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At what point do scientists consider something sentient vs random and/or genetic?

At what point do scientists consider something sentient vs random and/or genetic?


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When I was thinking about sentience from a scientific point of view, I was confused about the bio-electric mental difference between a paramecium, dog, human, and supercomputer.

At what point does electricity go from being random and genetic to creating logic gates for perceived "sentience" / intelligence?


if you have 300 neurons and 10 of them can put you in a depressed state, you are a sad eukariote.

To compare the logic gates of a worm and a mouse? which one is sentient? a slug literally has 10k neurons and a fly has 250k. that would make a slug 25 time sless sentient than a human, and a dog less sentient than a human, but a human is equally as sentient as a dog so numerically there may be now lower bounds.

Logic Gates are electronic switches which provide routing for AND/OR/NOT/EQUALS of data types, or objects. They come into existence when you have the first cilia and sensory cells. 20 nerves are a signal routing engine, logic system.

A neuron can roughly represented by 4-8 transistors, and a logic gate is a simple transistor routing/instruction, so a worm has about 2000 logic gate equivalents. https://en.wikipedia.org/wiki/List_of_animals_by_number_of_neurons

A logic gate is digital, a brain is analogue, no software, , so you inadvertantly weave smoke and mirrors to clarify your question.

The question evokes electrical sentience, synapses are electrochemical, slower than electricity and can varied in many ways chemically, and they are self organizing.

feeling, aware and knowing (reductionism of sentience) are much more debated topics in science. Relative to random and genetic logic gates for intelligence, that's unclear and you are discussing free will and decision (philosophy), intelligence has unclear relation to sentience/emotion.

Your question is confusing a vast range of scientific measures by using the term sentience, which is rarely used in science. Scientists write informally about sentience as an ethical issue based on their experience, but there's only fringe research on animal sentience. https://scholar.google.fr/scholar?hl=en&as_sdt=0%2C5&q=sentience+fish&btnG=

Animal psychology is a scientific topic, and sentience is metaphysical, it means feeling, aware and knowing, it's incommensurate and imprecise.

So scientists don't consider there to be such a point of sentience. They measure certain markers of sentience, such as

self awareness,

stress response,

emotional queues,

counting,

comparing,

memory,

puzzle solving,

social behaviour,

hormones, that kind of thing.

There are perhaps a 2 publications about sentience in fish, none about lizards or insects, and there are thousands of books and opinions about sentience in insects and other animals.

The brain increases in size from a dozens to billions of neurons. So the progression is in stages, so awareness is likely to be a complex series of steps.

A good animal psychologist can give you an entire book about the onsent of emotions and knowing in animals.


How are gene variants involved in evolution?

Evolution is the process by which populations of organisms change over generations. Genetic variations underlie these changes. Genetic variations can arise from gene variants (often called mutations) or from a normal process in which genetic material is rearranged as a cell is getting ready to divide (known as genetic recombination). Genetic variations that alter gene activity or protein function can introduce different traits in an organism. If a trait is advantageous and helps the individual survive and reproduce, the genetic variation is more likely to be passed to the next generation (a process known as natural selection). Over time, as generations of individuals with the trait continue to reproduce, the advantageous trait becomes increasingly common in a population, making the population different than an ancestral one. Sometimes the population becomes so different that it is considered a new species.

Not all variants influence evolution. Only hereditary variants, which occur in egg or sperm cells, can be passed to future generations and potentially contribute to evolution. Some variants occur during a person’s lifetime in only some of the body’s cells and are not hereditary, so natural selection cannot play a role. Also, many genetic changes have no impact on the function of a gene or protein and are not helpful or harmful. In addition, the environment in which a population of organisms lives is integral to the selection of traits. Some differences introduced by variants may help an organism survive in one setting but not in another—for example, resistance to a certain bacteria is only advantageous if that bacteria is found in a particular location and harms those who live there.

So why do some harmful traits, like genetic diseases, persist in populations instead of being removed by natural selection? There are several possible explanations, but in many cases, the answer is not clear. For some conditions, such as the neurological condition Huntington disease, signs and symptoms occur later in life, typically after a person has children, so the gene variant can be passed on despite being harmful. For other harmful traits, a phenomenon called reduced penetrance, in which some individuals with a disease-associated variant do not show signs and symptoms of the condition, can also allow harmful genetic variations to be passed to future generations. For some conditions, having one altered copy of a gene in each cell is advantageous, while having two altered copies causes disease. The best-studied example of this phenomenon is sickle cell disease: Having two altered copies of the HBB gene in each cell results in the disease, but having only one copy provides some resistance to malaria. This disease resistance helps explain why the variants that cause sickle cell disease are still found in many populations, especially in areas where malaria is prevalent.


Sandwalk

PZ Myers posted an interesting article on The state of modern evolutionary theory may not be what you think it is. He makes the point that there's more to evolution than natural selection.

I think this is an important point but I would not explain it the same way as PZ. He focuses attention on Neutral Theory and the fact that neutral, or nearly neutral, mutations are fixed by random genetic drift. Here's how he describes it .

The debate over adaptationism is a debate over mechanisms of evolution. Random genetic drift is a mechanism of evolution that results in fixation or elimination of alleles independently of natural selection. If there was no such thing as neutral mutations then random genetic drift would still be an important mechanism.

Let's say you have a clearly beneficial mutation with a huge selection coefficient of 0.1 (s = 0.1). Population genetics tells us that the probability of fixation is 2s or, in this case, 20%. That means that the allele will be eliminated from the population 80% of the time. That's random genetic drift. Similarly, some fairly deleterious mutations can sometimes be fixed by random genetic drift.

Random genetic drift is a mechanism of evolution that was discovered and described over 30 years before Neutral Theory came on the scene.

What Neutral Theory tells us is that a huge number of mutations are neutral and there are far more neutral mutations fixed by random genetic drift that there are beneficial mutations fixed by natural selection. The conclusion is inescapable. Random genetic drift is, by far, the dominant mechanism of evolution.

Many people seem to equate Neutral Theory with random genetic drift. They think that random genetic drift is only important when the alleles are neutral (or nearly neutral). Then they use this false equivalency as a way of dismissing random genetic drift because it only deals with "background noise" while natural selection is the mechanism for all the interesting parts of evolution. I think we should work toward correcting this idea by separating the mechanisms of evolution (natural selection, random genetic drift, and others) from the quality of alleles being produced by mutation (beneficial, detrimental, neutral).

The revolution is over and strict Darwinism lost. We now know that random genetic drift is an important mechanism of evolution and there's more to evolution than natural selection. Unfortunately, this blatantly obvious fact is not understood by the vast majority of people and teachers. There are even many scientists who don't understand evolution.

53 comments:

Did you see my comment on PZ's article giving you and Arlin Stoltzfus a shoutout? His Curious Disconnect series was fantastic, do you have any other guest posts by him?

I love the idea of constructive neutral evolution. It seems that Lenksi's results highlight the importance of it because the Cit+ gene was contingent on several neutral mutations being fixed in the populations that evolved it. You can always tell an IDiot hasn't done their homework when they attack "Darwinism" Evolutionary theory has "been there done that" and moved on for over half a century now!

I am not sure what has been proven:

1. That genetic drift is responsible for more changes of gene frequency than other evolutionary forces? True, but since these are zillions of little jiggles of gene frequency and some of the them cancel each other out, it is open to question as to whether this make genetic drift the major force in evolution. Whatever "major force" means.

2. That the many adaptations that we see are not the result of natural selection? Gould and Lewontin made the point in their "Spandrels of San Marco" paper that we could not assume that any adaptation we saw was itself directly brought about by natural selection for that purpose. But the high level of adaptation of living systems (a level they have to have, else they could not survive and reproduce) must have been the result of natural selection. Mutational processes alone and/or genetic drift alone just could not have made a bird that flies or a fish that swims, not ever.

3. That if we conclude that, in addition to natural selection, neutral mutation has caused a lot of molecular differences within and between species, then we have rejected the Modern Synthesis? That is just semantics, but it has consequences, and unfortunate ones. Are readers to infer that the lessons they learned in school, telling them that the adaptations of living organisms are the result of natural selection, are now to be discarded?

I think that it would be a tragedy if the promotion of a series of newer and newer evolutionary theories causes people to forget the one important point -- that if there is no natural selection you will not get (or maintain) adaptations.

Yes, let's celebrate the diversity of evolutionary forces, but let's not throw out the baby with the bathwater.

1. That genetic drift is responsible for more changes of gene frequency than other evolutionary forces? True, but since these are zillions of little jiggles of gene frequency and some of the them cancel each other out, it is open to question as to whether this make genetic drift the major force in evolution. Whatever "major force" means.

Setting aside the example I gave where even highly beneficial alleles are lost by drift, the real question is whether a substantial proportion of phenotypic changes are due to drift. I tell my students to look around them in class and observe all the genetic variation in the human population, some of which has become fixed in some populations. Is all that evolution due mostly to natural selection or random genetic drift?

I think that, as a general rule, most of the differences between closely related species are due to drift and not selection. That makes drift a major force in evolution.

2. That the many adaptations that we see are not the result of natural selection?

Nobody is denying the power of natural selection.

3. That if we conclude that, in addition to natural selection, neutral mutation has caused a lot of molecular differences within and between species, then we have rejected the Modern Synthesis?

First, let's stop saying that we're only talking about "molecular differences" when we talk about random genetic drift. That's a bad habit to get into and it it's often used as a way of dismissing the importance of drift and neutral mutations.

The answer to your question is, yes, I think we have to face up to the fact that the derived, hardened, version of the Modern Synthesis did not give due credit to random genetic drift and it completely ignored Neutral Theory. Even though everyone SHOULD be aware of drift and Neutral Theory, the fact is most aren't. The version of the Modern Synthesis that's being taught is misleading and it's probably best to discard it completely in order to get on with 21st century evolution.,

That is just semantics, but it has consequences, and unfortunate ones. Are readers to infer that the lessons they learned in school, telling them that the adaptations of living organisms are the result of natural selection, are now to be discarded?

In some cases, yes. They are going to be told that many of the things they thought were adaptations are only just-so stories and there's another perfectly scientific explanation in the form of random genetic drift. They will never be able to evaluate the scientific evidence for adaptation if they don't even realize that natural selection isn't the only possibility.

Evolutionary psychology will be the first victim but that won't be a bad thing.

I think that it would be a tragedy if the promotion of a series of newer and newer evolutionary theories causes people to forget the one important point -- that if there is no natural selection you will not get (or maintain) adaptations.

We all agree with you on that point. What we're arguing about is whether adaptionism—an almost exclusive focus on adaptation as the only important mechanism of evolution—has been harmful to the understanding of evolution. I am certain that it has.

Prof. Moran should note that many of the folks who comment on creationism who are not biologists (e.g. Mano Singham, a physicist, over at freethoughtblogs) refer only to evolution by natural selection. This seems to be the dominant meme in the non biologist scientific community.

Darwin was the first to recognize the diversity of evolutionary forces! In other words Darwin was not a strict Darwinist as misunderstood by PZ Myers. In other words - it's not always about optimal adaptation.

For example Darwin waxed eloquent on Sexual Selection in his 1871 book The Descent of Man and Selection in Relation to Sex

Sexual selection is not a separate evolutionary force

Would love to see more about the relationship between types of speciation (are speciation and "macroevolution" synonymous?), natural selection, and random genetic drift.

No, speciation and macroevolution aren't synonymous. Speciation is often seen as the dividing line between micro and macro. As for your request, have you read Speciation by Coyne & Orr?

There has already been an argument on Pharyngula about whether sexual selection is something separate from natural selection. Some people think it is, and I've never been able to understand why. Apparently Kevin Padian is a big advocate for that position. But again I don't understand why.

No, speciation and macroevolution aren't synonymous. Speciation is often seen as the dividing line between micro and macro.

Confused - I would have thought your second sentence would imply the opposite of your first. In other words, if one knows one is talking about macroevolution when one sees speciation.

The dividing line between A and B isn't necessarily either A or B. And while some people do consider speciation to be macroevolution, not even those people consider it to be all of macroevolution. Red is a color, but nobody thinks "red" is synonymous with "color".

Setting aside the example I gave where even highly beneficial alleles are lost by drift, the real question is whether a substantial proportion of phenotypic changes are due to drift. I tell my students to look around them in class and observe all the genetic variation in the human population, some of which has become fixed in some populations. Is all that evolution due mostly to natural selection or random genetic drift?

I think that, as a general rule, most of the differences between closely related species are due to drift and not selection. That makes drift a major force in evolution.

Of course, there is lots of drift. Of course, since much of the genome is junk, variations there are not the result of natural selection.

But keep in mind that if the population size is N, a selection coefficient much greater than 1/N will be quite effective in the long run. So if N is 1 million, a selection coefficient as low as 0.000001 cannot be ignored. (Yes, in hominoids, N is substantially lower than 1 million, but I'm talking about more typical species).

I think that, this point aside, we generally agree except for the issue of which label to put on theories.

The answer to your question is, yes, I think we have to face up to the fact that the derived, hardened, version of the Modern Synthesis did not give due credit to random genetic drift and it completely ignored Neutral Theory. Even though everyone SHOULD be aware of drift and Neutral Theory, the fact is most aren't. The version of the Modern Synthesis that's being taught is misleading and it's probably best to discard it completely in order to get on with 21st century evolution.,

Who is teaching this derived, hardened form of the Modern Synthesis? When did it arise? The Neutral Theory first appears no earlier than 1966-1968. Before that did George Gaylord Simpson ignore genetic drift? Did Sewall Wright? After it, did John Maynard Smith ignore neutral theory (he wrote papers on it, as it happens)? Does Brian Charlesworth? (He explained the degeneration of Y chromosomes by invoking Muller's Ratchet).

A big problem is that starting in the 1970s-1980s there were a host of young scientists who thought that they had to promote a "new paradigm" of their own or (horrors!) they would only be doing "normal" science. So those of us trying to achieve some clarity and understanding had to continually beat off waves of paradigm-mongerers. (Or perhaps the word should be paradigm-mongers). We continually had to point out that the brand-new Jim-Blotz-ian Synthesis was really wrong, and the brand-new Jane-Smith-ian Synthesis was really old wine in new bottles. This gets very tiring.

And it has one other negative effect. It persuades the public, through the popular science press, that all that old stuff that they heard about how the reason we have such good adaptations is natural selection, all that is now tossed out, and the new theory shows that it is "because of gene duplication", or "because of mutation of developmental regulatory sequences", or "because of a polyploid event". And the fact that natural selection tosses out most such events is not mentioned or appreciated.

Fine, maybe we now have a New Evolutionary Theory. And it will be proven wrong in 5 years and there will be a Newer Evolutionary Theory, and so on indefinitely. But what will the general public make of these endless declarations of the overthrow of existing evolutionary theories? 'Nuf said.


3. Different Phenomena Explained

A closer look at what is uncontroversially agreed upon, at least by those involved in the current debate, to be the foundation of the neo-Darwinian framework, the models of population genetics, and evo-devo helps to show that they explain different things. In section four below, I use this and the work of John Beatty (1995, 1997) to argue that a relative significance issue exists between neo-Darwinism and evo-devo.

3.1 The Population Genetics Foundation of Neo-Darwinism

Between 1918 and 1932, population geneticists Ronald Fisher, Sewell Wright, and J. B. S. Haldane developed the statistical models needed to explain the dynamic effects of mutation, migration, drift, and natural selection on gene frequencies of actual populations over generational time, thereby demonstrating the compatibility of Mendelian inheritance and Darwinian natural selection (e.g., Provine 1971 Lewontin 1980 Beatty 1986 Ridley 2004 Millstein and Skipper 2007). Simply put, these statistical models, according to William Provine, demonstrated how mutation, migration, drift, and natural selection could account for evolution (1980, p. 55). Indeed, Provine (1971) claims that Fisher, Wright, and Haldane did more than develop theoretical population genetics—they were the architects of the Modern Synthesis, during which they succeeded in quantitatively synthesizing Mendelian heredity, Darwinian selection, and statistical methods through the development of population genetics models (139–140). However, Provine later admitted that his initial description of the Modern Synthesis was inaccurate, and, in response, he argues that the Modern Synthesis is more accurately described as an “evolutionary constriction” (1989, p. 165). Provine (1989) claims that the Modern Synthesis was a time during which biologists from various fields winnowed down non-Darwinian alternatives (p. 176) because the mathematical and theoretical works of Fisher, Wright, and Haldane clearly showed that evolution could be explained with relatively few variables, far fewer variables than biologists had ever anticipated. It was during the Modern Synthesis that constriction based on the tools of population genetics spread throughout the study of evolution, and population genetics resulted in “a new way of seeing evolutionary biology” (p. 177).

Fisher’s most detailed explication of his general theory of evolution, which I refer to as his Genetical Theory of Natural Selection (GTNS) 5 , is found in his book of the same name, The Genetical Theory of Natural Selection ([1930b] 1958a). Here, Fisher relies on an analogy with statistical mechanics to demonstrate the relationship between Darwinian natural selection and Mendelian inheritance. Fisher’s particular aim was to explain how natural selection affects evolutionary change in populations given the principles of Mendelian inheritance (Fisher 1930 Skipper 2002, p. 343). The details of Fisher’s GTNS remain a topic of debate over 80 years after the publication of the first edition of his treatise. For example, papers by George Price (1972), Warren Ewens (1989), Anthony Edwards (1994), Anya Plutynski (2006), and Robert Skipper (2007) each argue for a particular interpretation of Fisher’s “Fundamental Theorem of Natural Selection,” which Fisher discusses in chapter two of The Genetical Theory of Natural Selection.

Generally, Fisher’s GTNS is understood as follows:

GTNS: Evolution occurs in large, randomly mating or panmictic populations and is driven primarily by natural selection, or mass selection, at low levels acting on the average effects of single allele changes (of weak effect) at single loci independent of all other loci (Skipper 2002, p. 343). 6

Wright’s earliest presentations of what he referred to as the Shifting Balance Theory (SBT) are his highly mathematical long paper of 1931 and its non-technical 1932 complement (Wright 1931, 1932 Skipper and Dietrich 2012, p. 16). In his four-volume Evolution and the Genetics of Populations (1968, 1969, 1977, 1978), Wright further develops his SBT. Throughout the course of his work, Wright describes the goal of his SBT in various ways. In 1931 and 1932, Wright claimed the goal of the SBT was to explain the ideal conditions needed for evolutionary change. By 1978, however, Wright strengthened this claim, stating that the SBT explained the “principal process by which cumulative evolutionary change occurred in nature” (Skipper 2002, 344). Wright readopted his statement from the 1931 and 1932 papers, once again claiming the goal of his SBT was to explain the ideal conditions required for evolution to take place (Skipper 2002 Skipper and Dietrich 2012).

To illustrate the three phase shifting balance process through which Wright believed evolution proceeded, he graphically depicted a two-dimensional metaphorical adaptive landscape that has become one of the most influential diagrams in evolutionary biology (Dietrich and Skipper 2012 Skipper and Dietrich 2012 for Wright’s adaptive landscape figures, see Figure 1 at the end of this article). The diagram represents possible gene combinations along with their adaptive values. The contour lines of the diagram depict the “hilly” surface of the landscape due to the epistatic relations between genes. The adaptive “peaks” of the landscape, designated by “+”, represent possible gene combinations with high adaptive value. The adaptive “valleys”, designated by “−”, represent possible gene combinations with low adaptive value. Wright was clear that due to the number of possible gene combinations, the actual population genetics of how evolution proceeds would require a diagram depicting several thousand dimensions (Wright 1932 Skipper 2002, p. 344 Dietrich and Skipper 2012).

Wright’s adaptive landscape figures (Wright 1932: 358, 361). 1A represents possible gene combinations and their respective adaptive values. 1B represents evolution on the landscape of 1A under different conditions. In A–E, the intensity of selection (s) and rate of mutation (u) vary, as does population size (N, nm). The view that Wright explains in the SBT is represented by F.

Wright’s adaptive landscape figures (Wright 1932: 358, 361). 1A represents possible gene combinations and their respective adaptive values. 1B represents evolution on the landscape of 1A under different conditions. In A–E, the intensity of selection (s) and rate of mutation (u) vary, as does population size (N, nm). The view that Wright explains in the SBT is represented by F.

Wright used his adaptive landscape to describe what he believed were the ideal conditions for a population to reach the optimal adaptive peak. Ideally, peak shifts take place in three stages or phases, according to Wright. First, genetic drift, typically maladaptive, moves semi-isolated subpopulations into adaptive valleys. In this first phase, drift changes the gene frequency distribution of subpopulations in such a way that subpopulations lose fitness, thus landing them in adaptive valleys. Second, within the subpopulations, mass selection acts to move subpopulations to adaptive peaks and out of adaptive valleys. In this second phase, mass selection changes the gene frequency distributions of subpopulations in such a way that the fitnesses of those subpopulations is raised, thus pushing them from adaptive valleys to adaptive peaks. Third, differential dispersion, or the migration of some members of more fit subpopulations to less fit subpopulations, drives interdemic selection, or selection between subpopulations, which pulls the global population up its optimal peak. In this third phase, interdemic selection changes the gene frequency distribution of the global population in such a way that the fitness of the entire population is raised.

As the foundation of neo-Darwinism, Fisher’s GTNS and Wright’s SBT illustrate the kinds of evolutionary phenomena explained by the framework. Fisher and Wright both provided mathematical models that attempt to explain how dynamic microevolutionary processes and population size and structure cause evolutionary change where evolutionary change is defined as change in the genetic compositions of populations. The models of population genetics provided the theoretical and statistical tools needed to investigate the possible causes of evolutionary change in different kinds of actual populations.

3.2 Evo-Devo Research

Evo-devo is partially comprised of several areas of research, many of which overlap. Müller (2007) provides an introduction to predominant areas of research within the field. A quick look at these research areas sheds light on the phenomena explained by evo-devo.

One predominant area of research within the field of evo-devo integrates comparative embryology, morphology, and genetics to focus on similarities and differences at multiple levels of biological organization, from the genetic, molecular, and cellular levels up, in order to understand how the ontogenies and morphologies of species have changed over time. Fossilized embryos and other evidence from paleontology allows for comparison of the morphogenetic and embryological differences between primitive and extant species (Müller 2007, p. 943). Comparative genomics compares sequences, expression patterns, and gene products and interactions, which allows for comparison of developmental sequences (Laubichler 2007, p. 349). The comparative approach provides evidence of significant changes in developmental pathways and morphologies in species over geologic time and provides evidence of phylogenetic relationships. This particular area of research utilizes comparative techniques to determine how aspects of development changed over time. Concepts and methodologies from paleontology, comparative embryology, comparative morphology, comparative genomics, and systematics are integrated to better understand the evolution of developmental processes and outcomes.

A second area of research within evo-devo focuses on the components and interactions of both genetically determined and non-genetically determined properties of developmental systems. What is of interest here are the properties of development that are not controlled directly by genes, such as self-organization, cell-cell signaling, and developmental timing, and how these epigenetic factors influence evolutionary changes. Changes in cell number or developmental timing can produce phenotypes found in ancestral organisms (Alberch and Gale 1985). The aim of this research is twofold. One goal is to better understand and explain the complex dynamics of development, as well as the effects of environmental influences on developmental systems and resulting morphologies. A second goal of this research is to understand and explain how particular changes to developmental systems can affect evolutionary change. Such research is closely related to experimental embryology (Laubichler 2007, p. 349), and thus borrows methodologies and concepts from its predecessor. Also integrated in this research are aspects of developmental genetics, systems biology, epigenetics, and ecology. 7

Another evo-devo area of research uses computational modeling and simulation to relate changes at the genetic level to changes at the cellular and tissue levels (Müller 2007, 943). Exciting results of this research include the computational ability to reconstruct gene expression during embryonic development in three-dimensions and the development of a quantitative approach to model the trajectories of ontogenetic shapes (Müller 2007, p. 943). Müller claims that the theoretical tools utilized in this research “help to localize the ontogenetic components of phenotypic change, assist in the organization of data and link evo-devo with quantitative genetics and with the study of morphological integration” (pp. 943–4).

3.3 Explanatory Differences

The areas of research within evo-devo explain morphological, or phenotypic, change within and across taxonomic levels over a range of time spans. Explanations of this kind include the origin of novel morphologies and changes in gene regulation, ontogenetic processes, and the diverse causally-relevant components of those processes, e.g., genes, molecular and environmental signals, transcription factors. Each of the aforementioned areas of research involve investigations of entities, activities, and the organization of those entities and activities at multiple levels of biological organization, including, at least, the genetic, molecular, cellular, tissue, and organismal levels. No particular level is privileged in evo-devo’s multi-level approach to mechanistically explaining phenotypic change.

As characterized by the current debate, neo-Darwinism, on the other hand, explains the effects of microevolutionary processes, most particularly natural selection, and population structures on the genetic makeup of organismal populations where phenotypes are narrowly thought of as a means of tracking genes. Such explanations pay no significant attention to the entities and processes involved in individual development, and the general explanatory focuses are the genetic and populational levels. Perhaps most indicative of the explanatory differences between neo-Darwinism and evo-devo are the different ways in which the two treat the relations between genes and phenotypes. According to the debate of interest here, neo-Darwinism places the causally complex processes of development that are the physiological links between genes and phenotypes into a black box and sets that box aside as explanatorily irrelevant while evo-devo takes the contents of the black box and attempts a multifaceted explanation of its origin and subsequent evolution. More simply, evo-devo explains phenomena that are seemingly explanatorily irrelevant within the neo-Darwinian framework as that framework is depicted by the current debate. The neo-Darwinian framework, absent significant embryological and developmental influence, explains populational changes using a phenotype concept that allows for gene tracking through generations.

Nonetheless, the phenomena explained by each are evolutionary phenomena. Changes in and maintenance of the genetic compositions of populations and heritable changes in morphologies and developmental processes are ways in which biological entities, understood to include super-organismic entities such as populations and species, are modified in relation to their ancestors over time. Natural selection, mutation, migration, drift, environmental factors, and heritability all play some role in both kinds of changes. That neo-Darwinism and evo-devo explain different evolutionary phenomena shows that evolutionary change is indeed heterogeneous. That is, not all evolutionary phenomena are the same evolution encompasses different phenomena that are explained by different explanatory frameworks. This heterogeneity is apparent within the current controversy—all engaged in it acknowledge, if only implicitly, that neo-Darwinism explains some evolutionary phenomena and evo-devo explains others.

As I see it, this heterogeneity and the different explanatory frameworks that explain different parts of it point to a relative significance issue. Moreover, I believe that the relative significance issue suggests that both of these explanatory frameworks will survive in evolutionary biology rather than form a synthetic theory that explains all of the phenomena in the heterogeneous domain. Again, my claim that the relative significance issue indicates that both frameworks will continue to develop unsynthesized says nothing of the possibility of a synthesis, and my claim need not be interpreted as staking a claim on whether neo-Darwinism and evo-devo are compatible. Instead, my claim, built using the conceptual tools of the ongoing debate, employs what is agreed upon within the debate, namely, that both well-supported frameworks explain different evolutionary phenomena, to address what I take to be the true underlying concern of the debate: the likely direction of neo-Darwinism and evo-devo.


Chance and Necessity

COMMENTARY: That's up to you.

One of the main disagreements between evolutionary biologists and "intelligent design" supporters is the role of "chance" (also called "randomness") in the origin of biological objects and processes (especially adaptations). In many cases, it seems that this disagreement is exacerbated by a disagreement about what the antonym of "chance" might be. In my experience, many people on both sides of the EB/ID disagreement think that the opposite of a "chance" event is an event that was "caused". However, this ignores the fact that many scientific explanations now include "chance" or "random" processes in causal explanations of natural objects and processes.

In this context, therefore, I propose that the antonym for "chance" is "necessity", as was first pointed out by Democritus of Abdera in the 4th century BC, whose two famous aphorisms were:

"All things are the fruit of chance and necessity"

"Nothing exists except atoms and the void".

The phrase "chance and necessity" is often used as a descriptive term in modern science. It means essentially "all natural/physical causes", or what one might consider to be the "Newtonian" world view. The reason that evolutionary biologists consider that Darwin founded the science of biology is that he proposed a theory of descent with modification and the origin of adaptations that was based entirely on "chance and necessity", thereby "unifying" biology with the other natural sciences.

However, it is clear that there is a myriad of objects and processes in the universe that are not entirely the "fruit of chance and necessity", just as there are clearly "things" that are neither "atoms" or "void". In purely physical terms, we now recognize at least three "things" in nature: mass, energy, and information. Only the first of these three qualifies under Democritus second aphorism, as neither energy nor information qualify as "things". Energy, of course, is interconvertable with matter according to Einstein's famous energy/matter equation. However, in the form of "pure" energy (such as electromagnetic radiation), energy is not detectable unless and until it interacts with matter (this is why outer space appears black, even though it is filled with light).

The "detectability" problem of energy is even more difficult in the case of information. It seems clear that all forms of information involve some sort of "translation", in which matter/energy relationships are "translated" into information, which can be stored and transmitted in forms that are not entirely reducible to the original matter/energy forms which they represent. As Korbzybski famously said, "the map is not the territory" the representation (in the form of information) is not the "thing" represented".

No one, including hard-core "naturalists", suggests that information doesn't exist. The problem (and this is where EB and ID run into serious difficulty), is how (and perhaps by whom) information can become "translated" in the first place. It is not even completely clear that simple "natural" processes (such as the photoelectric effect) do not include an exchange of "information" as well as an exchange of energy (in the form of a photon, for example). In quantum electrodynamics, does the exchange of a photon (or, even worse, a virtual photon) constitute an exchange of "information" between the interacting particles?

In classical physics, there is no "arrow of time". Newtonian mechanics can be run forward or backward in time, with no contradictions (and no way to tell which way the process is happening). However, in those branches of modern physics in which random processes play a part (statistical mechanics, thermodynamics, and quantum mechanics), randomness is necessarily tied to "time's arrow". The same is apparently the case with information, at least in its Shannon form.

Ergo, it seems to me that the problem of information is one that is necessarily tied with the concept of "chance". Indeed, I have come to think that information is a manifestation of one of the operations of "chance" in nature without information, chance overwhelms everything and the universe disintegrates into permanent incoherence.

This is clearly the case in biology. The "fixing" of information in the physical form of the genetic material is the only thing that makes biology possible. Without such "physicallization" of information (in the form of DNA, RNA, proteins, etc.) biological systems would be impossible, as they would disintegrate into incoherence.

Ergo, the transition from purely physical (i.e. mechanical/Newtonian) processes that do not include the translation and transfer of "translated" information to biological processes that necessarily involve the translation and transfer of "translated" information is the central problem of both biology and the physical sciences. As I have written before, I am not sanguine about our ability to answer this problem using historical information, as the transition occurred at a time (and perhaps in a place) which has left no traces from which we can infer its dynamics.

This leaves us with theoretical models, which are of course based on metaphysical assumptions about reality. I believe it would be fair to say that IDers assume that information can exist without a physical referrent (i.e. something that "carries" or "transmits" the information), whereas EBers (along with most other natural scientists) assume that information must have a physical referrent (i.e. it cannot exist in purely "disembodied" form).

Furthermore, it seems clear from previous discussions in this forum that IDers assume that information can be "foresighted" that is, it can somehow anticipate future outcomes, not by "induction" from the past but by some kind of "deduction" from the future. EBers (again, like most other natural scientists) assume that "time's arrow" cannot point backward, and that the future is therefore relentlessly driven by the past.

It seems to me that the foregoing lays out the problems which which any scientific theory of "origins" must come to grips:

• whether information can exist in purely "disembodied" form in nature, without a physical referrent

• whether the origin of the "translation" of information into physical form (i.e. the origin of the genetic translation machinery of living organisms) cannot take place without an input of "disembodied" information

• whether any form of information transfer can be genuinely "foresighted" (i.e. can be modified by events that have not yet happened, rather than simply predicting future events based on events that have happened in the past).

Evolutionary biologists (and the vast majority of all natural scientists) begin with a metaphysical world view in which their starting assumptions answer these three questions with NO. By contrast, most of the ID supporters with whom I have had such discussions begin with a metaphysical world view in which their starting assumptions are exactly the opposite: they answer these three questions with YES.

Personally, I believe that the metaphysical world view of most scientists is easier to work with, as it requires fewer "YES" answers to these questions (i.e. it requires fewer unverifiable assumptions about things that must exist for the universe to work). However, I freely admit that this belief is on a par with my acceptance of "Occam's razor" as a basic principle of scientific explanation. That is, "Occam's razor" clearly isn't "true", it's just useful as a rule of thumb in doing science.

So, where does this leave us? I think it explains why most scientists are uncomfortable with the word "design" being applied to biological objects and processes. As I have pointed out, Ernst Mayr argued for the legitimacy of the concept of design in biology, when what was meant by that term was the idea that organisms are "designed" by the information encoded in their genomes, interacting with the information obtained from interactions with their environments. This is because this view of biological "design" conforms to the three answers to the three questions listed above as answered by most scientists.

However, Mayr (and virtually all other evolutionary biologists) was uncomfortable with the idea that the process by which genomes and environments came into being was also "designed" - that is, that there was some foresighted process in which intention played a part in the bringing into existence of the physically embodied objects and processes in biology. Again, this is because this view of biological "design" does not conform to the three answers to the three questions listed above as answered by most scientists.

As always, comments, criticisms, and suggestions are warmly welcomed!

7 Comments:

I've always thought that the discussion between chance and necessity was a non-issue. They both seem to mischaracterize the constrained and unpredictable path that evolution takes.

Why not use "contingency" instead to reflect the interplay between "chance" and "necessity" in just one word?

Or, as Stephen Jay Gould said in The Panda's Thumb :
“Organisms are not billiard balls, propelled by simple and measurable external forces to predictable new positions on life’s pool table. Sufficiently complex systems have greater richness. Organisms have a history that constrains their future in myriad, subtle ways.”

Or Francois Jacob's expression from his 1977 paper "Evolution and Tinkering":
“It is hard to realize that the living world as we know it is just one among many possibilities that its actual structure results from the history of the earth. Yet living organisms are historical structures: literally creations of history. They represent, not a perfect product of engineering, but a patchwork of odd sets pieced together when and where opportunities arose. For the opportunism of natural selection is not simply a matter of indifference to the structure and operation of its products. It reflects the very nature of a historical process full of contingency.”

That's just my perspective anyway. Great post as always Allen. :-)

Here's a comment from my good friend, Will Provine:

What a thoughtful comment you made. I do have 2 serious drawbacks to it.

Many things in biology involve random factors. Random genetic drift is one of them. All evolutionists believe that there is a random parting of chromosomes in meiosis, and random breeding in the next generation. All senses of this randomness are based upon deterministic random number generators. In physics we have random processes for which we have no deterministic random number generators. There is no randomness in biology that is not based on deterministic random number generators. That makes a huge difference between physics and biology. In other words, the chance and necessity distinction means something in physics, but is meaningless in biology, where all chance is necessity.

My second point concerns your number one option for doing science:

• whether information can exist in purely "disembodied" form in nature, without a physical referent

In evolutionary biology, I rail against my colleagues, who treat natural selection as having no physical referent, or a made up one. Random drift is worse. All that is required is a small population of sexually breeding organisms. And almost everyone applies random drift to bacteria and other organisms that have no meiosis, and which makes absolutely no biological sense whatever. For this latter, biologists have no referent whatever, and merely invoke random genetic drift.

I agree with your point, but many working evolutionary biologists pay no attention to this problem. Then they treat ID’ers with zero respect when they point out that the evolutionists do about as they do.

I have recently come to avoid the use of the word "chance" in describing non-quantum-level natural phenomena. I tend to agree with my friend and mentor, Will Provine, who rejects the entire idea of "chance" and "randomness" as causes in biology, at least in phenomena above the quantum level. For example, it is often stated that the outcome of meiotic independent assortment is the result of "chance" or "random assortment", similar to that produced by the "random" shuffling of a deck of cards prior to dealing out a round of hands. However, as a grandson of a stage magician who could perform a "perfect shuffle" (i.e. every other card from alternate hands), I am convinced that neither meiosis nor card-shuffling (nor coin-tossing, etc.) are genuinely "random" in the same way that radioactive decay or other quantum processes are "random" or the result of "chance". That is, all events in the macroscopic universe are the result of necessity, and what appears to us to be "random" events are actually the result of massive contingency.

Which, by the way, is a reasonably concise description of what I believe to be the origin and evolution of life on Earth, including my life (of course).

As to the appropriate use of the term "design" in biology, I have come to have serious reservations about it as well. I tend to agree with Vrba and Gould that exaptation is perhaps as important as adaptation in biology. Indeed, I would go further and argue that virtually all characteristics of living organisms are exaptations , in the sense that they exist as the result of a long chain of contingent deterministic processes, rather than as the goal of an equally long chain of teleological processes. At first it would seem that the difference between these two is merely a matter of perspective, but I think the difference goes deeper.

If exaptations are outcomes , then they are produced by processes that do not require "disembodied" plans or programs at the beginning of the causal/deterministic chains which culminate in their coming into existence. However, if adaptations are goals , then this necessitates the a priori existence of the goal in "disembodied" form prior to the instantiation of the causal/deterministic chains which culminate in their coming into existence.

Just to confuse things even more, I note that mathematicians can speak of different orders of randomness.

There are regions in the genome that are particularly susceptible to mutations ("hotspots"). There are some point mutations that are more likely than others in particular regions. This is nothing radical for biologists, but one UD poster made a hooplah about it last year, suggesting that such mutations are thus "non-random", which means evolution is being directed, which makes Darwinism false, which validates "front-loading", blah, blah, blah.

Hm. I always thought the only sense of "chance" or "random" that was invoked in evolution was the zero correlation between the distribution of variation in the selective environment (roughly, the topography of the nearby fitness landscape) and the distribution of mutations that occur. Have I missed something?

I should have added that I tend to regard "information" as a property, not a thing. Hence it makes no more sense to worry about the existence of disembodied information than it does to worry about the existence of disembodied temperature. The notion of "existence" gets pretty slippery there.

Name: Allen MacNeill Location: Ithaca, New York, United States

I teach introductory biology and evolution at Cornell University in Ithaca, NY.


Principles of Evolution, Ecology and Behavior

Chapter 1. Introduction [00:00:00]

Professor Stephen Stearns: The lecture today is about neutral evolution. So let’s get going on that. I want to remind you, when people think about evolution they often think that it’s only natural selection. But it’s not. It is both micro and macro. So macro gives us history and constraint, and micro consists basically of natural selection and drift and developmental biology is involved in both.

So what we’re going to talk about today is basically neutral evolution. What happens to genes or traits that are not experiencing natural selection because they’re not making any difference to reproductive success? There’s actually a lot of that that goes on, and it’s very useful that it does. It gives us a baseline, it gives us a method of measuring things, and it gives us a lot of information about history.

So there are going to be three messages I want you to remember today. One is going to be how meiosis is like a fair coin. The probability that a gene will get into a specific gamete in meiosis is 50%. The second point is how the fixation of a neutral allele in a population is like radioactive decay and it’s like it in this sense: in neither the case of the fixation of neutral alleles, nor in the case of say looking at a gram of uranium-238, do you know which mutation will be fixed or which atom will decay. But, because there’s so many of them, in both cases you know very precisely how many events will happen in a certain period of time. Okay?

This is a kind of law of large numbers for random events. If a lot of random events go on, the average is a very predictable thing. But if you just examine one nucleotide in a genome, or one atom in a gram of uranium, you can’t predict when it will mutate, when it might be fixed, when it will decay.

The third thing that I want you to remember is this regular fixation of neutral alleles, this steady process whereby if you look at an entire genome, over a given period of time󈝶,000 years, 100,000 years–a certain very predictable, average number of mutations will be fixed if they’re neutral. So if you can locate the neutral ones in the genome, you can use them to estimate relationships and the times to the last common ancestors. Okay?

So there’s actually some interesting, rather abstract and rather big ideas in this lecture. Randomness is not something that everyone finds intuitive. Our brains are apparently not designed by natural selection to deal extremely well with Las Vegas, or the stock market. Okay? So we need to hone your intuition a bit about how random processes work.

By the way, people who do really well in calculus and analysis often find their introduction to probability and statistics a little confusing. The thing that’s going on here is that you have to learn to think about entire populations of things and about distributions and frequencies of things, rather than about billiard balls hitting each other on a table or planets being attracted to the sun, by gravity. It’s a different kind of thinking. It’s population thinking.

So the outline of the lecture is a bit about how neutrality arises. I want you to know mechanistically why it is that some genes are neutral the reasons why genetic variation might not produce any variation in fitness–that’s what we mean by neutral, there’s variation at one level but it doesn’t make any difference to reproductive success the mechanisms that cause random change and then the significance of neutral for molecular evolution. And now I’m briefly going to mention maladaptive evolution so that you can see how it is that an evolutionary process can actually result in a situation where organisms are not well adapted to their habitats. And with that we will have covered the major possible outcomes of evolution: adaptation, neutrality and maladaptation.

Chapter 2. Genes and Amino Acid Changes Not Reflected in Phenotypes [00:04:56]

Okay, here’s a nice abstract diagram to explain why neutrality arises. What I want you to imagine is a genotype space in which all possible genotypes for that organism might occur. Just think about that as being all the different ways that you might have been constructed if all of the possible recombination events in your father and mother had produced all the possible gametes and all the possible zygotes. There’s a genotype space for you.

Many of those genotypes will produce the same phenotype, and that’s because many of the genes and many of the nucleotides in the genome, many of the DNA sequences in the genome, are not making any difference to the proteins that are being produced. There are other things going on and we’ll run through them. Many phenotypes have the same fitness.

How many of you come from one-child families? Okay, all of your parents have the same fitness. How many from two-child families? All of your parents have the same fitness. Okay? This happens a lot. Basically when we say that many phenotypes have the same fitness, we just mean that in any population there will be a lot of organisms that all have two offspring or all have three offspring or something like that. The two offspring class all have the same fitness.

Then when we look at the whole halfway [this would only make sense when looking at the figure] here, we can see that G1, G2 and G3 are neutral with respect to each other, when measured in a certain environment, but they differ from G4. So here we have a lot of genetic variation that’s neutral, and it’s neutral for various reasons. We’re going to run through some of those reasons.

First, some of the mutations in DNA sequences are synonymous. That means they don’t produce any change in the amino acids that are coded in the proteins. Secondly, there are pseudogenes and other kinds of non-transcribed DNA in the genome. A pseudogene is a gene that resulted from a gene duplication event sometime in the past and never got used to make anything. And if you go through an entire genome, which you now can do for many organisms, looking for these things, you will find that they’re all over the place.

There have been many gene duplications in the past, and some of them resulted in genes that were then acquired by selection and used developmentally for some function. Others were not. The pseudogenes are the ones that weren’t used. Their usual fate is to be eroded by mutation. So gradually the useful information that was once in them gets destroyed by mutation, and if they sit around long enough they are no longer detectible you can’t tell anymore that they were once really a functional gene, before they got duplicated.

There’s neutral amino acid variation, for a variety of reasons. Some amino acids have very similar molecular size and charge properties, so that if you substitute them in a protein they don’t really make much difference to the shape or the charge distribution on the protein. And if you look at a whole protein, which is usually a pretty big thing–say if it’s an enzyme–normally it will have an active site that is in a very small spatial portion of it, so that the amino acid substations that are occurring right at the active site are making a big difference to its function, and then potentially down the line to fitness, and the amino acid substitutions that are occurring a long way from that active site are having little impact on the function of the protein, even if they have a different size or a different charge structure.

So there’s neutral amino acid variation, and finally there’s something which is a little bit more abstract, and basically it’s abstract because we don’t understand it very well–it’s a real phenomenon but we don’t always know what the mechanisms are–and that is the canalization of development. So I’ll run through these and then try to explain canalization a little bit in a few slides.

Here is, uh, the genetic code, and basically you can see here the nucleotide triplets that are translated into the various amino acids. And the take-home point, the first take-home point from this, is that for any particular amino acid–phenylalanine, for example, here there are two codes for phenylalanine, and look there are six codes for leucine. So any changes within this set of nucleotide sequences produce no change at all in the amino acid that goes into the protein. They are neutral with respect to each other, because they’re synonymous.

And you can get some hint of another level of synonymity by looking at the classes of positively-negatively charged amino acids, aromatic amino acids and so forth. Substitutions between aspartic acid and glutamic acid, that are both negatively charged, are less likely to make a fitness difference than a substitution say of lysine, for glutamic acid. So there is a level in the protein as well.

The pseudogenes I’ve talked about a little bit. They are not transcribed and all of their nucleotides are free to diverge at random. That means that there is no real editing process going on–natural selection isn’t preferring one mutation to another. It’s not any more likely to turn up in children or grandchildren than another. This gene has been turned off, and it will inevitably get eroded because all DNA sequences are subject to mutation and if a mutation occurs in a pseudogene, there isn’t any particular reason for repair mechanisms to pay any more attention to it than they do to anything else. Okay?

So these things are not especially repaired by repair mechanisms and they’re not at all repaired by natural selection. So this comment will apply to a lot of the DNA that’s not transcribed. Now fifteen, twenty years ago, when this class of DNA was discovered, people labeled it ‘junk DNA’ because they didn’t think it did anything, and of course it’s been then the pleasure of younger scientists to show the older ones that this stuff actually often does have a function–usually it’s a regulatory function. Some of it makes small RNA molecules that are used in regulation, but some of it is also being used as, uh, sites and signaling pathways and helping to regulate development.

However, some of it truly is junk. For example, there is a steady process by which viruses of various sorts splice themselves into the genomes of their hosts, and this is part of the adaptive strategy of viruses that they are able to hedge their bets by sticking themselves into a genome and hanging around for awhile and then popping out, at a point which might be advantageous to them but inconvenient for their host.

However, it’s a dangerous strategy because sometimes they stick themselves into parts of genomes that never get transcribed, and they never get out. So in fact the genomes of most of the organisms on earth are littered with the fossil skeletons of viruses. I read an estimate once that the human genome had a substantial percentage of fossil viruses in it. I have forgotten the exact figure at the time. This kind of thing was popular when DNA sequences were first starting to come out in large numbers. But just know that. Okay?

So there is junk DNA, and some of it’s there because either fossil viruses or transposons, jumping genes, got into positions where they could no longer be transcribed, and they then become a graveyard. Kind of an uncomfortable thought isn’t it, that you’re just carrying around a viral graveyard? But you are.

Chapter 3. Neutral Evolution in the History of Life [00:14:29]

Okay, neutral amino acid variation. I’ve talked about this a bit when I introduced the genetic code. So these are amino acid substitutions that aren’t producing any change in geometry or any charge change in the geometry and electrochemistry of a functional site within a protein. And I’d like to talk a little bit about a very early case of molecular evolution that’s the case of alpha-globin. So your hemoglobin has two alpha and two non-alpha chains. It has a beta chain if you’re an adult and it has a gamma chain if you’re an embryo. The reason it changes from a gamma to a beta is to change the oxygen binding properties, because embryos have to suck oxygen out of their mother’s blood. Okay?

If we look at these alpha-globin sequences, across a pretty broad range of vertebrates, and we take samples in such a way that we can look fairly far back in time, we can date these branch points approximately from the fossil records. Okay? So dogs and humans shared an ancestor probably somewhere late in the Cretaceous, mid–late mid-Cretaceous. Our last common ancestor with the kangaroo was at about 140 million years perhaps. The mammals were there while the dinosaurs were there. They were just small little guys, but there were mammals there. Our last common ancestor with the shark is back at about 440 million years.

So take the sequences for all the alpha hemoglobins that you pull out of these things–it’s a convenient molecule, you just need a blood sample–and plot them on a graph. So you estimate the time from the fossils and you estimate the average differences. This “k” is a measure of amino acid differences in a protein, and the straight line is what you would expect to get if the rate of amino acid substitution is random, just uniform, just steady. Okay?

It’s pretty close to the line. There are some deviations. But this is some of the earliest evidence–this was before DNA sequencing became easy, this was when protein sequencing was easier than DNA sequencing–this was some of the earliest evidence that there’s something like a molecular clock. In other words, if we got a vertebrate that we’d never seen before, living in some forgotten jungle, and it had a weird morphology and we didn’t know who its relatives were, and we wanted to find out when it might have shared an ancestor with something that we had, and it plotted right here–its difference with something that we were comparing it with right now, plotted right here–then we would have a good estimate of time to last common ancestor, for that new, undiscovered species, based on the assumption that it was experiencing evolution like all these other guys.

Okay, the fourth reason why genetic variation might be neutral is canalization. Now canalization in general means that there are developmental mechanisms that are limiting the range of phenotypic variation, so that even though there is a mutation in the genome, or there is a disturbing environmental effect on a genetically controlled pathway, that you’re still going to get the same phenotype.

Some things about your phenotype are extremely stable. They do not respond to mutation much at all. The fact that you have four limbs, the fact that you’ve got five fingers things like that are ancient and stable and there are developmental buffering mechanisms that keep them that way. So these things, these canalizing mechanisms, resist the tendency of variation in either genetic or environmental factors to perturb the phenotype they keep it in a stable state.

So what happens to the genes that are forming this phenotype but they’re being buffered by these developmental mechanisms? Well they are then freer to accumulate neutral variation, because basically the fitness consequences of a mutation in those genes have been removed, they’ve been buffered out. Now there’s been a lot of speculation about why canalization might evolve, or whether it might just be a byproduct. And frankly in most cases we have no idea. This is an open research question.

So one of the reasons people think that say whole organism traits, like say five fingers or four limbs, might be buffered is not because of selection to buffer those traits but because there are very, very strong selection forces operating at the micro level within cells on gene signaling pathways. So you buffer those, and then as a byproduct of that you get buffering at a higher level. We don’t know what’s the case, but we do know that canalization exists and we do know it has a consequence it allows hidden genetic variation to accumulate. So that’s the fourth major reason why there can be neutral genes.

Now, what causes random or genetic drift? That will generate neutrality, but then what happens to the genes that are neutral? Well these are the mechanisms that can introduce randomness into evolution most of them, there probably are a few others.

Chapter 4. Mechanisms of Neutral or Random Evolution [00:20:38]

The first is mutation. The second is the Mendelian lottery, which is the idea that meiosis is like a fair coin. Then we have some population level effects. So mutation you can think of as a molecular event. The Mendelian lottery is a cellular event. Founder effects and genetic bottlenecks are population effects. And then we have a demographic effect, which is variation in reproductive success in a population of any size. All of these things contribute to random change. And now I want to step through them and give you a more concrete feel for how they work.

There are some senses in which mutation is not random. Okay? Mutations occur at some sites more frequently than others. In a pathogenic bacterium that is encountering a challenging environment, it will up its entire mutation rate by down-regulating its DNA repair. It’s a fairly simple thing to increase the mutation rate on a whole genome. You just neglect to repair it and it will mutate faster. Okay? So if bacteria are moved into a new environment or, for example, if a pathogenic bacterium is put into a vertebrate with a very active and threatening immune system, it increases its mutation rate.

The transitions between the nucleotide classes–so purine to purine, pyrimidine to pyrimidine–are more frequent than transversions. So purines will mutate to purines more frequently than purines will mutate to pyrmidines.

And mutations do not produce random changes in phenotype space. This one again is a little bit abstract. Okay? But a mutation can only cause a change in the inherited set of possibilities. There is very, very little mutational variance in the human population for a sixth set of appendages, growing in the middle of our backs, that could be turned into the wings of angels very little. Okay? There is very little mutational variance in a clam for any organ that could be involved in air breathing.

So mutations do not cover all of conceivable phenotypic space. Mutations are only causing perturbations in the inherited set of possibilities that a given evolutionary lineage has produced. So they’re not making random changes in phenotype space. But they are random in an extremely important sense. There is no systematic relationship between the phenotypic effect of a mutation and the need of the organism in which it occurs. They’re random with respect to fitness.

So when those bacteria are going into the vertebrate immune systems and it would be extremely convenient for them to have a mutation that was just exactly the right thing that they needed to avoid that particular defensive maneuver on the part of their host, they don’t get it. Okay? All nature will give them is random mutations with respect to that particular function, and then if they have a lot of progeny, one of them may have the right one by luck.

Similarly, in your case, it might be extremely convenient for you to have an adaptation which allowed you to look at a computer screen for 48 hours without getting a headache and without having to get up to go to the bathroom. Okay? That mutation is not going to happen, because you need that function. Your genome is going to be covered by random mutations, and it may very well be that one of your children is able to look at that screen a little bit longer than you are. But that will be because it happened at random, not because somehow development or evolution could anticipate that that function was going to be useful.

So the process of mutation produces a lot of variation, and then natural selection edits it, it sorts it, it screens it. And at the point at which that variation is produced, the potential function of the variation is not a question, it’s not an issue it’s just making variations.

Okay, second, meiosis is like a fair coin. So this is something that you may find boring. You’ve all heard about meiosis. You’ve all heard about Mendel’s Laws. You know that the probability that a gamete will get into a particular–that a gene will get into a particular gamete is 50%. And you’re all familiar with this because you know that the probability that a child will be a boy or a girl is 50%, and that’s because at the sex chromosomes, and at all the other chromosomes that we have, the probability that the chromosome will go one way or the other is 50%.

That is absolutely amazing. Why is it that my Y chromosomes don’t get 80% of the action? Why is it 50%? There’s actually something very deep here. If you construct a system in which every one of the potentially competing elements has been forced to have the same chance, those elements must then cooperate, because the only way they can increase their own chances is by increasing everybody else’s as well.

And that is why this particular effect is called the parliament of the genes. It is a discovery that Nature, about probably two billion years ago, hit upon a principle that human political science didn’t discover until the Enlightenment, which is that democracies are stable. Meiosis is a democracy. In meiosis each gene has a fair chance, and that means that in a sense you’ve got a one-gene, one-vote situation.

So I’ll come back–I’ll come back to this fairness of meiotic segregation, but there’s a general idea behind that. I’ve just given you a little scenario that would suggest why it was selected it was selected to repress conflict. Every other aspect of genetics has evolved. So when you take genetics, or you take cell biology, or you take developmental biology, there were–there were selective processes that produce what you study, and there were alternatives that were rejected, and you’re looking only at a sample of what nature can produce. And that in itself becomes an interesting research program.

Okay, back to the parliament of the genes. I referred to conflict. Here’s the conflict. There are things called meiotic drivers. So there are genes which actually change Mendel’s Laws they change the probability that they will get into the next generation. Anybody already heard how a meiotic driver works? It’s kind of a cool system. They use a long-range poison and a short-range antidote. So a meiotic driver usually operates by killing off any cell that does not have a copy of itself, of its gene, and giving an antidote to its own cell.

So as the cells sit there, in the ovary or in the testes or in whatever organ that particular organism has, the biotic drivers are basically wiping out the competition and promoting their own interests. These things are all over the place. They are common in drosophila, and there is evidence that there have been meiotic drivers in the human genome. Okay?

Once the diploid state evolved, there was a long history of invasion by meiotic drivers, and the response to that is that all the other genes wanted to cause these meiotic drivers to go away. They were distorting their own interests. You’re sitting there on a chromosome, you’re innocent. Some wild bandit comes along and highjacks your interests, and now your probability of getting into the next generation is only 20% rather than 50%. Who wants that, you know? That’s not a good deal. So throughout the genome various mechanisms arose to repress meiotic drive and the result was a very complicated mechanism and we call it meiosis.

So that’s not the only possible reason for the complexity in fairness of meiosis. It is a plausible one. I invite you to consider the cultural evolution of democracy and decide whether it too might have been driven by a history of cheating, particularly the defection of leaders who no longer represented the interests of their people. I think there’s a similarity, and I think you’ll find it articulated in the Declaration of Independence.

Okay, mechanisms that cause random change also occur at the population level. One of them is the founder effect. Let’s suppose that I were to found a new population with only you it would have a high probability of blue eyes. And with you it would have a high probability of brown eyes. And in order to choose you I flipped a coin. Okay? At the founding of that population there was a random event, which was just sampling just sampling a couple of individuals out of a big population.

And the result of this is that there are certain diseases, human genetic diseases, that are rare in the human population in general, but are common in populations that were founded by just a few people, including Tay-Sachs disease in Quebec, porphyria in the Afrikaners of the Cape, and diabetes in Pitcairn Island. So you just take a little sample out of a big population and you get something that’s not representative, and sometimes that contains a genetic disease.

Another population level phenomenon that yields randomness is a bottleneck. So that will happen when a population crashes to a very, very small size, and then only a few alleles make it through. So you might have a lot of versions of a gene in a big population, but if you’re only founding a new population with two or three individuals, they’re–and they’re diploid, well two individuals only carry four copies of the gene. So if there had been twenty alleles in the original population, the maximum possible number that could get through that bottleneck is only four you’ve left behind sixteen.

It appears that this is what happened with the cheetahs. And they are apparently almost completely homozygous, particularly with respect to their immune genes. It is a weird biological fact that you can take a skin graft off of one cheetah and graft it to a cheetah, any other cheetah in the world, and the graft will take. In other words, their immune system finds a sample of skin from any other cheetah in the world to be their own skin. They don’t detect a difference. And that probably is a signal that cheetahs went through a very small population bottleneck within the last few thousand years.

Genetic drift is then a consequence of neutrality. It’s the random wandering of the frequencies of neutral genes. If you look through a microscope, Brownian motion is the jiggling of little dust particles that you see in the microscope, and it is actually the result of the random impacts of water molecules hitting that dust particle. Well the population level analog of heat in water is variation in population size–uh, excuse me, variation in family size. A gene which has gone through the Mendelian lottery of meiosis lands in a zygote. Okay? It got into the zygote. The zygote grows up.

This particular gene is neutral. It’s not making any difference to reproductive success. But that particular individual that it landed in could have a small family or a big family, for reasons that have nothing to do with the function of the gene. It’s just a flip of the coin that determines whether it will be in a family that produces two children, zero children, or a lot of children. Okay?

So that’s what I mean by combining the lottery of meiosis with variation in reproductive success. And this is a process that goes on in all populations. When people are first learning about genetic drift, they think oh, that’s something that happens in small populations, because small populations don’t have all the smoothing effects of the Law of Large Numbers. But this will happen in a population of any size. Okay? And basically what I mean by that is this interesting consequence of variation in reproductive success. If it’s correlated with a trait or with a gene, strongly, it produces natural selection. If it’s not correlated it produces drift.

Chapter 5. The Molecular Clock of Neutral Evolution [00:35:29]

So one of the real puzzles of evolution has to do with what causes a gene to end up at random in an individual making one, two or three, or zero recruits per lifetime what makes the difference between an adaptive and a neutral gene. I’ve sketched four possible answers to that question. In any particular case we normally do not know exactly which one is contributing the most to that.

So, what is it that happens to neutral alleles? [That’s not going to work. I’ll just have to draw over this.] If we draw time on the X-axis, and we draw frequency on the Y-axis, and a mutation occurs, the usual thing that will happen to a mutation is it will increase a little bit and disappear. Then we wait for awhile, another mutation occurs. We’re looking, by the way, across many different genes in the population. We wait awhile, another mutation occurs. It comes into the population.

The probability that it will ever get fixed is pretty low because the probability is proportional to the frequency excuse me, is proportional to 1/N, frequency equal to 1/N. When it’s rare, its frequency is very low and so its probability of being fixed is low. But once in awhile a mutation comes along that manages to go through all of this drift, and making it through organisms that had, on average, more than two progeny per lifetime, and it gets fixed.

And if you just look at this class of mutations, the time that it takes them to fix is proportional to the population size. So things will get fixed faster in small populations than they will in big ones. There will be more of them, more mutations will occur in a big population, but it will take them longer to get fixed.

Now because the bigger populations have more mutations, it turns out that their size exactly compensates for the longer fixation times. So if you’re just counting how many get fixed–it doesn’t matter whether you’re in a small population or a big one–the same number of mutations are getting fixed in both cases. That means that over the course of evolutionary history populations could’ve gone through crashes and explosions, and at the end of it, if you’re a geneticist studying the DNA, looking back, it doesn’t make any difference that the populations had crashes and explosions, in terms of how many neutral alleles got fixed. They were just getting steadily fixed, with no effect of population size.

So we don’t know which one will be fixed. We do know how many will be fixed. So this is why the molecular clock is like an atomic clock it’s driven by radioactive decay. We don’t know how many atoms–we don’t know which atom will decay, but in a second we know how many will, for a given radioactive substance.

The reason for this is that there’s regularity in large numbers. It emerges because there are a large number of independent events. Our haploid genome has about three billion base pairs. One mole of uranium has about 6 times 10 23 atoms–actually if it’s a mole it has exactly that many atoms–and these large numbers give the regularity to the process.

Okay, so this is what connects microevolution to macroevolution. It creates uniform substitution rates in neutral portions of the genome. And this is the assumption that molecular evolution makes when it reconstructs the Tree of Life. It allows us to estimate branch lengths and branch points to last common ancestors. It allows us to make comparative inferences on phylogenetic trees. And therefore neutral evolution is a actually a central tool in the construction of the evolutionary framework. It’s not something to be neglected it’s something to be understood, because it gives us a source of regularity that can take us back into deep time.

As an example, here are nucleotide substitutions occurring in flu. These are isolates that are still in the freezer. Okay? And they run here from about 1925 up to 1990. We don’t have any, any error of estimate in age we know when they were isolated. Okay? The population sizes have fluctuated dramatically. At some point, some of these flu strains were sitting in a few ducks or pigs in southeastern China. At other points, they were inhabiting a billion people around the world. They went through huge fluctuations, and a nice steady rate of substitution. Okay?

All the mechanisms of genetic drift are in play here, except meiosis, because flu is a virus, doesn’t go through meiosis. The effect of variation in population size was exactly compensated by the much slower rate of fixation of neutral mutations in larger populations. So even in an epidemic disease, like flu, the molecular clock is nice and steady.

A few caveats about that. Different proteins and different parts of proteins evolve at different rates. They only use non-transcribed DNA sequences. There are some differences among lineages because of different generation times.

And I’m not going to talk about maladaptation because I took too long to talk about neutrality. So you can read about maladaptation, and I’ll just give you the basic idea. Here’s the basic idea of maladaptation. If natural selection is strong in one place and organisms get really well adapted to it, but they move to another place, where they don’t do well, for whatever reason, we call the place that is producing an excess of organisms the source, and the place which is not good for the organisms a sink. The genes in the sink represent organisms usually that were adapted to the source. So if organisms get well adapted in one place and moved to another that’s quite different, and they never get an opportunity to come into evolutionary equilibrium with that new place, which we call the sink, then they are maladapted to the sink. That is the basic idea behind how maladaptation can occur. Okay?

So, let me jump ahead. I will just run quickly through these examples and get to the end, just to let you know what happens next time. These are the keys I want you to remember. I want you to remember how it is that meiosis is like a fair coin. I want you to remember how the fixation of a neutral allele is like radioactive decay. And I want you to remember that the regular fixation of neutral alleles generates a molecular clock that allows us to connect micro to macroevolution. Okay, that’s it.


# Lewis's Views on Evolution

Since Lewis rejects ID in the narrower sense, what does he think about Evolution? Lewis accepted both cosmic and biological evolution as highly confirmed scientific theories. He understood that when a scientific theory—which is a proposal about how some natural phenomenon is caused by some natural mechanism—is confirmed by many factors, we call it a fact. We should not understand the terms theory and fact as though “theory” means “not a fact” or “lacking adequate support.” Sometimes Lewis uses the term “hypothesis” as synonymous with a scientific theory, as do many scientists.

Regarding cosmic evolution, Lewis comments that his Space Trilogy contains “only enough science” to lift the reader’s imagination away from the ordinary but the science it does contain is informed by the basic scientific picture of the cosmos and space and the planets. In his more overtly philosophical (and apologetic) books, Lewis sometimes alludes to well-known information about the universe. In The Problem of Pain, he writes,

Look at the universe … By far the greatest part of it consists of empty space, completely dark and unimaginably cold. The bodies which move in this space are … few and so small in comparison with the [vastness] of space… (p. 13)

Elsewhere Lewis speaks of “nebulae” coming into being in the early history of the cosmos therefore he knew something about cosmology and astronomy.

Lewis then transitions to biological evolution in that same passage in The Problem of Pain:

n our own [galaxy and solar] system it is improbable that any planet except the Earth -sustains life. And Earth herself existed without life for millions of years and may exist for millions more when life has left her. And what is life like while it lasts? … [A]ll the forms … can live only by preying upon one another. (pp. 13-14)

Here he reflects on what science tells us about key elements of organic evolution—the struggle for survival and natural selection. He continues:

[T]hat man is physically descended from animals, I have no objection … For centuries God perfected the animal form which was to become the vehicle of humanity and the image of Himself … The creature may have existed for ages in this state before it became man … n the fullness of time, God caused to descend upon this organism … a new kind of consciousness which could say “I” and “me,” … which knew God … [and] could make judgements of truth, beauty, and goodness… (pp. 72-77)

Clearly, Lewis accepts the Darwinian concept of “common descent with modification.” In other writings, he calls biological evolution a “genuine scientific hypothesis” (“The Funeral of a Great Myth”, p. 83) and scientists who study it “real biologists” and “real scientists.” (p. 85) He even refers in various locations to the age of “monsters,” “dragons,” “huge, very heavily armored creatures,” the great reptiles, dinosaurs, which had to pass so that mammalian life could emerge and flourish. (p. 87 Mere Christianity, p. 218)

So, Lewis never voices any objection to the scientific facts of Evolution as though they are somehow incompatible with orthodox Christian doctrines— and, in fact, he was completely comfortable integrating Evolution into a comprehensive worldview. For Lewis, positively engaging the growing body of human knowledge does not mean accommodating the latest fad but responsibly reflecting on how the Christian vision makes best sense of the facts and broad principles we learn from a variety of sources, including the sciences. Since Lewis’s time, of course, the findings of the sciences have converged more strongly on the truths of Evolution, such that it now has as high a degree of confirmation as anything else we know in science.

Why do certain religious groups continue to have problems with Evolution? One factor is the low quality of science education in our schools that makes it difficult to have informed discussion in which all parties adequately understand the methods and aims of science. Also, we noted earlier the perception that Evolution contradicts a literal reading of Genesis, which, for Christian fundamentalism, violates biblical authority. But the factor that requires attention here is that some people—both Christian and non-Christian—see Evolution as implying that there is no God, as being a form of atheism. So, Evolution becomes identified with the view that matter alone is real, chance and randomness eliminate design and purpose, moral absolutes do not exist, and a human being is merely a complex animal with no special dignity. However, these are not scientific claims they define the philosophical worldview of Naturalism (or Materialism).

Lewis, of course, was a sworn opponent of Naturalism, but not of Evolution. He carefully distinguished Evolution as science from Evolution as co-opted by philosophical naturalism (“The Funeral of a Great Myth”, p. 83). Naturalism has been around since the dawn of philosophical thought in Greece 2,500 years ago. Its advocates have always claimed that “Naturalism-plus-the-science-of-the-day” explains all that needs to be explained, and that therefore theological and metaphysical explanations are obsolete. In our day, thinkers who take this approach have been dubbed “the New Atheists.” Lewis shrewdly cautions us not to fall for their spin:

Please do not think that one of these views [i.e., either Naturalism or Supernaturalism] was held a long time ago and that the other has gradually taken its place. Wherever there have been thinking men both views turn up … You cannot find out which view is the right one by science in the ordinary sense (Mere Christianity, p. 22).

Lewis is making two important points: (1) That it is pure propaganda that Supernaturalism was believed when people were prescientific and intellectually unsophisticated, but that science has now shown that Naturalism is true. In point of fact, classical Christian orthodoxy is always capable of the most sophisticated engagement with any new information. (2) That science—legitimately operating by methodological naturalism—cannot decide between the two philosophical options of Naturalism and Supernaturalism. For naturalists to think that science itself provides evidence for Naturalism is, ironically, to commit the same category mistake earlier attributed to ID: failing to distinguish what sorts of issues are properly addressed in the fields of science and philosophy, respectively. The New Atheists fallaciously claim that their philosophical position is closely linked to a scientific case for atheism which is supported by evolutionary science, whereas ID proponents fallaciously claim that their version of science exposes weaknesses in evolutionary approaches and thus provides grounds for thinking that something like Theism is true.

Lewis’s incisive criticisms of Naturalism masquerading as evolutionary science are still very relevant to the growing cultural discussion. Consider two famous examples of scientists promoting Naturalism in the name of science. In the 1980s, Cornell astronomer Carl Sagan burst on the scene with his book Cosmos (New York: Ballantine, 1980) and the PBS series it inspired. The first sentence of the book declares: “The cosmos is all that is or ever was or ever will be.” (p. 1) The sum total of reality is matter, continually and endlessly changing in space. There is no intelligent and benevolent being behind it all.

More recently, Oxford zoologist Richard Dawkins makes the New York Times Best Seller List from time to time with books arguing that Evolution combined with philosophical naturalism provides a complete and compelling explanation of the world. As a leader of the New Atheism, he writes in The Blind Watchmaker (New York: W.W. Norton & Co., 1986),

An atheist before Darwin could have said, following Hume: “I have no explanation for complex biological design. All I know is that God isn’t a good explanation, so we must wait and hope that somebody comes up with a better one.” I can’t help feeling that such a position, though logically sound, would have left one feeling pretty unsatisfied, and that although atheism might have been logically tenable before Darwin, Darwin made it possible to be an intellectually fulfilled atheist. (p. 6, emphasis added)

So, for Sagan and Dawkins, the philosophical view that physical stuff is ultimate reality can now be coupled with a comprehensive scientific account of how the physical realm developed and operates. You have the complete package: Naturalism co-opts Evolutionary Science. No need for a Creator-God the physical realm simply explains itself!


DNA: The Tiny Code That's Toppling Evolution

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Two great achievements occurred in 1953, more than half a century ago.

The first was the successful ascent of Mt. Everest, the highest mountain in the world. Sir Edmund Hillary and his guide, Tenzing Norgay, reached the summit that year, an accomplishment that's still considered the ultimate feat for mountain climbers. Since then, more than a thousand mountaineers have made it to the top, and each year hundreds more attempt it.

Yet the second great achievement of 1953 has had a greater impact on the world. Each year, many thousands join the ranks of those participating in this accomplishment, hoping to ascend to fame and fortune.

It was in 1953 that James Watson and Francis Crick achieved what appeared impossible—discovering the genetic structure deep inside the nucleus of our cells. We call this genetic material DNA, an abbreviation for deoxyribonucleic acid.

The discovery of the double-helix structure of the DNA molecule opened the floodgates for scientists to examine the code embedded within it. Now, more than half a century after the initial discovery, the DNA code has been deciphered—although many of its elements are still not well understood.

What has been found has profound implications regarding Darwinian evolution, the theory taught in schools all over the world that all living beings have evolved by natural processes through mutation and natural selection.

Amazing revelations about DNA

As scientists began to decode the human DNA molecule, they found something quite unexpected—an exquisite 'language' composed of some 3 billion genetic letters. "One of the most extraordinary discoveries of the twentieth century," says Dr. Stephen Meyer, director of the Center for Science and Culture at the Discovery Institute in Seattle, Wash., "was that DNA actually stores information—the detailed instructions for assembling proteins—in the form of a four-character digital code" (quoted by Lee Strobel, The Case for a Creator, 2004, p. 224).

It is hard to fathom, but the amount of information in human DNA is roughly equivalent to 12 sets of The Encyclopaedia Britannica—an incredible 384 volumes" worth of detailed information that would fill 48 feet of library shelves!

Yet in their actual size—which is only two millionths of a millimeter thick—a teaspoon of DNA, according to molecular biologist Michael Denton, could contain all the information needed to build the proteins for all the species of organisms that have ever lived on the earth, and "there would still be enough room left for all the information in every book ever written" (Evolution: A Theory in Crisis, 1996, p. 334).

Who or what could miniaturize such information and place this enormous number of 'letters' in their proper sequence as a genetic instruction manual? Could evolution have gradually come up with a system like this?

DNA contains a genetic language

Let's first consider some of the characteristics of this genetic 'language.' For it to be rightly called a language, it must contain the following elements: an alphabet or coding system, correct spelling, grammar (a proper arrangement of the words), meaning (semantics) and an intended purpose.

Scientists have found the genetic code has all of these key elements. "The coding regions of DNA," explains Dr. Stephen Meyer, "have exactly the same relevant properties as a computer code or language" (quoted by Strobel, p. 237, emphasis in original).

The only other codes found to be true languages are all of human origin. Although we do find that dogs bark when they perceive danger, bees dance to point other bees to a source and whales emit sounds, to name a few examples of other species" communication, none of these have the composition of a language. They are only considered low-level communication signals.

The only types of communication considered high-level are human languages, artificial languages such as computer and Morse codes and the genetic code. No other communication system has been found to contain the basic characteristics of a language.

Bill Gates, founder of Microsoft, commented that "DNA is like a software program, only much more complex than anything we've ever devised."

Can you imagine something more intricate than the most complex program running on a supercomputer being devised by accident through evolution—no matter how much time, how many mutations and how much natural selection are taken into account?

DNA language not the same as DNA molecule

Recent studies in information theory have come up with some astounding conclusions—namely, that information cannot be considered in the same category as matter and energy. It's true that matter or energy can carry information, but they are not the same as information itself.

For instance, a book such as Homer's Iliad contains information, but is the physical book itself information? No, the materials of the book—the paper, ink and glue contain the contents, but they are only a means of transporting it.

If the information in the book was spoken aloud, written in chalk or electronically reproduced in a computer, the information does not suffer qualitatively from the means of transporting it. "In fact the content of the message," says professor Phillip Johnson, "is independent of the physical makeup of the medium" (Defeating Darwinism by Opening Minds, 1997, p. 71).

The same principle is found in the genetic code. The DNA molecule carries the genetic language, but the language itself is independent of its carrier. The same genetic information can be written in a book, stored in a compact disk or sent over the Internet, and yet the quality or content of the message has not changed by changing the means of conveying it.

As George Williams puts it: "The gene is a package of information, not an object. The pattern of base pairs in a DNA molecule specifies the gene. But the DNA molecule is the medium, it's not the message" (quoted by Johnson, p. 70).

Information from an intelligent source

In addition, this type of high-level information has been found to originate only from an intelligent source.

As Lee Strobel explains: "The data at the core of life is not disorganized, it's not simply orderly like salt crystals, but it's complex and specific information that can accomplish a bewildering task—the building of biological machines that far outstrip human technological capabilities" (p. 244).

For instance, the precision of this genetic language is such that the average mistake that is not caught turns out to be one error per 10 billion letters. If a mistake occurs in one of the most significant parts of the code, which is in the genes, it can cause a disease such as sickle-cell anemia. Yet even the best and most intelligent typist in the world couldn't come close to making only one mistake per 10 billion letters—far from it.

So to believe that the genetic code gradually evolved in Darwinian style would break all the known rules of how matter, energy and the laws of nature work. In fact, there has not been found in nature any example of one information system inside the cell gradually evolving into another functional information program.

Michael Behe, a biochemist and professor at Pennsylvania's Lehigh University, explains that genetic information is primarily an instruction manual and gives some examples.

He writes: "Consider a step-by-step list of [genetic] instructions. A mutation is a change in one of the lines of instructions. So instead of saying, "Take a 1/4-inch nut," a mutation might say, "Take a 3/8-inch nut." Or instead of "Place the round peg in the round hole," we might get "Place the round peg in the square hole" . . . What a mutation cannot do is change all the instructions in one step—say, [providing instructions] to build a fax machine instead of a radio" (Darwin's Black Box, 1996, p. 41).

We therefore have in the genetic code an immensely complex instruction manual that has been majestically designed by a more intelligent source than human beings.

Even one of the discoverers of the genetic code, the agnostic and recently deceased Francis Crick, after decades of work on deciphering it, admitted that "an honest man, armed with all the knowledge available to us now, could only state that in some sense, the origin of life appears at the moment to be almost a miracle, so many are the conditions which would have had to have been satisfied to get it going" (Life Itself, 1981, p. 88, emphasis added).

Evolution fails to provide answers

It is good to remember that, in spite of all the efforts of all the scientific laboratories around the world working over many decades, they have not been able to produce so much as a single human hair. How much more difficult is it to produce an entire body consisting of some 100 trillion cells!

Up to now, Darwinian evolutionists could try to counter their detractors with some possible explanations for the complexity of life. But now they have to face the information dilemma: How can meaningful, precise information be created by accident—by mutation and natural selection? None of these contain the mechanism of intelligence, a requirement for creating complex information such as that found in the genetic code.

Darwinian evolution is still taught in most schools as though it were fact. But it is increasingly being found wanting by a growing number of scientists. "As recently as twenty-five years ago," says former atheist Patrick Glynn, "a reasonable person weighing the purely scientific evidence on the issue would likely have come down on the side of skepticism [regarding a Creator]. That is no longer the case." He adds: "Today the concrete data point strongly in the direction of the God hypothesis. It is the simplest and most obvious solution . . ." (God: The Evidence, 1997, pp. 54-55, 53).

Quality of genetic information the same

Evolution tells us that through chance mutations and natural selection, living things evolve. Yet to evolve means to gradually change certain aspects of some living thing until it becomes another type of creature, and this can only be done by changing the genetic information.

So what do we find about the genetic code? The same basic quality of information exists in a humble bacteria or a plant as in a person. A bacterium has a shorter genetic code, but qualitatively it gives instructions as precisely and exquisitely as that of a human being. We find the same prerequisites of a language—alphabet, grammar and semantics—in simple bacteria and algae as in man.

Each cell with genetic information, from bacteria to man, according to molecular biologist Michael Denton, consists of "artificial languages and their decoding systems, memory banks for information storage and retrieval, elegant control systems regulating the automated assembly of parts and components, error fail-safe and proof-reading devices utilized for quality control, assembly processes involving the principle of prefabrication and modular construction . . . [and a] capacity not equalled in any of our most advanced machines, for it would be capable of replicating its entire structure within a matter of a few hours" (Denton, p. 329).

So how could the genetic information of bacteria gradually evolve into information for another type of being, when only one or a few minor mistakes in the millions of letters in that bacterium's DNA can kill it?

Again, evolutionists are uncharacteristically silent on the subject. They don't even have a working hypothesis about it. Lee Strobel writes: "The six feet of DNA coiled inside every one of our body's one hundred trillion cells contains a four-letter chemical alphabet that spells out precise assembly instructions for all the proteins from which our bodies are made . . . No hypothesis has come close to explaining how information got into biological matter by naturalistic means" (Strobel, p. 282).

Werner Gitt, professor of information systems, puts it succinctly: "The basic flaw of all evolutionary views is the origin of the information in living beings. It has never been shown that a coding system and semantic information could originate by itself [through matter] . . . The information theorems predict that this will never be possible. A purely material origin of life is thus [ruled out]" (Gitt, p. 124).

The clincher

Besides all the evidence we have covered for the intelligent design of DNA information, there is still one amazing fact remaining—the ideal number of genetic letters in the DNA code for storage and translation.

Moreover, the copying mechanism of DNA, to meet maximum effectiveness, requires the number of letters in each word to be an even number. Of all possible mathematical combinations, the ideal number for storage and transcription has been calculated to be four letters.

This is exactly what has been found in the genes of every living thing on earth—a four-letter digital code. As Werner Gitt states: "The coding system used for living beings is optimal from an engineering standpoint. This fact strengthens the argument that it was a case of purposeful design rather that a [lucky] chance" (Gitt, p. 95).

More witnesses

Back in Darwin's day, when his book On the Origin of Species was published in 1859, life appeared much simpler. Viewed through the primitive microscopes of the day, the cell appeared to be but a simple blob of jelly or uncomplicated protoplasm. Now, almost 150 years later, that view has changed dramatically as science has discovered a virtual universe inside the cell.

"It was once expected," writes Professor Behe, "that the basis of life would be exceedingly simple. That expectation has been smashed. Vision, motion, and other biological functions have proven to be no less sophisticated than television cameras and automobiles. Science has made enormous progress in understanding how the chemistry of life works, but the elegance and complexity of biological systems at the molecular level have paralyzed science's attempt to explain their origins" (Behe, p. x).

Dr. Meyer considers the recent discoveries about DNA as the Achilles" heel of evolutionary theory. He observes: "Evolutionists are still trying to apply Darwin's nineteenth-century thinking to a twenty-first century reality, and it's not working . I think the information revolution taking place in biology is sounding the death knell for Darwinism and chemical evolutionary theories" (quoted by Strobel, p. 243).

Dr. Meyer's conclusion? "I believe that the testimony of science supports theism. While there will always be points of tension or unresolved conflict, the major developments in science in the past five decades have been running in a strongly theistic direction" (ibid., p. 77).

Dean Kenyon, a biology professor who repudiated his earlier book on Darwinian evolution—mostly due to the discoveries of the information found in DNA—states: "This new realm of molecular genetics (is) where we see the most compelling evidence of design on the Earth" (ibid., p. 221).

Just recently, one of the world's most famous atheists, Professor Antony Flew, admitted he couldn't explain how DNA was created and developed through evolution. He now accepts the need for an intelligent source to have been involved in the making of the DNA code.

"What I think the DNA material has done is show that intelligence must have been involved in getting these extraordinary diverse elements together," he said (quoted by Richard Ostling, "Leading Atheist Now Believes in God," Associated Press report, Dec. 9, 2004).

"Fearfully and wonderfully made"

Although written thousands of years ago, King David's words about our marvelous human bodies still ring true. He wrote: "For You formed my inward parts, You covered me in my mother's womb. I will praise You, for I am fearfully and wonderfully made . . . My frame was not hidden from You, when I was made in secret, and skillfully wrought. . ." (Psalms 139:13-15 Psalms 139:13-15 [13] For you have possessed my reins: you have covered me in my mother's womb. [14] I will praise you for I am fearfully and wonderfully made: marvelous are your works and that my soul knows right well. [15] My substance was not hid from you, when I was made in secret, and curiously worked in the lowest parts of the earth.
American King James Version× , emphasis added).

Where does all this leave evolution? Michael Denton, an agnostic scientist, concludes: "Ultimately the Darwinian theory of evolution is no more nor less than the great cosmogenic myth of the twentieth century" (Denton, p. 358).

All of this has enormous implications for our society and culture. Professor Johnson makes this clear when he states: "Every history of the twentieth century lists three thinkers as preeminent in influence: Darwin, Marx and Freud. All three were regarded as 'scientific' (and hence far more reliable than anything 'religious') in their heyday.

"Yet Marx and Freud have fallen, and even their dwindling bands of followers no longer claim that their insights were based on any methodology remotely comparable to that of experimental science. I am convinced that Darwin is next on the block. His fall will be by far the mightiest of the three" (Johnson, p. 113).

Evolution has had its run for almost 150 years in the schools and universities and in the press. But now, with the discovery of what the DNA code is all about, the complexity of the cell, and the fact that information is something vastly different from matter and energy, evolution can no longer dodge the ultimate outcome. The evidence certainly points to a resounding checkmate for evolution! GN


Frequently Asked Questions About "Intelligent Design"

Q: What is intelligent design?
A: Intelligent design (ID) is a pseudoscientific set of beliefs based on the notion that life on earth is so complex that it cannot be explained by the scientific theory of evolution and therefore must have been designed by a supernatural entity.

Q: Is ID a scientific theory?
A: No. A scientific theory must be testable and based on observable evidence. A scientific theory makes predictions about occurrences in the natural world that can then be tested through scientific experimentation. ID makes no predictions and cannot be scrutinized using the scientific method. So although proponents of ID couch their views in scientific terms, their assertion that ID is a scientific theory is false.

Q: How is ID like and unlike traditional creationism and creation science?
A: ID is the most recent incarnation of creationism. Unlike traditional forms of creationism, ID does not openly rely on a literal interpretation of the Bible. Nor does it take a stand on such issues as the age of the earth, in order to secure a broad base of support from creationists with differing views. Like traditional forms of creationism, it claims to have scientific evidence for the existence of design in the biological world unlike them, it refrains from claiming that the designer can be ascertained to be God. Yet, although some proponents have suggested that the designer could be a space alien or a time-traveler from the future, such possibilities are not seriously entertained. In its scientifically unwarranted criticisms of evolution, ID's arguments are a subset of those used by traditional forms of creationism.

Q: What is biological evolution?
A: Biological evolution is a scientific theory that explains how life on earth has changed over time. The belief that species have evolved existed before Darwin, and was first stimulated by finding fossils of animals that no longer exist. Evolution has undergone many important developments since Darwin's time, most notably the incorporation of genetics.

Q: Why isn't ID a possible alternative to evolution?
A: ID is not a scientific theory and therefore cannot be put forward as an alternative to the scientific theory of evolution. ID has no explanatory power or predictive power. It simply says that some things that seem very complex could not have happened based on natural causes. So where it sees complexity, it declares that it must have been created by a supernatural entity. This is not science.

Q: Who is behind the ID movement?
A: The ID movement is led by a small group of activists based at the Discovery Institute's Center for Science and Culture (formerly Center for the Renewal of Science and Culture) in Seattle, WA. There are very few credentialed scientists among the group's leadership, and those who are scientists typically studied in fields unrelated to biology. Their approach to religion is very different from the leading scientists in the United States who are religious. Most legitimate scientists who are people of faith accept the overwhelming evidence supporting the scientific theory of evolution and see no conflict between the two.

Q: What is the "Wedge Strategy?"
A: The Wedge Strategy is an internal memorandum from the Discovery Institute that was leaked to the Internet in 1999. Although ID proponents publicly declare that they are neutral on many questions related to their religious motivations, the Wedge document reveals in clear terms that their assertions are at best deceptive. The document specifically outlines plans to reverse prevailing scientific practices and methods, and makes clear that the motivations of ID's main supporters are religious, not scientific. It is indeed curious that they would choose deception to advance their religious beliefs.

Q: Why not "teach both sides"?
A: This would be like teaching astrology in an astronomy course or alchemy in a chemistry class. There are not "two sides" to the science. Evolution is a scientific theory that seeks to explain how life on earth has changed over time, while ID is simply an ideology that attacks science and asks that its ideas be accepted as if they are true. Evolution and ID address different topics, employ different methods and certainly should be judged by entirely different standards.

Q: How does ID undermine science education?
A: Teaching ID as a so-called "alternative" to evolution would misinform students as to the scientific standing of the theory of evolution and the workings of the scientific method. In addition, it would improperly prepare them for postsecondary science education, placing them at a significant disadvantage to their peers. All scientists and physicians who study such diseases as SARS and AIDS, as well as those who trace how bacteria become resistant to antibiotics, completely rely on evolutionary theory to understand the phenomena they are examining. We are certain that even ID proponents would prefer to rely on these scientists rather than a scientist who believes that SARS or AIDS was created by intelligent design and can be explained only by intelligent design.

Q: How does ID undermine religious freedom?
A: ID is attempting to insert its particular religious beliefs into science education - as if it were science. By trying to use governments to give the prestigious label of "science" to their controversial theories, they are misleading children and parents. By attempting to elevate a single religious viewpoint over others and situating religion in conflict with science, they are endangering the religious freedom of all Americans. In the words of Theologian John F. Haught, "If a child of mine were attending a biology class where the teacher proposed that students consider ID as an alternative to?evolution I would be offended religiously as well as intellectually." (Haught, J, rep. App. 3, tab F, at 7.)

Q: What's wrong with the claim that evolution is "just a theory"?
A: Calling evolution "just a theory" is deeply misleading because it confuses the everyday meaning of the word "theory" (a "hunch" or an "opinion.") with the scientific meaning (requiring an explanation that is testable, grounded in evidence and able to predict natural phenomena better than competing theories). The scientific theory of evolution is one of the most robust theories in modern science. It has been corroborated by hundreds of thousands of independent observerations and has succeeded in predicting natural phenomena in every field of the biological sciences, from paleontology to molecular genetics. No persuasive evidence has been put forward in the last 150 years to contradict the theory of evolution. In the words of Theodosius Dobzhansky, one of the most prominent geneticists of the 20th century, "Nothing in biology makes sense except in light of evolution."

Q: Does the scientific theory of evolution deny the existence of an intelligent designer or God?
A: No. Since the question of God's existence is outside the realm of science, the theory of evolution is silent on it. Darwin himself openly wondered about the existence of a supreme designer throughout his life, but kept these questions separate from his scientific work. Accepting evolution and belief in God are not mutually exclusive. Many scientists hold personal religious beliefs, including Dr. Francis Collins, leader of the Human Genome Project and an evangelical Protestant, and Dr. Kenneth Miller, a Catholic and a prominent biologist who was called as an expert witness in Kitzmiller v. Dover .

Q: Aren't there controversies among scientists about evolution?
A: There are many debates within science about aspects of any theory, and scientific theories are constantly being revised as new and compelling information is learned. In evolution, as in all areas of science, our knowledge is incomplete. There are many important debates within evolutionary theory. For example, what features of animals are due to sexual selection as opposed to natural selection? How much of evolutionary change occurs because of the need to adapt to changing environments versus random genetic change? Does natural selection occur only at the level of the individual organism or can it occur also at the level of groups or even species? The list goes on. None of these debates, however, undermines the scientific standing of evolution itself. In fact, each has added to our understanding of the ways in which evolution works, and strengthened the core elements of the theory.

Q: Why not teach ID as just one controversy about evolution along with others?
A: Unlike real scientific theories, ID cannot provide any evidence in favor of its conclusions - meaning that it is an ideology and not science.

Q: But what about gaps in the theory of evolution that cannot be explained by scientists?
A: Most important scientific theories have gaps that need to be filled, and unanswered questions do not render a theory invalid. Doubters of Galileo's theory of the earth's rotation around the sun asked, why, if the earth is spinning, don't we all fly off it? It took roughly a half-century for Isaac Newton to develop the theory of gravitational pull, which answers this question. A scientific theory is not disqualified simply because it raises new questions in fact, the ability of a theory to inspire new questions and experiments is a measure of its quality. Furthermore, most of the so-called "unexplainable gaps" pointed out by ID proponents have in fact been answered by scientists. For many years "creationists" argued that there were serious gaps in the "fossil record" and that there was no fossil record of transitional species. During the last twenty years several such transitional species have been found -- something that ID people are reluctant to admit -- making the original assertion more and more dubious.

Q: Have the ID critiques of evolutionary theory been published in peer-reviewed scientific journals?
A: Peer review is the standard process by which scientists judge each other's work and deem it acceptable for publication in scientific journals. Only one article supporting ID has ever been published in a peer-reviewed journal - the Proceedings of the Biological Society of Washington - and it was later disavowed by the Society's governing council. The writer was a philosopher of science, not a practicing scientist, and the article reported no original data. Other scientific publications by authors affiliated with ID were on subjects other than ID. Aside from this one instance, proponents of ID have published their work in the popular press, avoiding review by experts.

Q: What do ID proponents mean by "irreducible complexity" and how do they argue that this concept implies design?
A: Michael Behe, a Discovery Institute fellow, coined the term "irreducible complexity" as a description of organisms that are so complex that they could not come into existence gradually. He uses a mousetrap as an example: a mousetrap has many different parts, and if one of them did not work, you wouldn't have an inferior mousetrap, rather your mousetrap would not work at all. Therefore, the mousetrap couldn't work at all until all the parts were in place. In biology, structures that don't function are weeded out by natural selection, so Behe concludes that complex biological systems must have been designed with all their parts in place as well. However, evolution does not necessarily occur in a linear progression, with each new part being added on, one at a time. Instead, structures develop for one purpose, and then get co-opted for a different task. Scientists have been able to chart these changes in many organisms that seem irreducibly complex in their current form, showing how natural selection can produce stunning variety from the same building blocks. The failure of Behe's irreducible complexity argument is a perfect example of ID's failure as a whole: misunderstanding how evolution works, ID's proponents reject it in favor of divine intervention.


Sandwalk

I was doing some reading on lncRNAs (long non-coding RNAs) in order to find out how many of them had been assigned real biological functions. My reading was prompted by the one of the latest updates to the human genome sequence namely, assembly GRCh38.p3 from June 2015. The Ensembl website lists 14,889 lncRNA genes but I'm sure that most of these are just speculative [Ensembl Whole Genome].

The latest review by my colleagues here in the biochemistry department at the University of Toronto (Toronto, Canada), concludes that only a small fraction of these putative lncRNAs have a function (Palazzo and Lee, 2015). They point out that in the absence of evidence for function, the null hypothesis is that these RNAs are junk and the genes don't exist. That's not the view that annotators at Ensembl take.

This is getting to be a familiar refrain. I understand how modern scientists might be confused about the difference between the Watson and the Crick versions of the Central Dogma [see The Central Dogma of Molecular Biology]. Many textbooks perpetuate the myth that Crick's sequence hypothesis is actually the Central Dogma. That's bad enough but lots of researchers seem to think that their false view of the Central Dogma goes even further. They think it means that the ONLY kind of genes in your genome are those that produce mRNA and protein.

I don't understand how such a ridiculous notion could arise but it must be a common misconception, otherwise why would these authors think that non-coding RNAs are a challenge to the Central Dogma? And why would the reviewers and editors think this was okay?

I'm pretty sure that I've interpreted their meaning correctly. Here's the opening sentences of the introduction to their paper .

They think that the Central Dogma is a "protein-centered bias." They think the Central Dogma rules out genes that specify noncoding RNAs. (Like tRNA and ribosomal RNA?)

It's simply not true that scientists in the past viewed all noncoding DNA as junk, at least not knowledgeable scientists [What's in Your Genome?]. Furthermore, no knowledgeable scientists ever interpreted the Central Dogma of Molecular Biology to mean that the only functional genes in a genome were those that encoded proteins.

Apparently Lee, Vincent, Picler, Fodde, Berindan-Neagoe, Slack, and Calin knew scientists who DID believe such nonsense. Maybe they even believed it themselves.

Judging by the frequency with with such statements appear in the scientific literature, I can only assume that this belief is widespread among biochemists and molecular biologists. How in the world did this happen? How many Sandwalk readers were taught that the Central Dogma rules out all genes for noncoding RNAs? Did you have such a protein-centered bias about the role of genes? Who were your teachers?

Didn't anyone teach you who won the Nobel Prize in 1989? Didn't you learn about snRNAs? What did you think RNA polymerases I and III were doing in the cell?


References

Barad, Karen, 2007. Meeting the Universe Halfway: Quantum Physics and the Entanglement of Matter and Meaning, Duke University Press.

Carter, Christopher, 2010. The human genome is composed of viral DNA: Viral homologues of the protein products cause Alzheimer's disease and others via autoimmune mechanisms, naturepreceedings: http://precedings.nature.com/documents/4765/version/1.

Chaisson, Eric J., 2001. Cosmic Evolution: The Rise of Complexity in Nature. Harvard University Press: Cambridge, MA.

Dennett, Daniel. 1995. Darwin's Dangerous Idea. New York: Simon & Schuster.

Dyson, Freeman, 1999. Origins of Life: Revised Edition. Cambridge University Press: Cambridge.

Folsome, Clair, 1985. “Microbes,” in The Biosphere Catalogue, ed. T. P. Snyder (Fort Worth, Texas: Synergetic Press), 51–56.

Flegr, J., Klose, J., Novotná, M., Berenreitterová, M., and Havlícek, J., 2009. "Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study." BMC Infectious Diseases 9 (72): 72.

Loomis, R.S. and D.J. Connor, 1992. Crop Ecology: Productivity and Management in Agricultural Systems. Cambridge University Press: Cambridge, England.

Helmreich, Stefan, 2009. Alien Ocean: Anthropological Voyages in Microbial Seas. University of California Press.

Hird, Myra J., 2009. The Origins of Sociable Life: Evolution After Science Studies.Palgrave Macmillan.

Margulis, Lynn and Sagan, Dorion, 1997. What is Sex? Simon and Schuster.

McFall-Ngai, Margaret, 2011. “Origins of the Immune System,” Chapter 17 in Chimeras and Consciousness: Evolution of the Sensory Self, (Lynn Margulis, Celeste A. Asikainen, Wolfgang E. Krumbein, editors), MIT Press.

Milius, Karen, 2011. “Green Sea Slug Is Part Animal, Part Plant,” Science News, Wired Science:http://www.wired.com/wiredscience/2010/01/green-sea-slug/

Mitteldorf, J. and J. Pepper, 2009. "Senescence as an adaptation to limit the spread of disease." The Journal of Theoretical Biology, 260(2): 186-195.

Sagan, Dorion, 1992. “Metametazoa: Biology and Multiplicity. In Incorporations (Zone 6 Fragments for a History of the Human Body), Jonathan Crary and Sanford Kwinter, eds. Zone, pp. 362-385.

Sagan, Dorion and Margulis, Lynn, 2005. “Candidiasis and the Origin of Clowns,” New England Watershed, October, pp. 16-19. (Reprinted in Dazzle Gradually: Reflections on the Nature of Nature. Chelsea Green, pp. 146-152).

Schneider, Eric D., and Sagan, Dorion, 2004. Into the Cool: Energy Flow, Thermodynamics, and Life, 2nd edition, paperback. University of Chicago Press, Chicago.

Teresi, Dick, 2011. Discover Interview: “Lynn Margulis Says She's Not Controversial, She's Right: It's the neo-Darwinists, population geneticists, AIDS researchers, and English-speaking biologists as a whole who have it all wrong” http://discovermagazine.com/2011/apr/16-interview-lynn-margulis-not-controversial-right/article_view?b_start:int=1&-C=

Whitehead, Alfred North, 1962. Science and the Modern World, Lowell Lectures 1925. The New American Library, p. 10.