow cell extensions (filodigits [11]) supported by a tight actin-filament bundle that probably evolved from ancestral opisthokont filopodia in the common ancestor of holozoa, the clade comprising animals, choanoflagellates and Filosporidia (figure 1). Fascin that crosslinks filodigit actin filaments, villin at their base, signalling protein Vav-1 at their tips, myosin X (transporting proteins to their tip), and other functionally related proteins, all originated in the holozoan last common ancestor [13], as did several other myosins [14] that strongly substantiates the conceptual distinction of filodigits from more generalised filopodia of deeper branching protozoa that lack them as well as filodigits being the key morphological synapomorphy for holozoa [11]. Filodigits, absent from other protists, were presumably present in the immediate ancestors of the first stem choanoflagellates from which animals almost certainly evolved they apparently evolved at the same time as cadherins that might initially have been involved in holozoan biology long before animals recruited them for epithelial cell adhesion [15]. Of choanoflagellate orders, the mostly surface-attached Craspedida of more primitive morphology and feeding mode are excellent models for stem choanoflagellates also, except for having lost some key animal precursor proteins that remain in more distant protists planktonic Acanthoecida whose collar filodigits manipulate secreted silica strips into elaborate loricas (enabling a novel filter feeding mode) are highly derived, not directly relevant to animal origins [10].

Figure 1. Cell structure divergence in phagotrophic non-amoeboid flagellates provided the basis for evolving animals, fungi, plants and chromists. Pseudopodia evolved secondarily, myosin II providing the basis for pseudopodia in animals, Amoebozoa (and Percolozoa) and muscles. Chloroplasts, originating when the plant ancestor enslaved and modified undigested cyanobacteria, were transferred laterally (red arrow) to make chromists (e.g. brown seaweeds, diatoms, dinoflagellates) whose ancestor modified an enslaved undigested red alga. The most basic eukaryote structural dichotomy contrasts Euglenozoa (parallel centrioles cilia with paraxonemal rods cytopharynx for feeding) and excavates (Percolozoa, Eolouka, Neolouka: orthogonal centrioles: no paraxonemal rods feeding by phagocytosing prey drawn into a ventral groove by posterior ciliary currents). The pre-animal lineage lost excavate groove-feeding by evolving ventral ciliary gliding locomotion to generate Sulcozoa, protozoa with a dorsal proteinaceous pellicle (blue). Irrespective of whether the eukaryote tree is rooted within the protozoan subkingdom Eozoa as shown (most likely) or beside Eolouka-like Reclinomonas with the most primitive mitochondria, the immediate ancestors of animals (Choanozoa) arose by loss of the anterior cilium and sulcozoan dorsal pellicle to make opisthokonts (in red) with a radically simplified, more radially symmetric, microtubular cytoskeleton. Long actin-supported filodigits arose in the ancestor of Filosporidia and choanoflagellates and became a circlet of microvilli to make the choanoflagellate/sponge collar for catching bacteria. Filosporidia comprise Filasterea, Ichthyosporea, Corallochytrea [12]. The four derived kingdoms (e.g. ANIMALIA, PLANTAE) are shown in upper case all taxa in lower case belong to the basal eukaryotic kingdom Protozoa.

Among extant animals, only sponges could have evolved directly from protozoa without changing feeding mode. The key problems in understanding animal origins are therefore how and why sponges evolved from a craspedid-like stem choanoflagellate and later generated all other animals. I attempt to explain both after briefly outlining enabling protozoan innovations. I shall emphasize simple conceptual aspects of the choanoflagellate/animal transition, often overlooked but more important than discovering extra protozoan genes suitable as precursors to animal functions. Such ancestral features exist in both choanoflagellates and more distant protozoan relatives of substantially different cell structures and feeding mode [12].

In the light of site-heterogeneous trees using 187 protein sequences [16,17], figure 1 summarizes the major eukaryote clades and key steps in eukaryote cell evolution that paved the way for later innovations that generated animals. Like choanoflagellates, Filosporidia (next most distant animal cousins) belong to the protozoan phylum Choanozoa that ancestrally evolved a swimming mode with a single posterior cilium (i.e. opisthokont—‘posterior oar’ in Greek) like archetypal animal sperm or fungal zoospores that evolved by modifying ancestral opisthokont cell structure [11,16]. Immediate outgroups to opisthokonts are successively more distant branching predominantly biciliate lineages of phylum Sulcozoa that typically move not by swimming but by gliding on surfaces by ciliary surface motility propelling one semi-rigid cilium and feed by emitting newly evolved, bacteria-grabbing, branching pseudopodia from the cell's ventral ciliary groove [11,16].

Sulcozoan flagellates clearly could not have retained their characteristic locomotory or feeding modes had they evolved glue to stick together as a multicellular organism such mutants would necessarily quickly starve to death. Nor could their immediate ancestors—three successive groups of swimming, not gliding flagellates (i.e. Neolouka, Eolouka, Percolozoa) collectively called excavates because their ventral groove looks more obviously scooped out [11,17]. The groove phagocytoses prey propelled therein by both cilia, the posterior often having one or two lateral vanes to increase its thrust. Their ancient groove-supporting asymmetric cytoskeleton, with five distinct microtubular ciliary roots and many characteristic filaments, was inherited by Sulcozoa, initially with diverse minor modifications, but radically simplified and made more symmetric during the origin of the opisthokont body plan by anterior ciliary loss, possibly in association with a protochoanoflagellate feeding mode [11].

Knowing the structure and evolutionary potential of the closest relatives and ancestors of animals (figure 1) and that opisthokont cells were radically simplified compared with their ancestors does not directly explain animal origins, but helps distinguish central from peripheral aspects of the process and avoid pitfalls from erroneous assumptions about ancestors. Most things we inherit from our unicellular ancestors evolved before the excavate/Euglenozoa split. Only a few arose within the scotokaryote clade that embraces opisthokonts, Amoebozoa, Sulcozoa and Neolouka, and is sister to the cytologically substantially different plant/chromist clade (Corticata) [17].

Integrins and associated molecules used for epithelial cell adhesion to extracellular matrix (ECM) were secondarily lost by choanoflagellates and fungi without full genomes for the deepest branching Sulcozoa, the exact point of origin is unclear (figure 1): though not yet known for branches before Breviatea, integrins might have arisen earlier with scotokaryote pseudopodia, for mediating reversible adhesion to the substratum and/or pseudopodial actin bundle attachment/assembly via talin/vinculin that certainly evolved earlier [12], at least prior to Amoebozoa. If, instead, integrins help actin attachment to sulcozoan dorsal pellicles, they possibly arose one node earlier. Determining intracellular distribution and functions in early Sulcozoa would clarify the integrin adhesion system's original functions as genomes are known only from very simplified and derived Amoeboza lacking integrins, they are also needed for early diverging Amoebozoa with more complex extracellular coats/thecae [18] that might involve integrins. Though lacking typical integrins, Dictyostelium has a β-integrin-like adhesion protein [19] and its multicellular prefruiting 'slug' evolved ahaerens-like junctions involving preexisting actin-filament-binding catenins [20] (convergently with independently evolved animal adhaerens junctions) but unlike sponges and other animals could not recruit cadherins as they only evolved later (with filidigits in ancestral holozoa) [12].

On present evidence, excavates and Sulcozoa, successive ancestors of Choanozoa, never evolved multicellularity, nor did any Choanozoa except choanoflagellates whose unique cell structure and feeding mode preadapt them for evolving multicellularity. Therefore, discovery in non-choanoflagellate Choanozoa and Sulcozoa of integrins and of cadherins, and synaptic proteins and other neural channel proteins in choanoflagellates and filosporidia [15,21], does not explain how animals originated. It tells us (unsurprisingly) that pre-existing proteins were recruited for the job and diversified by gene duplication and divergence (standard for any substantial innovation) but not why these protozoa failed to become animals and only one lineage did. We must identify selective forces that make it impossible for most protists to evolve a body with a gut and explain why only one lineage ever did. I contend that it was not the presence of potential glue molecules, but the rare ability of choanoflagellate cells to stick together yet still feed as before that made stem choanoflagellates our ancestors. Inability to do this would strongly select against similar aggregative mutations in other groups.

3. Choanoflagellate and flagellate multicellularity

In choanoflagellate colonies, every cell can feed. To become a sponge, the majority must abandon feeding as collar cells, lowering feeding potential dramatically. A sponge could evolve only if a body were made where reduction in feeding capacity caused by a lower ratio of feeding to non-feeding cells was more than compensated by an indirect increase in feeding or survival efficiency. For understanding animal origins, the key problem is not how cells evolved a capacity to stick together (trivial)—or even why—but defining the selective forces that promoted the fundamental differentiation between sponge feeding cells (choanocytes) and non-feeding cells and between cells that stick together as epithelia and connective tissue cells embedded separately in a gelatinous mesohyl. Did epithelia evolve first or did epithelia and mesenchyme coevolve?

Four different ways of making multicellular choanoflagellates exist. Many become ‘colonial’ sessile organisms by evolving thin extracellular stalks that join cells together to form branched tree-like structures analogous to corals or plants [5,10]. Other flagellate groups also evolved multicellular sessile lineages with branching stalks many heterotrophic, e.g. biciliate bicoecids (heterokont chromists), pseudodendromonads (heterokont chromists), sessile ciliates (e.g. Carchesium, Zoothamnion) some algal, e.g. chrysophyte Dinobryon. Mucilaginous multicellular branching structures are formed by Rhipidodendron (cercozoan chromists) or Phalansterium (uniciliate Amoebozoa). As no branching protists evolved a multicellular tissue, similar ‘colonial’ choanoflagellates are probably not directly relevant to animal origins. Nonetheless, they show that various linked flagellates can still feed in the same way as when unicellular, and their frequency suggests that branching stalks advantageously enable them to sweep prey from a much larger water volume than can one sessile cell. Filtering more water by a different sessile body form is, I argue, the selective advantage that made sponges.

More rarely, choanoflagellate multicells arise by linking adjacent cells by their collar microvilli as in Proterospongia choanojuncta, but I doubt this had a potential to yield a sponge. Sponge collars also join laterally often by a second mucus mesh to achieve 100% removal of suspended bacteria [22], showing intercellular cooperation efficacy.

The loricate Diaphanoeca sphaerica, where cells often clump in hollow balls with cilia pointing inwards [23], exemplifies a third multicell type incapable of progressing to a tissue. Comparing this with a sponge choanocyte chamber [24] was misleadingly superficial as Diaphanoeca, like other loricates (Acanthoecida), are tiny cells suspended within a much larger lorica of siliceous strips porous to water currents carrying prey. Aggregating porous loricas by connecting longitudinal strips allows colonial feeding despite cilia pointing inwards, as the collar outer surface that traps food still faces outwards. Water and bacteria can pass through the lorica mesh or wide interlorica spaces, so feeding mode is unchanged compared with unicells cell bodies are not in contact so could not evolve into an epithelium to make a sponge. Acanthoecida are necessarily an evolutionary dead end.

Non-loricates (Craspedida) never aggregate with cilium facing inwards like sponges as that would suicidally stop collar-based feeding. Sphaeroeca is a multicellular planktonic craspedid whose colonies are hollow balls with a surface cell monolayer, associated by cell bodies not collars, analogous to the alga Volvox that Hardy [25] invoked as a potential animal ancestor because of its simple feeding. The craspedid Salpingoeca rosetta reversibly makes little multicellular balls, a capacity influenced by bacteria [26]. Numerous other flagellates, e.g. chrysophyte chromists, evolved similar free-swimming multicell balls. These would be incapable of progressing towards a multilayered Haeckelian gastraea, because gastrulation-like internalizing cells would prevent their feeding, without immediate benefit, and thus be strongly disadvantageous. However, by settling on stable surfaces as sessile filterers, they would encounter new selective forces favouring cell differentiation, enabling animal origin. Sponges evolved thus from a craspedid-like stem choanoflagellate.

4. Evolving a triploblastic presponge

Willmer emphasized the basic dichotomy between ciliated epithelial and non-ciliated, amoeboid, connective tissue cells as fundamental to animal development [27]. Figure 2 summarizes a potential pathway by which a stem choanoflagellate lineage, initially a standard swimming ball of choanocytes, could transform into a sessile precursor of sponges by evolving comparable somatic cell differentiation to anchor itself to a rock. The new cell type was a basal non-ciliate anchoring cell that secreted ECM—effectively a basal pinacocyte. An ECM of mucopolysaccharide and collagen would form a supportive mesohyl skeleton between two monolayer sheets of choanocytes—the ancestral choanoderm. The selective advantage of this novel three-layer structure would be filtering food from a much larger volume of water, just as branching colonial choanoflagellates do. ECM support would allow a much larger structure that could overtop simple branched choanoflagellates with choanocytes only. This could have increased food caught by choanocytes more than enough to compensate a presponge for loss of filter-feeding capacity by basal pinacocytes and ECM secretion costs. If so, selection for taller, wider multicellular filters processing larger volumes of seawater would immediately unavoidably ensue. Flow hydrodynamics for maximizing catch and architectural principles maximizing support and filter area would impose novel selective forces yielding similar structures to bivalve mollusc gills. Pinacocytes would develop contractile actomyosin and surface adhesion analogously to an amoeba to spread flattened extensions and cell contacts over the holdfast portion of the sessile lamina with least cost. They retained a capacity for phagocytosis, thus providing a primitive immune system by digesting potentially invasive bacteria for which mesohyl was a nice habitat and food.

Figure 2. Evolution of an archetypal animal, a presponge (vii), from a stem choanoflagellate (i–ii,v) prior to integrin loss by crown choanoflagellates. Choanoflagellates feed by catching bacteria (B) drawn by ciliary water currents (i, arrows) to their collar filters the cell body phagocytoses them (ii). Extant craspedid choanoflagellates may be unicells (i,ii) or daughter cells may stick together by branched stalks (iii) or collar microvilli (iv) to make sessile multicells or via cell bodies to make planktonic swimming balls of cells (v). The first animal could simply have evolved (horizontal black arrow) by such a ball of cells joined laterally by cadherins settling onto a rockface (cross-hatched), differentiating non-ciliated pinacocytes for attachment and for support secreting extracellular mesohyl (turquoise) by both cell types and attached to them via pre-existing integrins (vi). This simplest presponge presumbly budded off ciliated swimming balls for dispersal (blue arrow), and probably had to evolve nutrient transfer from choanocytes to pinacocytes. (vii) Competition for filtering larger water volumes led to larger, stronger, three-layer (prototriploblastic) feeding laminas with mesenchyme cells specializing in ECM secretion sandwiched between choanocyte epithelia. Larger laminas led to divergent selection for large eggs capable of rapid cleavage and more numerous smaller sperm, both originally differentiated from choanocytes (rightmost blue arrows). As size increased, the pluripotent nonciliated mesenchyme cells differentiated into proliferative stem cells (archaeocytes: thenceforth the usual precursors of eggs, choanocytes continuing to generate sperm) and terminally differentiated cells (lophocytes) secreting collagen fibres to increase mechanical strength.

The primary dichotomy between uniciliate choanocyte and non-ciliate pinacocyte is also mirrored by that between sperm and egg. Therefore, part of the same gene switches needed for somatic differentiation could also be used to differentiate gametes. Once a three-layered structure with just two somatic cell types evolved, presponges could become quite large (compared with choanoflagellate unicells) selection for rapid establishment of a large embryo would strongly favour oogamy (large egg and numerous small sperm) by modifying choanocytes, presumably hermaphrodite. The animal bauplan was in place once a selective force for ever-larger filtering structures built from two dissimilar cell types existed: two germ line and two soma cell types. Accidental fragments could also reproduce vegetatively as choanocytes retained pluripotency [28]. There was no necessary sacrifice of reproductive potential as in Dictyostelium dead stalk cells.

Another selective advantage of evolving mesenchyme and massive tissues perhaps gave extra impetus to early animal evolution. Mucilage easily harbours bacterial symbionts potentially able to provide enough extra food to repay a presponge several times over the trophic and reproductive costs of non-feeding cells. Cultivating cyanobacteria in ECM mucilage would make the photophagotrophic consortium an extremely effective competitor with merely branched choanocyte-only colonial choanoflagellates. Lichen fungi can survive solely by cultivating cyanobacteria a presponge could be even better off, being also a phagotroph able to grow far faster than a lichen in bacteria-rich water. Great Barrier Reef sponges 1–2 m high are often red through being packed with cyanobacteria whose biomass is greater than that of the sponge cells. Lake Baikal giant freshwater sponge tissues cultivate green algae. Both habitats are oligotrophic, making internal algae especially advantageous, but even in habitats rich in particulate food, the majority of sponge species are often photosynthetic [29]. In organic-rich habitats, a presponge could probably eat enough bacteria to subsist without growing algae. Even sponges without cyanobacteria or green algae have a huge bacterial symbiont biomass, often in special bacteriocytes, presumably providing trophic or other advantages such as antibiotic defence against invaders [30]. All choanoflagellates live with bacteria of many kinds. Choanoflagellate–bacteria interactions other than simple predator–prey must affect modern choanoflagellates [31], but could also have had a role in animal origins [32]. Making a tissue without cell walls invites others to eat it before bilateria, enemies were mainly microbial.

Extra cell types could be added relatively simply to help presponges to grow bigger and be less susceptible to environmental damage. An individual could grow basally across a rock and erect multiple laminae. Spatial controls evolved to prevent laminae from interfering with each other. Presumably, various morphologies and arrangements and ratios of the two basic cell types were experimented with, giving different compromises between maximizing feeding and mechanical stability. An early innovation necessary for large structures was to increase the ECM-synthesizing cells initially perhaps by evolving a third cell type—the ancestral archaeocyte that left the epithelium, entering the mesohyl for secreting ECM in all directions, making a triploblastic tissue with mesenchyme sandwiched between two epithelia. Nowadays archaeocytes and choanocytes are the demosponge stem cells, expressing PIWI double-strand RNA-binding domain proteins whose short-RNA related functions are associated with germline and stem cell maintenance in higher animals [28] as well as with RNAi and chromatin dynamics [34]. Generally, sperm arise from tiny choanocytes and eggs from many-fold larger archaeocytes [35] possibly therefore the non-ciliated archaeocytes originated from ancestral choanocytes as egg precursors independently of non-ciliated terminally differentiated pinacocytes that like spicule-forming sclerocytes and other non-stem cells do not express PIWI proteins. Very likely PIWI suppression in pinacocytes arose in the ancestral presponge with only two somatic cell types when its ancestral function of protecting proliferating cells from transposons (that goes back even to prokaryotes) became unimportant in the very first dead-end somatic cells.

5. Defects of some other scenarios

Site-heterogeneous multigene trees (technically the best) maximally support choanoflagellates being sisters to animals [1,33] they never branch within or as sister to sponges, as the implausible idea that choanoflagellates evolved reductively from sponges [36] requires. Myxozoan parasites having become somatically unicellular (spores are multicells with uniquely cnidarian nematocyst minicollagens [37]) is one of many examples of selectively comprehensible gross parasitic reduction, but does not make such selectively incredible drastic simplification of a free-living sponge even remotely likely and should not have been cited in its favour [36].

Site-heterogeneous multigene trees equally strongly show sponges as a clade, disproving Nielsen's assumption that eumetazoa are more closely related to homoscleromorphs than others, and invalidating his twin assumptions that ancestral animals were lecithotrophic and eumetazoa secondarily lost lecithotrophy [24]. His suggestion that the first event in animal evolution from a spherical choanoflagellate colony was evolving internal non-ciliate, non-feeding cells to make an ‘advanced choanoblastea’ exemplifies selectively untenable Haeckelian idealistic morphology such a change would drastically sacrifice feeding potential with no positive benefit and be quickly eliminated by competition. It has been insufficiently recognized that evolving a non-germline soma is not inherently advantageous, but a severe reproductive cost that has to be offset by an extremely strong novel selective advantage. Had a ‘choanoblastaea’ been advantageous, such two-layered pelagic choanoflagellates should still exist their supposed sponge descendants occupy a separate adaptive zone, so would not have competitively eliminated them as happened for the selectively plausible sessile intermediates of figure 2. The key innovatory sessile benthic stage (vi) of figure 2 provides a definite selective advantage for presponge non-feeding cells, unlike a pelagic choanoblastaea.

6. Evolving a water-pumping sponge

This presponge was not a sponge, for it lacked an aquiferous system (AS) with incurrent pores (ostia) and larger excurrent osculum or oscula. AS architecture has two advantages: (i) it increases food supply by pumping much larger water volumes past the choanoderm (ii) compared with the essentially ‘free-living gills’ of the presponge, placing the choanoderm inside a globular or encrusting body protects choanocytes from damage by sand and other things swept against them by vigorous water currents and from damage by the currents themselves. Essential innovations making a sponge were (i) controlled formation of ostia of appropriate size, frequency and distribution (ii) rearrangement of pinacocytes and choanocytes to internalize the latter, make a more compact less easily damaged body, and optimize water flow through internal choanoderm-lined channels. Ostia are intercellular in all Homoscleromorpha and most demosponges, but are formed by channels through specialized porocytes in Calcarea and not obviously homologous contractile porocytes in a few haplosclerid demosponges. I suspect they originated not by evolving a new cell type but by spatially controlling pinacocyte contacts and geometry porocytes evolved later independently in Calcarea and haplosclerids. If so, ostia arose as part of the supracellular rearrangements that made an axially polarized water channel system. This major innovation almost certainly depended on prior evolution of morphogen gradients and homeobox and other spatially controlled switch genes that sponges share with Eumetazoa [22,38]. Benefits of an effective AS might have been the prime driving force for the evolution of animal ‘head/tail’ polarity—nothing to do with heads or tails: the Wnt anterior–posterior axis system probably controls sponge AS development [39,40]. More likely, Wnt axial gradients arose earlier still in vendozoan presponges.

Making AS development and functioning more efficient probably entailed differentiating pinacocyte subtypes: specialization of some as myocytes to exert some control on oscular and ostial opening and multiplication of non-epithelial mesohyl cell types. The branched mesohyl cells that synthesize a variety of neurotransmitters are obvious candidates for precursors of eumetazoan nerve cells, requiring only the origin of electrosensitve channels to cause action potentials and synapses to make a nerve net. The syncytial body form and calcium/potassium action potentials of hexactinellid glass sponges are secondary, not the ancestral condition for sponges, as hexactinellids are related to demosponges not the deepest lineage [1]. They are therefore not directly relevant to origins of animals, sponges or eumetazoa. It was long overlooked that sponges of all four classes are contractile, as contractions are typically slow, taking 15 min to hours in demosponges pinacoderm mediates this [41]. Many are in constant motion, contracting ostia and water channels and relaxing body parts to modulate pumping [42]. Sponge behaviour primarily involves water-filtering and protection against damage by larger particles or storm surges, but can be adapted to seasonal temperature changes, increased suspended sediment, or even spawning by other sponges or used to expel wastes by ‘sneezing’. It is untrue that they lack sense organs [22]. All have non-motile oscular sensory cilia that use calcium channels for behavioural control [43]. Calcium control of ciliary reversal is well studied in Chlamydomonas and could be a general property of eukaryote cilia that evolved during the origin of two structurally and behaviourally dissimilar cilia in the eukaryote cenancestor [44]. In the demosponge Ephydatia, oscular sensory cilia lack the centre-pair microtubules as in eumetazoan sensory cilia [43]. Early sponges likely had a solenoid body form [38] with a higher ratio of choanocytes to non-feeding cells than the simplified asconoid of figure 3.

Figure 3. Origins of sponges, Cnidaria and bilateria with homologous body axis polarity. (i) Internalizing presponge choanoderm (yellow) by overgrowth of the pinacoderm (grey) and epithelial rearrangement into an asconoid body form, with incurrent ostia and exhalent osculum, could have established the sponge body plan without adding new cell types. The key innovation may have been Wnt axial prepatterning translated into spatially controlled differentiation by homeodomain transcription factors. (ii) Origin of perioscular and septal nematocysts for catching larger food and tentacular growth led to loss of ostia (as convergently in carnivorous sponges), so spongocoel became coelenteron and osculum the mouth pre-existing neurotransmitter-secreting cells made synapses (elaborations of cadherin-joined foci) with nematocytes, sensory cells, tentacular and perioral myocytes and each other, making a nerve net controlling feeding behaviour of this stem anthozoan. Not shown is that nematocytes probably originated aborally from sponge flask cells slightly earlier to improve larval settlement and ancestral cnidaria probably evolved pharnyx with bilaterally symmetric ciliary feeding currents and nematocyst-rich octomerous septa for trapping food for extracellular digestion before tentacles (see §8). In some anthozoan polyps, pharynx and coelenteron develop as separate cavities in solid tissue masses (iii) mouth and pharynx/coelenteron connection form by secondary channels opening later (iv). Bending the elongated pharyngeal primordium laterally to fuse basally with the body wall before the lower channel opened could make anus and coelom in one step (v) former endoderm becomes the coelomic and stomodaeal epithelium the gut lining.

The greater complexity of true sponges over presponges required planktonic ciliated larvae for dispersal to new fixed sites that grew big enough to transform immediately into a tiny triploblastic sponge with internal choanoderm able to feed at once. Abundant egg yolk enabled more rapid development than feeding by surface choanocytes, making sponge larvae lecithotrophic unlike planktotrophic presponge and ancestral eumetazoan ciliated larvae. Larvae evolved phototaxis using cryptochromes [45], not rhodopsin as in eumetazoa some respond to gravity and have behaviour of similar complexity to eumetazoan larvae with nerves. Like rhodopsin, calcium control of cell behaviour first evolved in eubacteria [46,47] not stem eukaryotes [48], which simply adapted it for the control of actomyosin that evolved in association with bacterial wall loss and the origin of phagotrophy and endomembrane system [44,49].

The phrase ‘from amoeba to man’ epitomizing Haeckel's early phylogenetic views doubly misleads. Amoebae are not primitive but arose from zooflagellate ancestors independently in each of the three ancestrally biciliate eukaryotic supergroups [18]. Epithelial polarized vesicle secretion selectively to apical and basolateral membranes, fundamental to animal organization, is prefigured in zooflagellate cell polarity that may hold molecular clues to its origin [50]. Subcellular differentiation merits intensive study in choanoflagellate models, including spatial differentiation of ciliary and cell membrane proteins. Very likely, membrane protein targeting also differs between intra- and extracollar regions and for microvilli. Selective protein targeting to different membrane regions must have evolved with cilia, exemplified, in exquisite detail, by cytoskeletal architecture and membrane protein targeting to the ciliary pocket of trypanosomes [51], which are Euglenozoa as far from us on the tree as can be (figure 1), showing eukaryotic cell asymmetry's antiquity. Understanding asymmetric cytoskeletons and spatial control of membrane protein secretion of the whole spectrum of zooflagellates as well as sponges will do far more than genomics for elucidating the physical forces that made animals. Making animals is a four-dimensional, not a one-dimensional problem. Many cytoskeletal protein sequences evolve rather fast and have numerous confusing paralogues, not lending themselves easily to one-dimensional bioinformatics. We need phylogenetically informed molecular cell biology with a developmental slant of the form-generating molecules (and their three-dimensional structure, a huge crystallographic challenge) to understand cell morphogenesis, the basis for animal bodies and nervous systems. To learn about learning, we must understand molecular bases of neuronal form, prefigured in branching sponge cells and synapse dynamics. Unlike stem choanoflagellates, merely temporarily polarized aciliate amoebae never evolved into Hacekel.

7. Zoophyte 1 origin of eumetazoa and the nervous system

The larger larvae of true sponges provided a novel, hitherto unexploited, food for predators. One stem sponge lineage, I suggest, evolved nematocysts to catch and digest them, thereby becoming the ancestor of coelenterates (Cnidaria, Ctenophora), a clade on the best multigene trees [33]. Nematocyst discharge of ECM [54] anchors the aboral pole of settling cnidarian planula larvae [55] just as do secretory flask cells at the aboscular pole (similarly anterior when swimming) of sponge larvae [56]. Flask cells are the only larval sponge cell type to coexpress the majority of post-synaptic protein homologues [57], so I suggest, evolved directly into nematocytes by evolving capsular/tube minicollagens [58] and cnidoin elastomer that facilitates their nanosecond discharge [59]. Nematocytes are not independent effectors [60] but innervated by chemical synapses (responsive to glutamate and GABA (γ-aminobutryic acid) in Hydra [61]), and thus post-synaptic effectors. I suggest their primary function was to mediate larval settlement and their more complex feeding role evolved only after synapses first evolved between sensory cells and nematocysts and were then secondarily formed with muscles and probably simultaneously with larval ciliated cells, improving adult feeding and larval guidance. If so, chemical synapses arose to facilitate rapid concerted ECM discharge by the aboral cluster of secretory cells that cnidarian and sponge larvae share. Sponges already had glutamate, GABA and NO control of behaviour [62], and synaptic proteins had polarized secretory functions as early as the ancestral unicellular holozoan [21] very few synaptic proteins are restricted to animals with synapses, choanoflagellates have many [63]. As Trichoplax (unlike sponges) has numerous presynaptic protein precursors as well as gap junctions, chemical and electrical synapses probably both originated after the pre-cnidarian lineage diverged from placozoa yielding an anthozoan-like stem coelenterate. Thus, neither muscular [60] nor ciliary control [64] initiated neurogenesis, but neurosecretion, the third, underappreciated universal effector. 1

Key to neurogenesis was a multicellular precursor with neurotransmitter-making cells and already adjacent receptor and effector cells linkable by evolving synapses under a strong selective advantage, exactly as this flask cell to nematocyte transition postulates without missing links or improbable events. Thus, improving the sessile zoophyte lifestyle by increasing survival (e.g. against waves tearing settling larvae from rocks) at the crucial, but uniquely vulnerable, pelagic–larval/benthic–adult transition was, I contend, the selective force for evolving synapses, ultimately leading to brains, culture and science. Synapses evolved to make ciliated larval settlement faster and more effective by neural coordination of concerted banks of nematocysts under the control of ciliated sensors that selected the best sites. Flask cell precursors concentrate at the aboral pole. Nematocysts remain there to mediate settlement but concentrated also around the osculum (making it a mouth) and along ancestral anthozoan protosepta to trap food.

Adding synaptic junctions not only between sensory cells and nematocysts, but between sensory cells and branched pre-existing branched transmitter-making cells (making internuncial neurons) and myocytes, would establish local neuromuscular control by a nerve net. This speeded oscular contraction making it an effective mouth, its reversible closure plus adhaerens junctions being key innovations for initial extracellular digestion of larger prey caught by oral and septal nematocysts. Having established neuromuscular synapses, pre-existing voltage-dependent Na + and K + channels (both originating in bacteria) were modified to generate sodium/potassium action potentials in longer nerve cell branches for distant coordination of feeding responses, making eating more efficient—a selective advantage an automatic corollary of this explanation of synaptic origin. Action potentials evolved many times, thus easily—not only in hexactinellids, but also filamentous fungi, plants and ciliate protozoa [65]. Axons easily evolved by centrosomally directed cytoskeletal elongation. During gradual changeover, choanocytes and nematocysts could both be used for feeding: no traumatic hopeful-monster, but simple gut evolution from ideal precursors. Catching larger prey was made more efficient by circum-oscular projections evolving into stem anthozoan tentacles. Pre-existing myocytes contracted tentacles to place the prey inside the osculum for better absorption.

Before tentacles evolved, partially redirected ciliary currents (importing food and exporting waste through the mouth) likely made an asymmetric single-siphonoglyph protopharynx and eight functionally complementary nematocyst-rich septa (arguably modified from internal projections within a sponge of more complex AS morphology than the figure 3 asconoid depicted for simplicity) trapping food within the incipient gut evolved octomerous bilateral symmetry in the ancestral coelenterate. Much later a few demosponges convergently evolved carnivory, some like Cnidaria losing choanocytes and AS [66], without nematocysts or nerves, showing they can evolve carnivory, but carnivory per se does not make nerves.

Without giving reasons, Nielsen unjustifiably asserted ‘it seems impossible to derive eumetazoans from an adult sponge’ [24, p. 148]. On the contrary, to evolve a coelenterate from a stem sponge depended on preexisting epithelial adhaerens junctions, enabling extracellular digestion [24], thus converting spongocoel into gut lumen and required only two key cellular innovations: secretory nematocysts for enhancing larval settling and trapping metazoan prey action potentials in protoneurons as well as loss of choanocyte collars and ostia. Neither is mechanistically or selectively unlikely given copious sponge molecular precursors and complex homologous axial triploblastic organization, both key innovations would have been evolutionarily far easier than origins of either presponges or sponges, so coelenterates should have evolved essentially immediately after sponges, which fits the fossil record. A flask-cell/nematocyst transition makes a cnidarian more simply than Nielsen's assumption of neotenous conversion of a lecithotrophic homoscleromorph sponge larva into a planktotrophic eumetazoan larvae that added an entirely novel adult sessile stage by loss of the whole sponge adult, which did not explain how or why nematocysts originated or how they were linked with synaptic origins. His scenario is far more complex and less plausible selectively than nematocysts converting stem sponge larvae to planulas and switching adults from bacterial to metazoan prey. Nielsen [67] correctly argued that ciliated larvae were present in ancestral eumetazoa and later independently lost by those lacking them, but basal sessile eumetazoan adults did not, as he supposed, evolve from them independently of adult sponges. Thus, the ancestral animal life cycle was a non-Haeckelian alternation of feeding planktonic larvae and sessile feeding adults, lecithotrophy and direct development being multiply derived. Neoteny (accelerated sexual development) probably did occur in the independent of origins of Trichoplax (gut loss by secondary flattening when switching to benthic feeding after adhaerens junctions and gap junctions, but before tentacles/neurons, evolved) and Ctenophora.

8. Coelenterate unity and diversification

I have argued that the ancestral coelenterate was a bilateral octomerous stem anthozoan that lost choanocyte microvilli as neurally controlled nematocyst/tentacle feeding on larger prey improved, its mouth evolving from the osculum, and ostia closed (except for a pore at the body base in many anthozoa several in ctenophores) suppressing water channels, yielding a single body cavity, the coelenteron. Choanoderm and endoderm are homologous [68], as are larval swimming with anterior sensory cilia and posterior aboral settlement, and Wnt signalling patterns specifying oral–aboral axes and nervous systems in eumetazoa, including coelenterates [69–71] and sponges [40].

Contrary to dogma, Anthozoa, Scyphozoa and Cubozoa are mostly triploblastic with true mesoderm [72–74]. The Huxley/Haeckel idea that diploblasty preceded triploblasty is wrong. Huxley invented the diploblast concept for Hydrozoa, the only true diploblasts [73]. Phylogenetically they nest deeply within Cnidaria as sister to the triploblastic jellyfish, together making clade Medusozoa [1]. Medusozoa arguably originated by an early anthozoan evolving vegetative scyphistoma-like transverse budding to make planktonic tentaculate forms that could disperse and feed immediately as a medusa without needing metamorphosis from a planula. Sponge and anthozoan larvae and large planktonic protists were probably its initial prey, but as bilateria evolved giving larger necton Scyphozoa and Cubozoa diversified nematocysts and poisons for larger more active prey, but Anthozoa typically kept to smaller snacks, developing large individual polyps (sea-anemones) or most often spreading multipolyp modular body forms and reef formation with dinoflagellate photosynthetic symbionts in oligotrophic waters. Hydrozoa focused on a branching hydroid form with only tiny dispersive medusae and simplified both by narrowing the mesogloea, so became diploblastic. Hydromedusae swim by jet propulsion via whole body contraction that may have been mechanically favoured by extreme mesogloeal thinning through losing mesenchyme cells.

Probably before Medusozoa originated, a stem coelenterate switched completely from benthic to planktonic life by evolving multiaxonemal macrocilia and comb plates (with reversible beat, but swimming typically with mouth anterior, opposite to medusae) and losing nematocysts no longer required for settlement and accelerating oral and sexual development. This radical shift in adaptive zone and developmental fate of the ancestral planula larva entailed numerous unique innovations giving Ctenophora such a different body form from crown cnidarian adults, and unique embryology. In Cnidaria, the larval nervous system is concentrated largely aborally but degenerates during metamorphosis after settlement, being replaced by an oppositely polarized adult system with an oral focus [75]. Unsurprisingly, by eliminating settlement and metamorphosis, ctenophores retained the originally larval neural organization, uniquely developing the statocyst as a neural focus. Ctenophore homologies should be sought with transient larval cnidarian, not adult nervous systems. Although most larval cnidaria lack mouths, some anthozoan larvae have them—accelerated developments independent of the profound ctenophore neoteny.

Ideas that the nervous system evolved twice or was lost by sponges [54–56] are unwarranted [76]. The long ctenophore stem on sequence trees suggests episodic evolutionary hyperacceleration that probably largely erased true phylogenetic signal, allowing slight systematic biases summed over many genes to place them (arguably misleadingly) often below sponges [1], not as sister to Cnidaria as some good trees [33] and organismal characters favour. Complex character loss is far easier than gain Myxozoa, somatically secondarily unicellular parasites once wrongly considered Protozoa, lost their nervous system, being robustly phylogenetic sisters to Polypodium, a tentaculate triploblastic polypoid cnidarian (class Polypodiozoa) whose highly modified planula endoparasites sturgeon oocytes [1]. Polypodium triploblasty supports treatment as a separate class outside diploblastic Hydrozoa [77], their actinula-like stolonoid parasitic phase suggesting that the Myxozoa/Polypodium clade might be sister to Hydrozoa, as some trees indicate [77]. Myxozoan branches on multiprotein trees that show them as sister instead to all other Medusozoa [1] might have put them artefactually one node too deep, but they could reasonably be genuine sisters of all Medusozoa, as the polyp-like free-living adult has an apparently primitive nerve net [77], as expected if its ancestor evolved directly from a stem anthozoan and its traditional assignment to Medusozoa were incorrect.

Others advocate one neural origin and invoke tree artefacts, giving more supporting details [78]. Saying synaptic origin ‘might occur more than once during ∼600 million years of animal evolution’ [79, p. 607] is 100-fold misleading fossil ctenophores and cnidaria originated essentially simultaneously (Ctenophora 540 Ma [80] Cnidaria 560 Ma [81]) as sequence trees' close branching and poor resolution confirm. It was no coincidence benthic nematocystous anthozoa and pelagic ctenophores likely diverged within 5 Ma of synaptic origin (a complex arguably unique innovation), divergently perfecting benthic tentacular feeding (Cnidaria) or pelagic ciliary current feeding (Ctenophora) by amplifying and recruiting partially different subsets of the choanozoan/sponge protein repertoire. Cambrian ctenophores lack tentacles and have more comb plate rows (reflecting divergent evolution of details of mosaic development from the pluripotent stem cnidarian ancestor), a major subgroup being armoured the two long tentacles with colloblasts, to give a greater reach, evolved substantially later in the palaeozoic after bigger prey evolved (secondarily lost in Beroe [1]). The benthic coeloplanids are phylogenetically derived [1] with no role in ctenophore or bilaterian origins.

Rapid divergence of Anthozoa (benthic nematocystous adults) and Ctenophora (pelagic direct developing ciliary feeders the first) neatly partitioned the Early Cambrian adaptive zone for predating larger prey. By not settling, ctenophores could evolve anal pores at the statocyst pole, enabling more efficient unidirectional ingestion and defecation currents independently of unianal bilateria, allowing secondary biradial gut symmetry by losing the siphonoglyph (convergently with scleractinian corals). Like ctenophores, early adult anthozoa probably relied on ciliary feeding (often helped by mucus secretion as in scleractinia). More complex barbed nematocysts (from the likely ancestral atrichous isorhizas) and toxins evolved divergently only after bilateria arose and became cnidarian prey.

9. Origin of bilateria and the coelom

The first bilaterian and coelom could have evolved most simply through repercussions of a single key mutation modifying early pharyngeal development of a stem anthozoan polyp. The anthozoan pharynx (stomodaeum) develops separately from the coelenteron cavity by an apical inwardly projecting tissue mass that secondarily develops an inner cavity (e.g. Renilla) or by apical invagination (Alcyonium) the stomodaeal cavity/invagination joins the coelenteron secondarily when the two separating epithelia at the stomodaeal base degenerate, making a novel opening [82]. A mutation, causing an extended pharynx primordium like that of Renilla to fuse basally with the side of the developing coelenteron wall before the breakthrough, would immediately connect the pharyngeal cavity not with the coelenteron but through the body wall to the outside (figure 3). This one-step anal breakthrough [83] would convert the muscular pharynx into a through gut, and transform the coelenteron into a closed coelom, creating a viable ‘hopeful monster’. If the stem anthozoan had one siphonoglyph like octocorals and cerianthid and some actiniarian Zoantharia (often misleadingly called hexacorals), it was already bilaterally symmetric (most likely) if it were biradial with two siphonoglyphs such as some Zoantharia (Antipatharia, some sea anemones), the lateral breakthrough directly made it bilateral. Being hermaphrodite with vegetative reproduction, it could have multiplied enough to invalidate the classic objection against hopeful monsters that they could never find a similar mate.

If the anthozoan that did this was a facultative burrower, as some are, then the coelom could have increased the mechanical efficiency of burrowing (often postulated as its original function) almost without further modification, and separated its mechanical functions from those of a gut. The new through gut could retain digestive and absorptive functions, likely improved by modifying their positional control to regionally differentiate the former pharynx and be suppressed in the former coelenteron, now coelom. By focusing on burrowing and processing ingested sediment, nematocysts were lost and tentacles modified in function to simple mouthparts (or lost in some lineages). Such a radical change would necessarily dramatically affect embryology unsurprisingly, thereupon two different ways immediately arose to stabilize mouth/anus formation in this protobilaterian: the proterostome/deuterostome bifurcation.

Sequence phylogeny makes it virtually certain that the deuterostome ancestor was non-cephalized, whether a burrower like acorn worm or tentaculate like pterobranchs, possibly colonial like tunicate and salp. All these could readily have arisen from this tentaculate/burrowing intermediate. Lophotrochozoa also appear primitively to have had non-cephalized tentaculate or burrowing forms. The common ancestor of both groups can be argued to have been a tentaculate form, retaining pharyngeal ciliary currents that Anthozoa use in feeding, but a better burrower than burrowing sea anemones. This protobilaterian would be preadapted as ancestor of all major deuterostome and lophotrochozoan groups acquiring ecdysis and very different mouthparts was more radical, yielding a priapulid-like ecdysozoan ancestor. Site-heterogeneous multigene analyses show that deuterostome acoels lost gut [84,85] and proterostome entoprocts, and independently cephalized Platyhelminthes and Gnathifera (miniaturized interstitial specialists) all lost coeloms independently [84,85]. Whether Xenacoelomorpha are sisters to deuterostomes [84] (thus also lost coeloms) or Nephrozoa [85,86] (so possibly ancestrally acoelomate), they probably arose by simplifying an anthozoan-like ancestor. Xenacoelomorph early divergence, even if true, would not contradict that or justify Hyman's influential antipathy to all ‘coelom early’ theories for bilateria [87].

Although lacking synapses, sponge tissues and embryology are as complex as in Cnidaria [22,88–91] Hyman [92] wrongly but influentially denied that by labelling sponges a cellular and coelenterates a tissue constructional grade sponge pattern formation and morphogenesis involve many of the same genes as in other animals, e.g. notch [38]. When I first propounded the ideas summarized in §§2–9 at a 1984 symposium on lower invertebrate origins and relationships [93], only two other speakers took seriously my argument that coeloms evolved in the ancestral bilaterian: Rieger, who had evidence for coelom losses in annelids, and Nielsen who shared my heterodox but right [85] view of Bryozoa as a clade (entoprocts secondarily acoelomate). Almost none thought choanoflagellates relevant to animal origins. Sponge expert Bergquist, the only other participant considering sponges relevant to eumetazoa, agreed that Hyman's dogma that sponges lack proper tissues and are radically simpler than Cnidaria is wrong. The audience of morphologists burst out laughing when I said sequencing mitochondrial genomes of all animal phyla could test my ideas. The symposium volume excluded my invited chapter as a referee called it ‘a farrago of nonsense’, so I took a sabbatical to learn to clone and sequence genes, starting with cnidaria, sponges and choanoflagellates [7]. Cnidarian mitochondrial genomics initiated by my 1987 cloning Sarcophyton mitochondrial genome [94] confirmed my 1984 theses that Anthozoa were ancestral to Medusozoa, triploblastic jellyfish ancestral to Hydrozoa, and Eumetozoa ancestrally bilaterally symmetrical and triploblastic [95]. Radial symmetry of Medusozoa and hydrozoan diploblasty is indeed derived. The only primitively radiate animals are sponges.

Hyman's assertion [87] that non-cephalized, often tentaculate bilaterian phyla and classes were obviously all decephalized and simplified by losing mouthparts, sense organs and brains never convinced me. A few, notably barnacles, probably are, but most are not. Arthropod, gnathiferan, mollusc, annelid and vertebrate heads are not morphologically homologous, arguing for independent origins. Their common ancestors more likely than not were non-cephalized tentaculate filter feeders. That all animals have homologous ‘head–tail’ patterning involving Wnt and homeobox gene switches does not make heads homologous. Such genes are just transcriptional switches that connect patterning gradients and downstream cell differentiation and morphogenetic cellular processes that actually make non-homologous structures such as mandibles, chelicerae, rotifer jaws or mollusc radula. Thinking human and grasshopper heads structurally homologous is as bad as calling a vacuum cleaner and light bulb homologous, because identical switches can turn both on. The notion that all animal eyes are homologous, because Pax transcription factors induce all, similarly erroneously confuses organizational levels. Rhodopsin is homologous between proteobacteria and animals, but vertebrate eyes are not structurally homologous with octopus or Drosophila eyes these eyes evolved independently by modifying eukaryote cells (not strictly homologous with the bacteria that invented rhodopsin) and arranging them into contrasting supracellular structures. It is too often overlooked that structural homologies like those of tetrapod limb bones are at a higher level of organization than are transcription factors or building blocks such as collagen that they may share with morphologically non-homologous arthropod or annelid limbs and can often be recognized unambiguously entirely independently of gene sequences there is almost certainly no ‘pentadactyl-limb gene’. Non-homologous structures (e.g. cilia and muscle or nematocysts and leg bones) are often built partly of homologous components.

10. Vendozoa: diversified presponges?

Rejecting the then prevalent idea that Ediacaran macrofossils antedating the Cambrian explosion included bilateria [96], I argued in 1984 and subsequently [83] that the Cambrian explosion was simply the origin of bilateria, and Vendobionta were all Cnidaria. Critical reevaluation of frondose rangeomorph Vendozoa makes it unlikely they are Cnidaria [97,98]. I now agree with Seilacher [99] that typical modular quilted foliate Vendozoa are not from any extant phyla, though non-foliate approximately 560 Ma old Haootia might be a muscular cnidarian impression [81]. However, I reject his idea that Vendozoa are complex, possibly syncytial protists (vendobionts) unrelated to animals [100], his analogy with quilted caps of giant unicellular green alga Acetabularia being superficial. Acetabularia is not syncytial its form requiring cell walls is adapted for photosynthesis. Habitat proves that Vendozoa were not generally phototrophs [101]. Syncytial algae such as Codium are never quilted. Absorptive feeding by filamentous syncytial fungi like zygomycetes would cease if they evolved that body form. Large fungal fruiting bodies are non-trophic for spore dispersal. Syncytial sponges evolved secondarily from cellular ancestors. The largest protozoan syncytia (myxogastrid Mycetozoa) are naked phagotrophs with no architectural potential to evolve a vendozoan body form, unassignable to any protist group. Vendozoan complexity required extensive connective tissue to make quilt seams as struts supporting two outward facing trophic epithelia. Broken frondule internal structure [102] suggests cellular tissue not syncytia.

That Vendozoa were osmoheterotrophs [103] is implausible such organisms should be finely divided like a fungal mycelium. Feeding by harbouring chemotrophic bacteria is theoretically possible [104], as in Pogonophora or anaerobic bivalves, but these clearly betray an annelid and mollusc ancestry unlike Vendozoa both evolved in Lophotrochozoa with a long history of oral/gut feeding (some carnivorous sponges similarly supplement their diet). I do not see how such a symbiosis could have originated and propelled the origin of a complex macrorganismal tissue. Instead, I suggest that quilted Vendozoa were a major presponge radiation (‘Avalon explosion’ [105]) approximately 30 Ma before the AS originated. Rangeomorphs with attachment discs could be bifacial fronds bearing choanocytes on both sides. Dickinsoniids without discs might be flattened presponges living on soft surfaces and differentiated into an upper filter-feeding choanoderm and lower surface without choanocytes (possibly also phagocytosing bacteria beneath it [106]). Often confused with bilateria, dickinsoniid self-mobility is a palaeontological misinterpretation, making it improbable that they are Placozoa [106] quilt terminal addition does not prove that they are bilateria [107].

It is theoretically possible that Vendozoa arose independently of sponges by evolving a connective tissue in another colonial flagellate group—Phalansterium and spongomonads are possibilities that in principle might retain their feeding mechanism after evolving a multicellular differentiated tissue. But I strongly doubt any did, as evolving a multicellular phagotroph with tissues is difficult (see above) except via a flagellate/sponge pathway, and vendozoan timing just before sponges and eumetazoa can hardly be mere coincidence. Vendozoa flourished 580–541 Ma, becoming extinct at the Cambrian explosion approximately 541 Ma. Their reduced disparity and diversity 5 Ma before the Cambrian explosion [108] I attribute to competition from stem sponges with AS, making bilaterian grazing just the final straw that extinguished Vendozoa.

Several simpler, seemingly non-quilted, sessile Ediacaran fossils could also be presponges, e.g. the tubular Funisia [109]. The 1 mm Eocyathispongia [110] is more reasonably interpreted as a 600 Ma old presponge than as a sponge, as it lacks evidence for an AS, the tiny putative intercellular spaces being insufficient evidence for ostia and channels penetrating the body wall. This interpretation of Ediacaran fossils implies that presponges preceded sponges by scores of millions of years. Oldest undoubted sponges are 535 Ma old hexact spicules, claims for earlier sterols being demosponge-specific being erroneous [111]. Crown sponges must be older, at least as old as Eumetazoa (minimally 541 Ma), but not necessarily older if Eumetazoa evolved from stem sponges. Arguably, spicules evolved independently in calcareous and siliceous sponges by evolving specialized amoeboid sclerocytes only after spicular protection against early pre-molluscan grazers became advantageous sponge carbonic anhydrases related to those of eumetazoa diversified immensely in Calcarea, aiding calcification [112]. Unique sponge anti-predator secondary metabolites would also have diversified thenceforth. A 40 Ma lag between presponge and sponge origins is reasonable, as rearrangements making an AS were radical, probably mutationally and mechanistically more difficult than the choanoflagellate–presponge transition.

I regard Vendozoa as the oldest phylum of kingdom Animalia, distinct from Porifera, Placozoa and Eumetazoa. I divide it into subphylum Petalonamae [113] for petaloid quilted taxa (even Kimberella may belong here [101]) and for non-quilted ones (e.g. Eocyathispongia) new subhylum Varisarca: Diagnosis: extinct macroscopic sessile multicells inferred to be ciliary filter feeding phagotrophs with epithelial/ECM organization body form: variable arrangements of thin sheets, neither arranged in a quilted array (unlike Petalonamae), nor having ostia and internal water channels (unlike Porifera) non-mobile as adults. Etymology Vari variable sarco Gk flesh signifies variable body forms of epithelioid/ECM presponge fleshy organization.

Vendozoa likely had Wnt/catenin axial patterning and ciliated planktonic larvae for dispersal, as without an AS they could not have easily brooded larvae as most sponges do (perhaps secondarily as protection after coelenterates evolved). If Placozoa are sisters of Eumetazoa as most multigene trees suggest, Placozoa were secondarily simplified by AS or coelenteron loss, evolving neotenously by prolonging the usual larval presettling benthic creeping phase by evolving extracellular digestion of benthic microbes and losing metamorphosis. Only if nested within Eumetazoa (Coelenterata plus bilateria) as some unconvincing trees suggest, need they have lost neurons also, like Myxozoa. Only if branching deeper than sponges and Eumetozoa, which multigene trees mostly exclude, could Trichoplax be direct descendants of presponges.

11. Cambrian body plan quantum evolution made major new adaptive zones

The Cambrian explosion is the most striking animal example of ultrarapid origins of novel body forms: Simpson's quantum evolution, convincingly attributed to the invasion of previously unexploited major adaptive zones [114]. Some lesser examples (e.g. land invasion generating tetrapods) may have been initiated by behavioural changes allowing entry into pre-existing vacant habitats and associated body plan modifications. Behaviour changed markedly during animal phylum origins—contrast crawling molluscs, burrowing annelids, walking/swimming arthropods and sedentary filtering Bryozoa—but in most cases, mutations creating truly novel body plans effectively simultaneously created body plans and their adaptive zones. Origins of sponges, cnidaria, ctenophores and coelomate bilateria made organisms with novel body plans and thereby new adaptive zones they cannot sensibly be regarded as responses to environmental change or entry into pre-existing adaptive zones. They were internal non-responsive innovations that worked. Darwin recognized that evolution would necessarily be exceptionally fast immediately a really new organismal type arose. But overawed by Lyellian uniformitarianism, and without understanding how quickly key mutations early in development can suddenly radically change animal phenotypes (exemplified by the above-discussed origins of Porifera, Cnidaria, ctenophores and bilateria), he greatly underestimated how fast it could be, mistakenly supposing animal phyla must have taken eons to evolve from a protozoan and that absence of Precambrian animal fossils meant that the palaeontological record is immensely more incomplete than study of microscopic fossils now shows.

There truly was an Early Cambrian explosion of animal (and protist) phyla, now ecologically and evolutionarily quite easy to understand. Such an explosion is expected for the very reasons that Darwin and Simpson convincingly explained. When a bilaterian with through gut and coelom arose, it created a new competitor-free adaptive zone and was bound to diversify rapidly into all body plans developmentally readily made by simple modifications and able to survive ecologically [83]. It would be a much greater puzzle if all bilaterian phyla had not evolved within 20–30 Ma. It is no longer a mystery why they did: self-creation of radical novelty dramatically alters selective forces and makes novel ancestors with unprecedented evolutionary potential. Animal developmental complexity allows the magnitude of mutational and phenotypic change to be disassociated: small key mutations can effect huge changes. Surprisingly easily, in the right organismal, phylogenetic, developmental and ecological context, they can make new phyla, probably on a similar timescale to the origin and evolutionary radiation of Darwin's finches (2–3 Ma [115]). As stressed above, origins of Cnidaria, ctenophores and bilateria were probably mechanistically much easier than of presponges or sponges, given the intermediates proposed here, so it is now entirely unsurprising that sponges, cnidaria, ctenophores and bilateria appear palaeontologically to have originated in a single geological blink (that makes early sequence tree resolution so hard). That is a nice congruence of palaeontological evidence, sequence tree proportions, and the present organismal evolutionary analysis and synthesis. Once the fundamental triploblastic zoophyte life cycle (pelagic ciliated larva, axial patterning, metamorphosis, triploblastic sessile adults) yielded the first sponge, as soon as the osculum became a mouth its immediate descendants could rapidly generate all other extant animal phyla (body plans and adaptive zones) in a radiative explosion that simultaneously eliminated Vendozoa.

A widespread explanatorily empty speculation that many groups originated long before their objective fossil dates is fuelled by deep uniformitarian prejudices about evolutionary rates that palaeontology long ago refuted, and three other prejudices/biases that synergistically led to the notion of a ‘slow burning fuse’—a journalistic slogan, not critical evolutionary thought, evaluation or synthesis. First is excessive confidence in the certainly false idea of a ‘molecular clock’ and in the reliability of current implementations of oxymoronic ‘relaxed clock’ computer programs [116]. Second is uncritical acceptance of the dubious identity of some fossils used for calibration, driven by palaeontologists’ ‘my fossil is older than yours’ competition [117]. Third is a dearth of coherent imaginative but critical synthesis as done by Darwin and Simpson, often harmfully dismissed as speculation and deterred by journal publishing and refereeing practices, but attempted here instead of merely listing genes from protist genomes potentially significant for originating animal multicellularity.

12. Conclusion: from zoophytes to mobile animals

The best way to understand megaevolutionary events is by a coherent synthesis unifying data of every kind using explicit reasoning and well-tested explanatory principles. Haeckel's idea that animals evolved from a protozoan ancestor directly via a gastraea with triploblastic body, mouth, gut and anus, and that the animal archetype was a flatworm-like bilateral mobile predator like us minus coelom and anus must be wrong. A gastraea is far too complicated to evolve in one step. Instead, a choanoflagellate became a triploblastic sponge (arguably in two separate stages), a sponge became an anthozoan cnidarian, stem anthozoa generated pelagic ctenophores and independently an ancestral sessile bryozoan-like bilaterian, whose headless zoophyte descendants independently evolved morphologically contrasting heads through inventing burrowing, crawling or swimming, in annelids, molluscs, arthropods and vertebrates all acoelomate bilateria arose secondarily by coelom occlusion. Nematocyst-triggered origin of neurons and zoophyte origin of bilateria adumbrated here put sessile headless animals central to eumetazoan and bilateria origins, just as they are to the already widely accepted choanoflagellate-sponge transition (here explicitly elucidated and divided into two possibly temporally distinct phases). All three problems are more deeply illuminated by a unifying zoophyte perspective than by Haeckel's anthropomorphic, self-mobile adult bias. Sessile presponge headless zoophytes with dispersive ciliated larvae were the first animals muscle-driven mobility is secondary. Heads followed rather than led basic animal innovations. Can a simpler path fit the facts?


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