The Searchers

AUTHORS: William A. Dembski and Robert J. Marks II

SOURCE: Proceedings of the 2009 IEEE International Conference on Systems, Man, and Cybernetics. San Antonio, TX, USA – October 2009, pp. 2647-2652

COMMENTARY: Allen MacNeill

First, congratulations to Drs. Dembski & Marks! Publication is the life blood of all career academics and the living heart of the intellectual process. It takes courage and hard work (and a little bit of luck) to get your original work published, and more of the same to weather the criticism that inevitably ensues. But, just as one cannot have a fencing match without an opponent, real progress in any intellectual endeavor cannot come from consensus, but only from the clash of ideas and evidence.

And so, to specifics:

I have no quibble with most of the mathematical analysis presented. Indeed, given the assumptions upon which the authors' Conservation of Information (COI) theory is based (with which I do not necessarily agree, but which are clearly presented in their paper), the analysis presented is apparently not completely outside the domain of No Free Lunch (NFL) theorems in general.

However, the same cannot be said for the application of these ideas to biological evolution. To be specific, consider the following quote [Dembski & Marks (2009) pg. 2651, lines 2-5]:

"From the perspective of COI, these limited number of endpoints on which evolution converges constitute intrinsic targets, crafted in part by initial conditions and the environment." [emphasis added]

This is indeed the crux of the issue vis-a-vis biological evolution. While it is clearly the case that Simon Conway-Morris asserts that there is an apparently limited number of biological "endpoints", it is neither the case that Morris' viewpoint represents the core of evolutionary theory, nor that his point is relevant to the analysis of COI presented in Dr. Dembski and Marks' paper.

To be specific, the highlighted qualifier from the quote above – crafted in part by initial conditions and the environment – is precisely the issue under debate between evolutionary biologists and supports of intelligent design (ID).

Taken at face value, this qualifying simply phrase means that, given specific starting conditions and a specific time-varying environmental context, the various mechanisms of evolution (e.g. mutation, natural selection, genetic drift, inbreeding, etc.) tend to converge on a relatively limited set of genotypic and phenotypic "endstates" (i.e. what could be loosely referred to as "evolutionary adaptations").

This is simply another way of defining evolutionary convergence, and in no way constitutes evidence for intrinsic evolutionary teleology. On the contrary, it simply provides support for the hypothesis that, given similar conditions, similar outcomes result.

Furthermore, it assumes that virtually all characteristics of living organisms are adaptations (that is, genotypic/phenotypic characteristics that fulfill some necessary function in the lives of organisms). However, this is manifestly not the case, nor is it an absolutely necessary component of current evolutionary theory. On the contrary, many (perhaps the majority) of the characteristics of living organisms are not adaptive. This is certainly the case at the level of the genome, as evidenced by the neutral and nearly neutraltheories of molecular evolution.

Finally, Morris' (and, by extension, Dembski and Marks') position completely omits any role for historical contingency, which both the fossil and genomic record indicate are of extraordinary importance in macroevolution. As Dembski and Marks state, the "endpoints" (perhaps it would be more precise to refer to them as "way stations") of macroevolution depend fundamentally on initial conditions and the environment. But this is not fundamentally different from Darwin's position in the Origin of Species:

"The complex and little known laws governing variation are the same, as far as we can see, with the laws which have governed the production of so-called specific forms. In both cases physical conditions seem to have produced but little direct effect; yet when varieties enter any zone, they occasionally assume some of the characters of the species proper to that zone." [Darwin, C. (1859) Origin of Species, pg. 472, emphasis added]

Moreover, Dembski and Marks' analysis completely ignores the appearance (or non-appearance) of new genotypic and phenotypic variations, and on the accidental disappearance of such characteristics (via extinction), without regard to the adaptive value of such characteristics, or the lack thereof.

In other words, Dembski and Marks' analysis, while interesting from the standpoint of what could be called "abstract" search algorithms, completely fails to address the central issues of evolutionary biology: the source of evolutionary novelty (i.e. the "engines of variation"), the effects of changing environmental conditions on the actual forms and functions of living organisms, and the fundamental importance of historical contingency in the ongoing evolution of genotypes and phenotypes.

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

--Allen

"Can Natural Selection Produce New Information?"

Here's another in a series of responses to some common assertions/misunderstandings of evolutionary biology by creationists and "intelligent design" supporters. One of the most common arguments against the theory of evolution is that natural selection cannot produce genuinely new information:

"Natural selection does not produce new information. On the contrary, it only reduces existing genetic information. Evolutionary biologists shouldn't invoke mutations as a source of new information, because all known mutations involve a net loss of information."

This viewpoint demonstrates a basic misunderstanding of the process of evolution bynatural selection. According to Darwin (and virtually all evolutionary biologists), natural selection has three prerequisites:

1) Variety, generated by the "engines of variation";

2) Heredity, mediated by the transfer of genetic material (either vertically - from parents to offspring - or horizontally - via viral transduction, retrotranscription, etc.); and

3) Fecundity, that is, reproduction, usually at a rate that exceeds replacement (according to Malthus).

Given these three prerequisites, the following outcome is virtually inevitable:

4) Demography: Some individuals survive and reproduce more often than others. Ergo, the heritable variations of such individuals become more common over time in populations of those organisms.

Natural selection is synonymous with #4; it is an outcome of the three processes listed as prerequisites, not a "mechanism" in and of itself.

Ergo, the real dispute between evolutionary biologists and "intelligent design" supporters is not over natural selection per se, but rather the properties and capabilities of the "engines of variation". I have written extensively about these here and here.

Yes, natural selection (i.e. #4, above) is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term "natural preservation" rather than "natural selection". However, it is also clear that the "engines of variation" - that is, the processes the produce phenotypic variation among the members of populations of living organisms - are both extraordinarily creative and extraordinarily fecund. The real problem in biology is therefore not producing new variation, but rather limiting the production of new variation to the point that the "engines of variation" do not cause the inevitable disintegration of living systems.

As just one example of this problem, the genetic elements known as transposons generate a huge amount of new genetic variation, much of which is either phenotypically neutral or deleterious to the organism. There are biochemical mechanisms by which cells can monitor the incidence of transposition in themselves, and limit its consequences (up to and including the active self-destruction of the cell via apoptosis).

At the same time, there is very good evidence in the genomes of many organisms that retrotransposition events mediated by transposons have occasionally produced genetic changes that have resulted in increased survival and reproduction of the organisms in which such events have taken place. There is a large and growing literature on this phenomenon, all of which points to the inference that retrotransposition via transposons both creates new genetic and phenotypic variation, and that in some cases such variation can provide the raw material for evolutionary adaptations, which are preserved via natural selection.

So, if someone really wants to find out where the Intelligent Designer might create new variations, they should follow the lead of Darwin's good friend, Asa Gray, and look for the telltale evidence (if any) for such intervention in the "engines of variation". Of course, they would have to show pretty conclusively (using empirical investigations and statistical analysis) that such "creation events" are not the result of purely natural, unguided processes. If they can do this, they will undoubtedly win a Nobel Prize and a Crafoord Prize (plus a MacArthur or two).

Notice that this will involve looking carefully into the mechanisms by which new variations are produced, rather than pointing to the outcomes of such processes (i.e. natural selection) and simply asserting that "you can't get here from there". Simply asserting (without empirical evidence) that something can't happen isn't "doing science" at all. In fact, it's doing just the opposite...

...it's doing ID the way it's always been done up until now; by press release, rather than by empirical research.

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

--Allen

Teleology vs Teleonomy: Can a "Program" Exist Before Its "Programmer"?

This post is a follow-up to the previous post on the subject of the "randomness" in the processes that generate the variation that is necessary for biological evolution.

Can a "program" exist before its "programmer" (and therefore bring it into being)? This seems to be the core of the disagreement between ID supporters and mainstream scientists. The former (which include Charles Darwin's very close friend, Asa Gray) advocate the idea that the variation upon which natural selection and other evolutionary processes work is neither random nor unintentional. The latter (which include Darwin and his intellectual heirs) do not disagree with the idea that such variation is not "random". What they disagree with is the idea that there is some "intention" or "plan" guiding the variation that occurs, so that certain outcomes (including, but not limited to, the origin of humans) are more likely than others.

To answer the question that stands at the head of this post, I think it's essential to emphasize (as I did in the original blogpost) that the terms “foresighted” and “goal-oriented” are not equivalent, nor are the processes to which they are applied. As I have pointed out in many posts, there is no inherent contradiction between a process being purely "natural" (i.e. the result of the operation of purely natural processes) and being "goal-oriented".

Ernst Mayr (surely no advocate of "intelligent design") argued forcefully (and, in my opinion, convincingly) that biological organisms are indeed "goal-oriented". That is, their genomes provide a program, the function of which is to bring about a particular state of affairs: the survival and reproduction of the organism via its interactions with its environment.

The origin of the genome (i.e. the "program" itself) is an entirely different situation, however. Ever since Darwin it has been a standard assumption that the evolutionary processes by which the genetic "programs" that direct the assembly and operation of living organisms are not goal-oriented. These evolutionary processes – natural selection, sexual selection, founder effects, genetic bottlenecks, neutral "drift" in deep evolutionary time, exaptation, heterochronic development, changes in homeotic development, interspecific competition, species-level selection, serial endosymbiosis, convergence/divergence, hybridization, phylogenetic fusion, background and mass extinction/adaptive radiation, and internal variance – do not require any kind of "goal orientation" to produce the living entities and processes we observe around and within us. And, since such processes do not require goal-orientation or intentionality, these are not included in evolutionary explanations. Some, but not all, evolutionary biologists extend this idea to the assumption that goal-orientation or intentionality do not exist in nature, in the absence of pre-existing genomic "programs").

The main reason for this assumption has been that it is extremely problematic to agree on how one would go about showing that the aforementioned evolutionary processes have indeed been goal-oriented. The most serious objection to this idea is that there seems to be nowhere for such a "directing agency" to exist in material form, nor any natural means by which its goals could be impressed upon physical organisms.

The genomes of organisms are physical/chemical "stuff", which is translated via physical/chemical "machinery" into biological entities and processes. That is, there is a physical/chemical "vehicle" in which the information for assembling and operating organisms is carried and expressed.

The same would not the case for the putative source of the "evolutionary program" which might direct the evolution of the genomes of living organisms. Since such an "evolutionary program" would cause the evolution of the "genomic programs" which direct the assembly and operation of living organisms, such a program would necessarily have to exist before the origin and evolution of biological genomes, as it would be necessary for it to do so to direct their coming into being.

This presents two serious problems:

• By what mechanism(s) would such an "evolutionary program" cause "genomic programs" to come into existence, and

• Precisely where in the physical universe would such a pre-existing "evolutionary program" itself exist?

We seem to have two direct logical contradictions in terms:

• How can a non-natural "evolutionary program" cause a natural "genomic program" to come into existence, and

• How can a programmer pre-exist the program which brings itself into existence?

There is a proposed answer to these two questions, but one which most ID supporters seem loathe to invoke:

• That the "pre-existing program" that directs the evolution of the genomic programs of living organisms is woven into the structure of physical reality itself.

This is the line of inquiry pursued by Ilya Prigogine and Stuart Kauffman (among others), but which is rejected out-of-hand by nearly all ID supporters (most notably Michael Behe, William Dembski, and Phillip Johnson), who prefer a purely "supernatural" source for the "pre-existing program" by which evolution has been directed).

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

--Allen

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

Random Mutation and Natural Selection Revisited

AUTHOR: Allen MacNeill

SOURCE: Original essay

COMMENTARY: That's up to you...

Promoters of "intelligent design theory" and other forms of creationism often assert that random mutation plus natural selection (RM+NS) are insufficient to explain the diversity of life on Earth. In particular, people like William Dembski assert that RM+NS cannot work fast enough (even given billions of years) to produce the complex living organisms we observe around us.

In so doing, they attack evolutionary theory using a "straw-man argument," because modern evolutionary theory is not limited to RM+NS alone to produce adaptations, nor to explain the diversity of life on Earth. In particular, while there is no empirical evidence that would lead one to believe that mutations are produced by an "intelligent designer," it is also not true that mutations alone must supply the variation necessary for evolution by natural selection.

In particular, while it is true that any given mutation is random (as far as we can tell), a series of mutations which are then preserved as the result of natural selection aren't really random at all, at least not in the way that is often depicted by critics of evolutionary theory. In classical evolutionary theory, as first mathematically formalized by R. A. Fisher, the variation that is necessary for the raw material for natural selection is the result of a large number of individual alleles, all producing variations of the same trait, such as height or skin color in humans. In this model, a normal distribution of heights or skin colors are produced by combinations of different alleles, each influencing some fraction of the overall height, producing what Fisher and others called "continuous variation." Selection then preserved one or a few of the various allele combinations by preserving the individuals that carried the controlling alleles.



In this model, evolutionary change would necessarily be slow and gradual, as changes in the overall mean value for any trait would require the gradual accumulation of mutations in each of the many alleles that controlled the trait. Since the observable mutation rate is very low (at least, the rate of mutations that significantly affect most phenotypic traits is very low), the argument was that directional change in any given trait was something like a wagon train: only as fast as its slowest constituent. That is, change in the overall distribution of the trait (such as height) depended on the rate of mutation of all of the alleles controlling it, and required that a sufficient proportion of the alleles that were preserved by selection mutate and then be selected in the same "direction" (e.g. for greater height).

However, subsequent field and laboratory investigations into the genetic and developmental control of such variable traits have shown the multiple allele/continuous variation model upon which the "modern synthesis" was based is, in fact, not the way most traits apparently evolve. For example, consider a mutation that causes an increase in size of a particular anatomical feature (e.g. a finch's beak). Most such features are regulated by a set of genes that are themselves regulated by a homeotic gene (or a few such homeotic genes; in the case of Darwin's finches, the controlling homeotic gene is called bmp4, for "bone morphology protein 4") [1]. Homeotic genes, like many but not all genes, do not produce a purely monotonic trait (i.e a trait with no variation). Instead, they produce a trait that varies somewhat between individuals, in what approximates a normal distribution. In the case of finch beaks, this means that in any population of finches, there are some individuals with small beaks, some with large beaks, and most with intermediate beaks. All of these finches could easily have the same allele for the homeotic gene controlling the trait. The variation in beak size would therefore be the result, not of the expression of different alleles, but rather of the different outcomes of the expression of the same allele of the homeotic gene, developing differently in different individuals as the result of a combination of chance and environmental conditions (this is how humans differ in heights, for example).



Now consider a situation in which an environmental change (for example, a drought), selected for individual finches with larger beaks. At the level of the controlling homeotic gene, this could mean one of two things: either the larger beaks are still within the developmental limits of the original allele, or another allele (i.e a mutant) has arisen, with an overlapping developmental pattern but a higher mean value for beak size. If the former is the case, then a return to the original environment would result in a return to the original mean beak size.

However, if the latter were the case, then there would be a built-in bias toward finches with larger beaks in the resulting population. This would also mean that the "base" allele - i.e. the new mutant allele - would start out producing a larger mean beak size along with the usual normal distribution of beak sizes. If the environmental change persisted, new alleles might arise, but they would begin with a "norm of reaction" that would produce significantly larger mean beak sizes, along with a normal distribution with significantly larger beaks at the upper tail of the distribution.

In other words, the existing alleles for such a trait would bias subsequent mutations in the "direction" of larger beaks, simply because the pool of potential new alleles would already start out biased in that direction. Therefore, the mutations and developmental changes that were available from one generation to the next would be biased in the direction of whatever phenotypic trait resulted in the highest reproductive success.

This process, called genetic accommodation [2], is part of the new science of evo-devo, which renders much of the classical "evolutionary synthesis" obsolete, and at the same time explains how such phenomena as punctuated equilibria can be integrated into a unified theory of evolutionary development. In particular, genetic accommodation and similar processes can explain how natural selection alone can produce both rapid and directional change in phenotypes over time, thereby making any resort to "intelligent design" unnecessary and irrelevant.

REFERENCES CITED:

[1] Pennisi, E. (2004) Bonemaking protein shapes beaks of Darwin's finches. Science, Vol. 305. no. 5689, p. 1383, available at : http://www.sciencemag.org/cgi/content/summary/305/5689/1383

[2] West-Eberhard, M. J. (2003) Developmental Plasticity and Evolution. Oxford, UK, Oxford University Press. See especially pages 147 to 158.

--Allen