RM & NS: The Creationist and ID Strawman

AUTHOR: Allen MacNeill

SOURCE: Original essay

COMMENTARY: That's up to you...

Creationists and supporters of Intelligent Design Theory ("IDers") are fond of erecting a strawman in place of evolutionary theory, one that they can then dismantle and point to as "proof" that their "theories" are superior. Perhaps the most egregious such strawman is encapsulated in the phrase "RM & NS". Short for "random mutation and natural selection", RM & NS is held up by creationists and IDers as the core of evolutionary biology, and are then attacked as insufficient to explain the diversity of life and (in the case of some IDers) its origin and evolution as well.

Evolutionary biologists know that this is a classical "strawman" argument, because we know that evolution is not simply reducible to "random mutation and natural selection" alone. Indeed, Darwin himself proposed that natural selection was the best explanation for the origin of adaptations, and that natural selection itself was an outcome that necessarily arises from three prerequisites:

• Variety: significant differences between the characteristics of individuals in populations);

• Heredity: genetic inheritance of traits from parents to offspring; and

• Fecundity: reproduction, often resulting in more offspring than are necessary for replacement.

Given these prerequisites, the following outcome is virtually inevitable:

• Demography: some individuals survive and reproduce more often than others, and hence their heritable characteristics become more common in their populations over time.

As I have alread pointed out in an earlier post, the real creative factor in evolution isn't natural selection per se, it's the "engines of variation" that produce the various heritable characteristics that natural selection then preserves from generation to generation. According to the creationists and IDers, the only source of such variation is "random mutations", and so there simply isn't enough variation to provide the raw material for evolutionary change.

In my earlier post on the "engines of evolution" I promised a list of the "engines of variation" that provide the raw material for evolutionary change. It's taken me a while, but here it is. This list includes "random mutation,' of course, but also 46 other sources of variation in either the genotypes or phenotypes of living organisms. Note that the list is not necessarily exhaustive, nor are any of the entries in the list necessarily limited to the level of structure or function under which they are listed. On the contrary, this is clearly a list of the minimum sources of variation between individuals in populations. A comprehensive list would almost certainly include hundreds (and possibly thousands) of more detailed processes. Also, the list includes processes that change either genotypes or phenotypes or both, but does not include processes that are combinations of other processes in the list, again implying that a comprehensive listing would be much longer and more detailed.

Anyway, here is the list of the "engines of variation", arranged according to level of structure and function (if a term is underlined, you can click on it and be taken to a definition and explanation of that term, usually at Wikipedia):

SOURCES OF HERITABLE VARIATION BETWEEN INDIVIDUALS IN POPULATIONS

Gene Structure (in DNA)

1) point mutations

2) deletion and insertion (“frame shift” / "indel") mutations

3) inversion and translocation mutations

Gene Expression in Prokaryotes

4) changes in promoter or terminator sequences (increasing or decreasing binding)

5) changes in repressor binding (in prokaryotes); increasing or decreasing binding to operator sites

6) changes in repressor binding (in prokaryotes); increasing or decreasing binding to inducers

7) changes in repressor binding (in prokaryotes); increasing or decreasing binding to corepressors

Gene Expression in Eukaryotes

8) changes in activation factor function in eukaryotes (increasing or decreasing binding to promoters)

9) changes in intron length, location, and/or editing by changes in specificity of SNRPs

10) changes in interference/antisense RNA regulation (increasing or decreasing binding to sense RNAs)

Gene Interactions

11) changes in substrates or products of biochemical pathways

12) addition or removal of gene products (especially enzymes) from biochemical pathways

13) splitting or combining of biochemical pathways

14) addition or alteration of pleiotropic effects, especially in response to changes in other genes/traits

Eukaryotic Chromosome Structure

15) gene duplication within chromosomes

16) gene duplication in multiple chromosomes

17) inversions involving one or more genes in one chromosome

18) translocations involving one or more genes between two or more chromosomes

19) deletion/insertion of one or more genes via transposons

20) fusion of two or more chromosomes or chromosome fragments

21) fission of one chromosome into two or more fragments

22) changes in chromosome number via nondisjunction (aneuploidy)

23) changes in chromosome number via autopolyploidy (especially in plants)

24) changes in chromosome number via allopolyploidy (especially in plants)

Eukaryotic Chromosome Function

25) changes in regulation of multiple genes in a chromosome as a result of the foregoing structural changes

26) changes in gene expression as result of DNA methylation

27) changes in gene expression as result of changes in DNA-histone binding

Genetic Recombination

28) the exchange of non-identical genetic material between two or more individuals (i.e. sex)

29) lateral gene transfer via plasmids and episomes (especially in prokaryotes)

30) crossing-over (reciprocal and non-reciprocal) between sister chromatids in meiosis

31) crossing-over (non-reciprocal) between sister chromatids in mitosis

32) Mendelian independent assortment during meiosis

33) hybridization

Genome Structure and Function

34) genome reorganization and/or reintegration

35) partial or complete genome duplication

36) partial or complete genome fusion

Development (among multicellular eukaryotes, especially animals)

37) changes in tempo and timing of gene regulation, especially in eukaryotes

38) changes in homeotic gene regulation in eukaryotes

39) genetic imprinting, especially via hormone-mediated DNA methylation

Symbiosis

40) partial or complete endosymbiosis

41) partial or complete incorporation of unrelated organisms as part of developmental pathways (especially larval forms)

42) changes in presence or absence of mutualists, commensals, and/or parasites

Behavior/Neurobiology

43) changes in behavioral anatomy, histology, and/or physiology in response to changes in biotic community

44) changes in behavioral anatomy, histology, and/or physiology in response to changes in abiotic environment

45) learning (including effects of use and disuse)

Physiological Ecology

46) changes in anatomy, histology, and/or physiology in response to changes in biotic community

47) changes in anatomy, histology, and/or physiology in response to changes in abiotic environment

So, next time you hear or read a creationist or IDer cite "RM & NS" as the sole explanation for evolutionary change, point out to them and everyone else that there are at least 47 different sources of variation (including "random mutations"), and at least three different processes that result from them: natural selection, sexual selection, and random genetic drift.

Comments, criticisms, and suggestions (especially additional items for the list) are warmly welcomed!

--Allen

More on Transcribed But Non-Translated RNA

On the same subject as the previous post (The Gene Is Dead, Long Live The Gene!), here is the following:

MikeGene at Telic Thoughts ( see Error Correction Runs Yet Deeper) wrote this about the new findings vis-a-vis transcribed but not translated RNAs:

According to Mats Ljungman, a researcher at the University of Michigan Medical School, as many as 20,000 lesions occur daily in a cell’s DNA. To repair all this continual damage, how does the cell first detect it? Ljungman’s research identified the logical candidate – RNA polymerase (the machine that reads the DNA and makes an RNA copy). Apparently, whenever the RNA polymerase encounters a lesion, it signals to p53, a master protein that activates all sorts of DNA repair processes.

According to the press release:

“These two proteins are saying, ‘Transcription has stopped,’” says Ljungman. These early triggers act like the citizen who smells smoke and sounds a fire alarm, alerting the fire department. Then p53, like a team of fire fighters, arrives and evaluates what to do. To reduce the chance of harmful mutations that may result from DNA damage, p53 may kill cells or stop them temporarily from dividing, so that there is time for DNA repair.

Recently, the ENCODE consortium determined that the majority of DNA in the human genome is transcribed:

This broad pattern of transcription challenges the long-standing view that the human genome consists of a relatively small set of discrete genes, along with a vast amount of so-called junk DNA that is not biologically active.

Of course, one could also argue that all this transcription simply speaks to the sloppy and wasteful nature of the cell. Yet here’s a thought. It would seem to me that Ljungman’s research now raises a third possibility: all that transcription is just another layer of error surveillance.

To which I replied:

That is a VERY interesting hypothesis. It could work like this: by incorporating large amounts of transcribed (but not translated) DNA into the human genome, the cell is essentially presenting a much larger "target" for mutation-detection by the p53 surveillance system. In essence, a cell that has been especially challenged by mutation-producing processes would be much more likely to send out the "fire alarm," since it would be much more likely to have transcription terminated and thereby triggering the p53 "stopped transcription" alarm. To extend the "fire alarm" analogy, imagine a house that is unusually likely to have a fire; perhaps it's very hot, or dry, or has smoldering fires in several locations. As the old saying goes, "where there's smoke, there's fire," and a fail-safe cancer/mutation detection system would be much more likely to detect potential "hot-cells" if there were a large amount of transcription going on.

Indeed, this would be most important in cells in which relatively little transcription of functional (i.e. protein-encoding) genes normally takes place, but which are still subject to mutation and potential cancer induction. By running the "non-coding transcription program constantly in the background, such cells could still alert the cancer/mutation surveillance system, even when they themselves aren't actively coding for protein.

Now, since transcription is itself a costly process, doing a lot of it for non-coding genes would also be costly. Cells would therefore be selected via a cost-benefit process for the amount of non-coding "surveillance transcription" they could do. that is, the more likely a cell/organism is to have a cancer/mutation event, the more valuable its non-coding/surveillance transcription system would be, and therefore the more non-coding DNA it should have. This immediately suggests a possible test of hypothesis: those cells (or organisms) that are more likely to suffer from cancer/mutation events would therefore have more non-coding "surveillance transcription" DNA sequences.

For example, since animals are much more likely to be harmed by uncontrolled cell division (i.e. cancer, induced by mutation), then one would predict that animals would have more non-coding/surveillance transcription sequences than, say, plants. Also, animals that live longer (and would therefore have a larger "window" for suffering mutations), should also have relatively large amounts of non-coding/surveillance transcription sequences.

Somebody should check this out (if they haven't already).

Nick (Matzke?) then commented:

The old C-value paradox may have some relevance here. Does the amount of non-coding/surveillance transcribed sequences correlate with the total amount on non-coding sequence? For example, do puffer fish have fewer non-coding transcribed sequences than zebrafish, or do they have the same amount of transcribed DNA with the difference in genome size being due to non-coding, non-transcribed sequence?

Encode's data would seem to argue for a close correlation between total genome size and amount of transcribed non-coding sequence. If that observation is generally applicable to other organisms, thenC value might be one way to test MikeGene's and Allen's hypotheses. The idea that transcription of non-coding DNA is another layer of mutation detection/error correction would imply that organisms with larger genomes have more mutation detection capability. Do animals with smaller genomes require less error detection because they live in less mutagenic environments? The dramatic differences in genome size among related organisms that live in similar environments would seem to argue against that hypothesis. Compare genome sizes of freshwater pufferfish and zebrafish, both of which live in freshwater streams, or look at the variation in genome size among salamanders of the genus Plethodon

To explore this issue, check out the very cool Animal Genome size database:

You can also test Allen's lifespan hypothesis. For example, zebrafish and small tetras with lifespans of 2 or 3 years have approximately the same genome size as common carp with lifespans of 20+ years.

One of the ID supporters on the list then challenged me to explain how such a complex error-surveillance system could have evolved via non-directed natural selection. This was my reply (Nota bene: the following is, of course, an HYPOTHESIS only):

Consider two virtually identical phylogenetic lines, A and B. At time zero, individuals in both lines start out with virtually no transcribable but non-coding DNA (abbreviated TNCDNA). If we assume a constant mutation rate for both lines, individuals in both lines would have essentially the same probability of dying from cancer.

Assume further that, over time, sequences of non-TNCDNA accumulate in the genomes of each line. This can happen by any one (or more) of several known mechanisms, such as gene dupilcation (without active promoter sequences), random multiplication of tandem repeats, retroviral or transposon insertions of non-TNCDNA, etc.

Then, at time one, an individual (or more than one) in line B have an active promoter inserted in front of one or more of their non-TNCDNA sequences in one or more of their cells, by the same mechanisms listed above. Now, these individuals have a lower probability of dying from the resulting cancer, since their p53-regulated surveillance systems would be more likely to eliminate the affected cells. Again, this would be a side-effect of the larger "mutation sponge" their cells would present to potentially mutagenic processes. Such individuals would therefore have more descendants, and over time the average size of all of the "mutation sponges" in the subsequent populations would increase. Natural selection in action, folks.

Now, as to the question of where the p53 surveillance system came from in the first place, proteins like p53 are common intermediates in intracellular signalling systems. Assume that the ancestor of p53 was a protein with some other signalling function. At some point, an individual that had p53 doing that other function has a mutation that changes the shape of p53 in such a way that it becomes part of a regulatory pathway that triggers apoptosis, thereby eliminating the cell. If the altered p53 no longer participates in the original pathway, and if that alteration is damaging, such individuals would be elimated, and the original function of p53 would be preserved.

However, if the altered p53 (now participating in the regulation of apoptosis) were also activated by the cells' normal "transcription termination signalling system" as described in Mike's original post, then individuals with the altered p53 would be less likely to die from cancer, and their descendants (who now produce the altered form of p53) would become more common over time.

Mike's original post notes that the research report cited the relatively recent observation that many cells actually suffer multiple mutations much of the time. This is precisely the situation that Darwin originally stated was a prerequisite for natural selection: not genetic mutations (Darwin didn't know about them), but increased heritable variation (which Darwin couldn't explain, but could point to as an observable phenomenon in living organisms). In other words, as both EBers and IDers both point out, phenotypic variations are very, very common, and so are the genetic changes with which they are correlated. Most of these variants are either selectively neutral (c.f. Kimura), nearly neutral (c.f. Ohta), or deleterious to some degree. Such changes either accumulate (if they are neutral or nearly so) or are eliminated (if they are deleterious).

But, in those relatively rare occasions when they result in increased relative survival and reproduction, they increase in frequency in those populations in which they exist. By this process of "natural preservation" (Darwin's preferred name for the process he and Alfred Russell Wallace proposed as the primary mechanism for descent with modification) results in the accumulation of both neutral and beneficial characters and the elimination of deleterious ones.

And by the way, the foregoing is why Darwin (and not Edward Blythe) is credited with the concept of "natural selection/preservation": Blythe only described the elimination of deleterious characters, and never realized that the preservation of beneficial characters could result in the origin of adaptations. Blythe, in other words, only recognized what EBers call "stabilizing selection," but missed the much more interesting and important "directional selection," which Darwin cited as the causal basis for evolution of adaptations.

Comments, criticisms, and suggestions are warmly welcomed!

--Allen

What is the "engine" of evolution?

AUTHOR: Allen MacNeill

SOURCE: Original essay

COMMENTARY: That's up to you...

Ever since Darwin, the primary "engine" of evolution has been considered to be natural selection. However, if one takes a closer look at this, it is clear that natural selection is not an "engine," it is an outcome. If evolution is defined as change in the characteristics of the members of a population over time and natural selection is defined as unequal non-random survival and reproduction (or, more parsimoniously, differential reproductive success), then the underlying cause of the changes that are differentially preserved over time is the real "engine" of evolution by natural selection.

And what might this "engine" of change be? Exactly what Darwin said it was in the Origin of Species: the "laws of variation" of which naturalists of his time were almost "completely ignorant." That is, given that some variations are heritable and that they can be passed from parents to offspring in the process of reproduction, then it is the processes that cause such variations that are the real "engine(s)" of evolution, including evolution by natural selection.

Darwin was on the right track when later on he sought out the specifics of the "engines of variation" in Variation of Animals and Plants Under Domestication, published in 1868. Darwin suggested that the rate of variation changed over time, in response to specific changes in the environment. For example, he pointed out that the variation between domesticated animals and plants was considerably greater than that found in the wild. This suggested to him that something about domestication – increased food, improved nutrition, lack of predators, etc. – caused an increase in the production of variations that were then exploited by animal and plant breeders.

However, it is now generally accepted that the only real difference between domesticated and wild animals and plants, in terms of variation, is that the conditions of domestication allow more variants to survive and reproduce, rather than causing more of them to be produced in the first place. I do not know enough genetics to say whether or not this is the case, but it seems to me at least that Darwin's idea is worth empirical investigation. Here are the relevant questions (which may or may not already have answers):

• Is the rate of generation of genetic and phenotypic variation a constant?

If the answer to this question is "yes," then all we need to investigate is the actual genetic and developmental mechanisms by which such variations are generated. However, if the answer is "no," then the rate of generation of genetic and phenotypic variations is variable, which immediately suggests more questions:

• Is the increased rate of generation of variations correlated with any identifiable factor in either the genetics/development or the environment of organisms in which such variable rates of variation are observed?

If the answer to this question is "no," then we may safely assume that the underlying "engine(s)" of variation is/are entirely random, insofar as we can observe it changing randomly over time. However, if the answer is "yes," then there are more questions:

• Via what mechanism(s) is the increased rate of variation generated, and are the "triggers" for such increased variation endogenous, exogenous, or some combination of the two?

Clearly, the "engine(s)" of variation are prodigious, as it/they have been able over time to modify something as simple as a mycoplasm into an oak tree or a blue whale. Some supporters of "intelligent design" (ID) would dispute this statement, of course, claiming (without any empirical evidence) that "you can't get here from there." However, we clearly have gotten here from there; the real question is "how?" There are logically at least two possibilities:

• The process(es) by which the "engine(s) of variation" have produced the necessary variation have operated endogenously by means of a prodigious (and undirected) "random variation generator," the products of which have been sorted over time by natural selection (i.e. the Darwinian hypothesis), or

• The process(es) by which the "engine(s) of variation" have produced the necessary variation have operated endogenously by means of a less prodigious "non-random variation generator," the products of which have been sorted over time by natural selection (i.e. the ID hypothesis).

Noticing that the only difference between these two possibilities is the amount of variation and its source immediately suggests a way of testing the two hypotheses: do the currently identified mechanisms of genetic and phenotypic variation produce enough variation to get from there to here, or not? If the answer is "yes," then the ID hypothesis is unnecessary, and therefore irrelevent to science.

So, the next obvious question is, what are the currently identified mechanisms of genetic and phenotypic variation, and do they provide enough variation to get here from there? The answer to this question will be posted soon -watch this space.

And as always, comments, criticisms, and suggestions are warmly welcomed!

--Allen

Unraveling Where Chimp And Human Brains Diverge

SOURCE: Terra Daily News

COMMENTARY: Allen MacNeill

Just in time for our discussion of human-chimpanzee differences in our evolution course at Cornell, here is an article describing recent research into how human an chimpanzee brains differ. Commentary follows:

Los Angeles CA (SPX) Nov 14, 2006: Many of the human-specific gene networks identified by the scientists related to learning, brain cell activity and energy metabolism.

Six million years ago, chimpanzees and humans diverged from a common ancestor and evolved into unique species. Now UCLA scientists have identified a new way to pinpoint the genes that separate us from our closest living relative - and make us uniquely human. The Proceedings of the National Academy of Sciences reports the study in its Nov. 13 online edition.
"We share more than 95 percent of our genetic blueprint with chimps," explained Dr. Daniel Geschwind, principal investigator and Gordon and Virginia MacDonald Distinguished Professor of Human Genetics at the David Geffen School of Medicine. "What sets us apart from chimps are our brains: homo sapiens means 'the knowing man.'

"During evolution, changes in some genes altered how the human brain functions," he added. "Our research has identified an entirely new way to identify those genes in the small portion of our DNA that differs from the chimpanzee's."

By evaluating the correlated activity of thousands of genes, the UCLA team identified not just individual genes, but entire networks of interconnected genes whose expression patterns within the brains of humans varied from those in the chimpanzee.

"Genes don't operate in isolation - each functions within a system of related genes," said first author Michael Oldham, UCLA genetics researcher. "If we examined each gene individually, it would be similar to reading every fifth word in a paragraph - you don't get to see how each word relates to the other. So instead we used a systems biology approach to study each gene within its context."

The scientists identified networks of genes that correspond to specific brain regions. When they compared these networks between humans and chimps, they found that the gene networks differed the most widely in the cerebral cortex -- the brain's most highly evolved region, which is three times larger in humans than chimps.

Secondly, the researchers discovered that many of the genes that play a central role in cerebral cortex networks in humans, but not in the chimpanzee, also show significant changes at the DNA level.

"When we see alterations in a gene network that correspond to functional changes in the genome, it implies that these differences are very meaningful," said Oldham. "This finding supports the theory that variations in the DNA sequence contributed to human evolution."

Relying on a new analytical approach developed by corresponding author Steve Horvath, UCLA associate professor of human genetics and biostatistics, the UCLA team used data from DNA microarrays - vast collections of tiny DNA spots -- to map the activity of virtually every gene in the genome simultaneously. By comparing gene activity in different areas of the brain, the team identified gene networks that correlated to specific brain regions. Then they compared the strength of these correlations between humans and chimps.

Many of the human-specific gene networks identified by the scientists related to learning, brain cell activity and energy metabolism.

"If you view the brain as the body's engine, our findings suggest that the human brain fires like a 12-cylinder engine, while the chimp brain works more like a 6-cylinder engine," explained Geschwind. "It's possible that our genes adapted to allow our brains to increase in size, operate at different speeds, metabolize energy faster and enhance connections between brain cells across different brain regions."

Future UCLA studies will focus on linking the expression of evolutionary genes to specific regions of the brain, such as those that regulate language, speech and other uniquely human abilities.

COMMENTARY:

Sounds to me like the differences are probably the result of different patterns of gene regulation in humans and chimps, rather than entirely different coding regions in the DNA of the two species. In other words, we share a common set of genes for making our brains, but those genes are regulated differently in the two species. This would explain a lot: why, for example, there is so little difference between human and chimp DNA, and how the two species could have diverged so quickly from a common ancestor six million years ago (or less, as some of the archaeological data seem to indicate).

It will be very interesting to see how this story develops, as we get higher and higher resolution "maps" of human and chimp brains and the genetic mechanisms that produce them.

--Allen