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

Jerry Fodor on Why Pigs Don't Have Wings



AUTHOR: Jerry Fodor

SOURCE: Why Pigs Don't Have Wings
(London Review of Books 29(20):19-22, 18 October 2007)

COMMENTARY: Allen MacNeill

Cognitive scientist and frequent critic of evolutionary psychology, Jerry Fodor, has a long article in the most recent issue of the London Review of Books in which he attacks what most people think of as the core of evolutionary biology: natural selection and adaptations. Fodor has attacked evolutionary psychology before, and spends most of his ammunition attacking it again in this article. However, he now has bigger (Darwin) fish in his sights: "Darwinism" – yes, he uses exactly the same term as the one so favored by creationists and ID theorists. Indeed, the article under discussion here has been lauded by prominent young-Earth creationist and ID theorist, Paul Nelson.

This isn't the first time left-leaning philosophers such as Fodor have joined forces with creationists, nor will it be the last. However, what I would like to discuss (in later posts) is Fodor's serious misrepresentations of evolutionary biology in general, and evolutionary psychology in particular. But, before I do that, you should go and read Why Pigs Don't Have Wings, paying special attention to Fodor's criticisms of natural selection and its role in evolutionary biology. And while you're at it, you might check out this essay by Fodor as well: Against Darwinism.

Then come back here (in a day or two), and I'll get started fisking both articles.

--Allen

Darwin Day in America



TITLE: Darwin Day in America

AUTHOR: John West

COMMENTARY: Allen MacNeill:

Meanwhile, back at the Discovery Institute/Neo-Creationism Propaganda Ministry, John West has published a much-balleyhooed book that makes the case that virtually all of society’s ills can be traced to poor old Charles Darwin and his latter-day minions. I’m going to force myself to read Darwin Day in America, not because I expect to find any new arguments or evidence in it (IDers like John West and his fellow creationists aren’t interested in new ideas, and are positively repelled by evidence, especially if it involves entering a lab or going out into the field), but because I want to be prepared for the mini-tidal wave of disinformation that it might generate vis-a-vis the pernicious effects of “Darwinism” on society.

This despite the fact that (according to the DI/NCPM’s favorite statistics), less than 10% of Americans believe in non-theistic evolution, and even fewer are atheists. Two thoughts immediately come to mind:

• Shouldn’t the prisons be stuffed with evolutionary biologists and atheists (i.e. greater than 10% of the prison population), and

•Isn’t this in a perverse way empirical evidence that evolutionary biologists and atheists have an influence on society out of all proportion to our numbers?

Ah, but that would imply a direct contradition in logic: something that the DI/NCPM is, of course, perfectly comfortable with, but which strikes the <10% of the population that attempts to be rational as…well, irrational.

So it goes…

--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

The Gene Is Dead: Long Live The Gene!



TITLE: Genome 2.0: Mountains Of New Data Are Challenging Old Views

AUTHOR: Patrick Barry

SOURCE: Science News

COMMENTARY: Allen MacNeill

First, an introductory comment:

In a previous post (New Definitions Of A Gene), I discussed new ideas of what genes might be according to recent discoveries in genetics and genomics. Now comes the absolutely stunning news that between 74% and 93% of the typical mammalian genome is transcribed into RNA, but not translated. This DNA accounts for almost all of what was recently referred to as "junk DNA." This discovery has shaken some of the fundamental principles of genetics, and promises to do even more to the underlying assumptions of neo-Darwinian evolutionary theory.

In particular, the "neutral theory" of Motoo Kimura and the "nearly neutral theory" of Tomoko Ohta may need to be extensively revised, if not entirely replaced. These theories are based on the assumption that the vast majority of the DNA of most organisms, especially eukaryotes, is selectively neutral (i.e. is not acted upon by natural selection). Furthermore, central to these theories is the idea that the neutrality of most of the genome is the result of its not being transcribed or translated into protein (and therefore ultimately into some component of organisms' phenotypes). However, if most of this DNA is transcribed, but not translated, then these theories (which form part of the foundation of current neo-darwinian evolutionary theory) will probably have to be revised, or even jettisoned.

Here is the text of the entire article. Pay particular attention to the various hypotheses presented for what all that transcribed but not translated RNA is doing in cells. This discovery opens up a huge new area of research, and seriously undermines the estimate of the number of "genes" mapped by the Human Genome Project:

***************************************************************************

When scientists unveiled a draft of the human genome in early 2001, many cautioned that sequencing the genome was only the beginning. The long list of the four chemical components that make up all the strands of human DNA would not be a finished book of life, but a road map of an undiscovered country that would take decades to explore.

Only 6 years later, the landscape of the genome is already proving to be dramatically different than most scientists had expected.

The established view of the genome began to take shape in 1958, just 5 years after Francis Crick and James D. Watson worked out the structure of DNA. In that year, Crick expounded what he called the "central dogma" of molecular biology: DNA's genetic information flows strictly one way, from a gene through a series of steps that ends in the creation of a protein. That principle developed into a modern orthodoxy, according to which a genome is a collection of discrete genes located at specific spots along a strand of DNA. This old view got the basics right: that genes encode proteins and that proteins do the myriad work necessary to keep an organism alive.

Researchers slowly realized, however, that genes occupy only about 1.5 percent of the genome. The other 98.5 percent, dubbed "junk DNA," was regarded as useless scraps left over from billions of years of random genetic mutations. As geneticists' knowledge progressed, this basic picture remained largely unquestioned. "At one time, people said, 'Why even bother to sequence the whole genome? Why not just sequence the [protein-coding part]?'" says Anindya Dutta, a geneticist at the University of Virginia in Charlottesville.

Closer examination of the full human genome is now causing scientists to return to some questions they thought they had settled. For one, they're revisiting the very notion of what a gene is. Rather than being distinct segments of code amid otherwise empty stretches of DNA—like houses along a barren country road—single genes are proving to be fragmented, intertwined with other genes, and scattered across the whole genome.

Even more surprisingly, the junk DNA may not be junk after all. Most of this supposedly useless DNA now appears to produce transcriptions of its genetic code, boosting the raw information output of the genome to about 62 times what genes alone would produce. If these active nongene regions don't carry code for making proteins, just what does their activity accomplish?

"What we thought was important before was really just the tip of the iceberg," says Hui Ge of the Whitehead Institute for Biomedical Research in Cambridge, Mass.

With the genome sequence in hand, exploration has moved at a brisk pace during the past 6 years. A milestone was reached in June, when a project called the Encyclopedia of DNA Elements (ENCODE) thoroughly mapped the functional regions in 1 percent of the human genome. The effort involved was staggering: Thirty-five teams of scientists from around the world worked for 4 years and compiled more than 600 million data points, the consortium reported in the June 14 Nature.

From the accumulating mountains of data, scientists are building a new picture of how the genome works as a whole. They have found mutations in nongene regions of DNA that are linked to common diseases such as diabetes and forms of cancer. And some researchers propose that DNA once labeled junk could have spawned the complex bodies of higher organisms—even the complexities of the human brain.

Second Fiddle To A Superstar

In the emerging picture of the genome's functioning, many of the key elements identified so far are molecules of RNA, a chemical cousin of DNA.

In the old central dogma, RNA had a strictly subservient role in the all-important task of making proteins. An RNA molecule is made from units of genetic code strung together, much like DNA. But while DNA has two strands twisted together into a double helix, RNA usually has only a single strand.

Protein synthesis begins when the two strands of a section of DNA unzip. Units of RNA then pair up with their counterparts on one of the DNA strands, forming a complementary messenger RNA (mRNA) molecule. The mRNA detaches and floats off to other parts of the cell, where it hooks up with machinery that transcribes its coded message into a protein.

If RNA's only job were making proteins, then nearly all the RNAs produced in cells should be transcripts of protein-coding genes. (A small fraction of RNAs serve in the protein-transcription machinery.) But in 2005, Jill Cheng and her colleagues at Affymetrix, a genomics company in Santa Clara, Calif., showed that less than half of the RNA produced by 10 of the chromosomes in human cells represented transcripts of traditional genes. In the team's experiments, 57 percent of the RNA was transcribed from noncoding, "junk" regions.

The results from ENCODE were even more striking. In the slice of DNA studied in that project, between 74 percent and 93 percent of the genome produced RNA transcripts. What becomes of this tremendous output is uncertain. John M. Greally of the Albert Einstein College of Medicine in New York says it's likely that some portion of it is made accidentally and simply discarded. But the discovery that so much of the genome is being transcribed into RNA underscores how out-of-date the central dogma has become.

Indeed, the closer researchers look, the more functions they find that RNA transcripts perform. An alphabet soup of new acronyms describes the newfound roles of RNAs. First there were short nuclear RNAs (snRNAs) and short nucleolar RNAs (snoRNAs), both of which reside inside the nucleus and help control production of other RNAs. These were joined by microRNAs (miRNAs) and short interfering RNAs (siRNAs), which can modulate the activity of protein-coding genes. In mice, about 34,000 of the RNA transcripts produced by the genome are nonprotein-coding, outnumbering the roughly 32,000 transcripts that code for proteins, according to a 2005 study by an international group of scientists called the Functional Annotation of Mouse Consortium.

These new families of RNAs add a layer of regulation that fine-tunes the production of proteins. While scientists already knew that some proteins influence the activity of other genes, "there are many more RNAs than proteins that play a regulatory role," Ge says.

Gene regulation may not sound sexy, but it's a powerful way for a cell to evolve complex behaviors using the tools—proteins—that it already has. Consider the difference between a one-bedroom bungalow and an ornate, three-story McMansion. Both are made from roughly the same materials—lumber, drywall, wiring, plumbing—and are put together with the same tools—hammers, saws, nails, and screws. What makes the mansion more complex is the way that its construction is orchestrated by rules that specify when and where each tool and material must be used.

In cells, regulation controls when and where proteins spring into action. If the traditional genome is a set of blueprints for an organism, RNA regulatory networks are the assembly instructions. In fact, some scientists think that these additional layers of complexity in genome regulation could be the answer to a long-standing puzzle.

Genome As Network

The biggest surprise in the first sequence of the human genome was how few protein-coding genes it contained.

"We humans do not have that many more genes than simpler organisms like flies or mice," Ge says. Earlier guesses of the number of genes in humans ran as high as 100,000, but the published sequence in fact contained only about 23,000. That's not much more than the roughly 21,000 genes possessed by the roundworm, a microscopic creature without a brain. If protein-coding genes are the only functional elements in an organism's DNA, where does the extra information come from that's needed to assemble and operate the complex bodies and brains of people, as compared with the simplicity of roundworms? "If we just look at the number of genes, it doesn't make sense," Ge says.

While the number of genes isn't much different in roundworms and people, the human genome is 30 times the size of the roundworms'. People have a much larger quantity of DNA beyond what codes for proteins. Since much of this "junk" DNA is being transcribed into RNA, perhaps it's responsible for much of the complexity of human bodies and brains. In fact, organisms simpler than roundworms, such as single-celled bacteria, carry little noncoding DNA and may have no regulatory RNA at all.

"Scientists have been suspecting that it is the regulatory networks that lead to this amazing complexity" in higher organisms, Ge says.

John S. Mattick of the University of Queensland in Brisbane, Australia, points to a known example of the importance of regulatory RNAs: their crucial role in fetal development. For example, most multicellular animals possess a gene called Notch that helps guide neural development. While the gene itself has much the same form in both simple and complex animals, its activity is regulated by miRNAs that are highly variable from one animal to another. Such miRNAs also influence a gene called Hox, which acts in many animals to define a fetus' body axis and the placement of its limbs.

What's more, the changes that distinguish human brains from those of chimpanzees and other apes could be due in part to evolutionary changes in RNAs that don't encode proteins. A group led by Katherine S. Pollard of the University of California, Davis identified DNA sequences shared by people and chimpanzees, but with large differences, meaning that they have evolved rapidly since the two species shared a common ancestor.

The researchers found that one of these sequences is a noncoding region of DNA that's related to brain function, they reported in the Sept. 14, 2006 Nature. Pollard and her colleagues speculate that this region produces a regulatory RNA and that changes in this RNA contributed to the evolution of the human brain.

With regulatory RNAs appearing to play such an instrumental role in animal development, it's no surprise that scientists are finding disease-associated mutations in regions of the genome formerly regarded as junk.

David Altshuler of the Broad Institute in Cambridge, Mass., and his colleagues looked for DNA mutations in 1,464 patients with type 2 diabetes. Three of the mutations that correlated with the disease were in DNA segments that don't code for proteins, the team reported in the June 1 Science. Other scientists have found mutations in noncoding DNA that link to diseases such as autism, breast cancer, lung cancer, prostate cancer, and schizophrenia.

To be sure, the specific functions of most of the noncoding DNA remain unknown. Projects such as ENCODE have focused on identifying the broad functional categories for active regions of the genome without working out the specific cellular function of each transcript, a task that will take biologists years, if not decades.

In fact, scientists debate whether some fraction of the genome's copious RNA output might do nothing at all. It may simply be that once the cellular machinery that transcribes DNA into RNA gets started, it sometimes doesn't know when to stop. On the other hand, making lots of RNA that does nothing would be a waste of a cell's energy. That's something that natural systems tend to avoid, so the fact of its production argues for at least some of this RNA being biologically active.

The Gene Is Dead

In the old view, each gene sat in splendid isolation on its segment of the genome. Other genes might be nearby, but scientists assumed that they didn't overlap each other.

Now it's clear that a single length of DNA can be transcribed in multiple ways to produce many different RNAs, some coding for proteins and others constituting regulatory RNAs. By starting and stopping in different places, the transcription machinery can generate a regulatory RNA from a length of DNA that overlaps a protein-coding gene. Moreover, the code for another regulatory RNA might run in the opposite direction on the facing strand of DNA. According to the ENCODE project results, up to 72 percent of known genes have transcripts on the facing DNA strand as well as the main strand.



"The same sequences are being used for multiple functions," says Thomas R. Gingeras of Affymetrix. That introduces complications into the evolution of the genome, which had until recently been assumed to act through single DNA mutations affecting single genes. Now, "a mutation in one of those sequences has to be interpreted not only in terms of [one gene], but [of] all the other transcripts going through the region," Gingeras explains.

The implications of this single mutation–multiple consequence model are still a matter of debate. In some cases, the RNA transcripts from DNA that overlaps a protein-coding gene regulate that same gene, so a mutation could affect both the structure and the regulation of a protein. But often, those transcripts regulate genes that are far away, or even on different chromosomes. This complex interweaving of genes, transcripts, and regulation makes the net effect of a single mutation on an organism much more difficult to predict, Gingeras says.

More fundamentally, it muddies scientists' conception of just what constitutes a gene. In the established definition, a gene is a discrete region of DNA that produces a single, identifiable protein in a cell. But the functioning of a protein often depends on a host of RNAs that control its activity. If a stretch of DNA known to be a protein-coding gene also produces regulatory RNAs essential for several other genes, is it somehow a part of all those other genes as well?

To make things even messier, the genetic code for a protein can be scattered far and wide around the genome. The ENCODE project revealed that about 90 percent of protein-coding genes possessed previously unknown coding fragments that were located far from the main gene, sometimes on other chromosomes. Many scientists now argue that this overlapping and dispersal of genes, along with the swelling ranks of functional RNAs, renders the standard gene concept of the central dogma obsolete.

Long Live The Gene

Offering a radical new conception of the genome, Gingeras proposes shifting the focus away from protein-coding genes. Instead, he suggests that the fundamental units of the genome could be defined as functional RNA transcripts.

Since some of these transcripts ferry code for proteins as dutiful mRNAs, this new perspective would encompass traditional genes. But it would also accommodate new classes of functional RNAs as they're discovered, while avoiding the confusion caused by several overlapping genes laying claim to a single stretch of DNA. The emerging picture of the genome "definitely shifts the emphasis from genes to transcripts," agrees Mark B. Gerstein, a bioinformaticist at Yale University.

Scientists' definition of a gene has evolved several times since Gregor Mendel first deduced the idea in the 1860s from his work with pea plants. Now, about 50 years after its last major revision, the gene concept is once again being called into question.

REFERENCES CITED:

Cheng, J. . . . and T.R. Gingeras. 2005. Transcriptional maps of 10 human chromosomes at 5-nucleotide resolution. Science 308(May 20):1149-1154. Available at http://www.sciencemag.org/cgi/content/full/308/5725/1149.

Chopra, V.S., and R.K. Mishra. 2006. "Mir"acles in hox gene regulation. Bioessays 28(May):445-448. Abstract available at http://dx.doi.org/10.1002/bies.20401.

Claverie, J.-M. 2005. Fewer genes, more noncoding RNA. Science 309(Sept. 2):1529-1530. Abstract available at http://www.sciencemag.org/cgi/content/abstract/309/5740/1529.

Diabetes Genetics Initiative of Broad Institute of Harvard and MIT, Lund University, and Novartis Institutes of BioMedical Research. 2007. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science 316(June 1):1331-1336. Abstract available at http://www.sciencemag.org/cgi/content/abstract/316/5829/1331.

Gerstein, M.B., et al. 2007. What is a gene, post-ENCODE? History and updated definition. Genome Research 17(June):669-681. Available at http://www.genome.org/cgi/content/full/17/6/669.

Gingeras, T.R. 2007. Origin of phenotypes: Genes and transcripts. Genome Research 17(June):682-690. Available at http://www.genome.org/cgi/content/full/17/6/682.

Kapranov, P. . . . and T.R. Gingeras. 2007. RNA maps reveal new RNA classes and a possible function for pervasive transcription. Science 316(June 8):1484-1488. Abstract available at http://www.sciencemag.org/cgi/content/abstract/316/5830/1484.

______. 2002. Large-scale transcriptional activity in chromosomes 21 and 22. Science 296(May 3):916-919. Available at http://www.sciencemag.org/cgi/content/full/296/5569/916.

Mattick. J.S. and I.V. Makunin. 2006. Non-coding RNA. Human Molecular Genetics 15(April 15):R17-R29. Available at http://hmg.oxfordjournals.org/cgi/content/full/15/suppl_1/R17.

Mattick, J.S. 2005. The functional genomics of noncoding RNA. Science 309(Sept. 2):1527-1528. Abstract available at http://www.sciencemag.org/cgi/content/abstract/309/5740/1527.

______. 2004. RNA regulation: A new genetics? Nature Reviews Genetics 5(April):316-323. Abstract available at http://dx.doi.org/10.1038/nrg1321.

Moore, M.J. 2005. From birth to death: The complex lives of eukaryotic mRNAs. Science 309(Sept. 2):1514-1518. Abstract available at http://www.sciencemag.org/cgi/content/abstract/309/5740/1514.

Pollard, K.S., et al. 2006. An RNA gene expressed during cortical development evolved rapidly in humans. Nature 443(Sept. 14):167-172. Abstract available at http://dx.doi.org/10.1038/nature05113.

Prasanth, K.V., and D.L. Spector. 2007. Eukaryotic regulatory RNAs: An answer to the 'genome complexity' conundrum. Genes and Development 21(Jan. 1):11-42. Available at http://www.genesdev.org/cgi/content/full/21/1/11.

Strausberg, R.L., and S. Levy. 2007. Promoting transcriptome diversity. Genome Research 17(July):965-968. Abstract available at http://www.genome.org/cgi/content/abstract/17/7/965.

The ENCODE Project Consortium. 2007. Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project. Nature 447(June 14):799-816. Available at http://dx.doi.org/10.1038/nature05874.

Wienholds, E., and R.H.A. Plasterk. 2005. MicroRNA function in animal development. FEBS Letters 579(Oct. 31):5911-5922. Available at http://dx.doi.org/10.1016/j.febslet.2005.07.070 .

Weinstock, G.M. 2007. ENCODE: More genomic empowerment. Genome Research 17(June):667-668. Available at http://www.genome.org/cgi/content/full/17/6/667.

Willingham, A.T., and T.R. Gingeras. 2006. TUF love for "junk" DNA. Cell 125(June 30):1215-1220. Available at http://dx.doi.org/10.1016/j.cell.2006.06.009.

Zamore, P.D., and B. Haley. 2005. Ribo-gnome: The big world of small RNAs. Science 309(Sept. 2)::1519-1524. Abstract available at http://www.sciencemag.org/cgi/content/abstract/309/5740/1519.

Further Readings:

Bower, B. 2006. Evolution's DNA difference: Noncoding gene tied to origin of human brain. Science News 170(Aug. 19):116. Available to subscribers at http://www.sciencenews.org/articles/20060819/fob4.asp.

Hesman, T. 2000. The meaning of life. Science News 157(April 29):284-285. Available at http://www.sciencenews.org/articles/20000429/bob9.asp.

Travis, J. 2002. Biological dark matter. Science News 161(Jan. 12):24-25. Available at http://www.sciencenews.org/articles/20020112/bob9.asp.

SOURCES:

David P. Bartel
Whitehead Institute
Nine Cambridge Center
Cambridge, MA 02142

George Church
Harvard Medical School
Genetics NRB Room 238
77 Avenue Louis Pasteur
Boston, MA 02115

Anindya Dutta
University of Virginia Health System
P.O. Box 800733
Charlottesville, VA 22908

Hui Ge
Whitehead Institute
Nine Cambridge Center
Cambridge, MA 02142

Mark B. Gerstein
Yale University
266 Whitney Avenue
New Haven, CT 06511-8902

John M. Greally
Albert Einstein College of Medicine
Jack and Pearl Resnick Campus
1300 Morris Park Avenue
Ullmann Building, Room 911
Bronx, NY 10461

James Keesling
University of Florida
358 LIT
Gainesville, FL 32611

Elliott H. Margulies
Genome Technology Branch
National Human Genome Research Institute
Bethesda, MD 20892-8004

Zhiping Weng
Boston University
44 Cummington Street
Boston, MA 02215

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

Evolution and Religion: Is Religion Adaptive?




ANNOUNCEMENT: Seminar in History of Biology

AUTHOR: Allen MacNeill

COMMENTARY: Allen MacNeill

First the announcement, followed by a brief commentary:

I am very excited to announce the following course, to be offered this summer in the six-week summer session at Cornell University:

COURSE LISTING: BioEE 467/B&Soc 447/Hist 415/S&TS 447 Seminar in History of Biology

SEMESTER: Cornell Six-Week Summer Session, 06/26/07 to 08/02/07

COURSE TITLE: Evolution and Religion: Is Religion Adaptive?

COURSE INSTRUCTOR: Allen MacNeill, Senior Lecturer in Ecology & Evolutionary Biology, Cornell University

COURSE DESCRIPTION: This seminar addresses, in historical perspective, controversies about the cultural, philosophical, and scientific implications of evolutionary biology. Discussions focus upon questions about gods, free will, foundations for ethics, meaning in life, and life after death. Readings range from Charles Darwin to the present (see reading list, below).

In 1871, Charles Darwin wrote in The Descent of Man that “…a belief in all-pervading spiritual entities seems to be universal.” A century later, Donald Brown, in his encyclopedic analysis of human universals, noted the same thing: that the capacity for religion is a universal trait, found in all human cultures. However, there is considerable individual variation in this capacity, ranging from people whose entire lives revolve around their religious beliefs to those who entirely lack them.

To an evolutionary biologist, such pan-specificity combined with continuous variation strongly suggests that one is dealing with an evolutionary adaptation. And indeed, in the past few years the publication of hypotheses for the evolution of the capacity for religion has become an explosive growth industry and a hot topic of debate. In this seminar course, we will take up this debate by considering three alternative hypotheses: that the capacity for religion is (1) an evolutionary adaptation, (2) a side-effect of an evolutionary adaptation, or (3) a “mind virus” with no direct evolutionary implications. We will read from some of the leading authors on the subject, including Scott Atran, Pascal Boyer, Richard Dawkins, Daniel Dennett, Andrew Newberg, and David Sloan Wilson. Our intent will be to sort out the various issues at play, and to come to clarity on how those issues can be integrated into the perspective of the natural sciences as a whole.

In addition to in-class discussions, course participants will have the opportunity to participate in online debates and discussions via the instructor's weblog. Students registered for the course will also have an opportunity to present their original research paper(s) to the class and to the general public via publication on the course weblog and via THE EVOLUTION LIST.

INTENDED AUDIENCE: This course is intended primarily for students in biology, history, philosophy, and science & technology studies. The approach will be interdisciplinary, and the format will consist of in-depth readings across the disciplines and discussion of the issues raised by such readings.

PREREQUISITES: None, although a knowledge of comparative anthropology, evolutionary psychology, and general evolutionary theory would be helpful.

DAYS, TIMES, & PLACES: The course will meet on Tuesday and Thursday evenings from 6:00 to 9:00 PM in Mudd Hall, Room 409 (The Whittaker Seminar Room), beginning on Tuesday 26 June 2007 and ending on Thursday 2 August 2007. We will also have an end-of-course picnic at a location TBA.

CREDIT & GRADES: The course will be offered for 4 hours of credit, regardless of which course listing students choose to register for. Unless otherwise noted, course credit in BioEE 467/B&Soc 447 can be used to fulfill biology/science distribution requirements and Hist 415/S&TS 447 can be used to fulfill humanities distribution requirements (check with your college registrar's office for more information). Letter grades for this course will be based on the quality of written work on original research papers written by students, plus participation in class discussion.

COURSE ENROLLMENT & REGISTRATION: All participants must be registered in the Cornell Six-Week Summer Session to attend class meetings and receive credit for the course (click here for for more information and to enroll for this course). Registration will be limited to the first 18 students who enroll for credit.

REQUIRED TEXTS (all texts will be available at The Cornell Store):

Atran, Scott (2004) In Gods we trust: The evolutionary landscape of religion. Oxford University Press, paperback, 388 pages, ISBN #0195178033

Boyer, Pascal (2002) Religion explained: The evolutionary origins of religion. Vintage Books, paperback, 448 pages, ISBN #0099282763

Dawkins, Richard (2006) The God delusion. Houghton Mifflin, hardcover, 416 pages, ISBN #0618680004.

Dennett, Daniel (2007) Breaking the spell: Religion as a natural phenomenon. Penguin Books, paperback, 464 pages, ISBN #0143038338

Newberg, Andrew & D'Aquili, Eugene (2001) Why god won't go away: Brain science and the biology of belief. Ballantine Books, paperback, 240 pages, ISBN #034544034X

Wilson, David Sloan (2003) Darwin's cathedral: Evolution, religion, and the nature of society. University of Chicago Press, paperback, 268 pages, ISBN #0226901351

OPTIONAL TEXTS (all texts will be available at The Cornell Store):

Darwin, Charles (E. O. Wilson, ed.) (2006) From So Simple a Beginning: Darwin's Four Great Books. W. W. Norton, hardcover, 1,706 pages, ISBN #0393061345

Eibl-Eibesfeldt, Irenaus & Salter, Frank (1998) Indoctrinability, ideology, and warfare: Evolutionary perspectives. Berghahn Books, hardcover, 490 pages, ISBN #1571819231

Fitzduff, Marie & Stout, Chris (2006) The psychology of resolving global conflicts: From war to peace: Volume 1: Nature vs nurture. Praeger Security International, hardcover, 354 pages, ISBN #0275982084

Guthrie, Stewart (1995) Faces in the clouds: A new theory of religion. Oxford University Press, paperback, 336 pages, ISBN #0195098919

Hamer, Dean (2005) The God gene: How faith is hardwired into our genes. Anchor, 256 pages, ISBN #0385720319

Newberg, A. & Waldman, M. (2006) Why we believe what we believe: Uncovering our biological need for meaning, spirituality, and truth. Free Press, hardcover, 336 pages, ISBN # 0743274970

Persinger, Michael (1987) Neuropsychological bases of god beliefs. Praeger Publishers, 175 pages, ISBN #0275926486

Wolpert, Lewis (2006) Six impossible things before breakfast: The evolutionary origins of belief. W. W. Norton, 243 pages, ISBN #0393064492

COMMENTARY:

I realize that putting myself in between such formidable opponents is perhaps asking for trouble...but I couldn't possibly get into any more trouble than I did last summer, could I? Once again, we shall rush in where angels fear to tread, and consider a very topical topic. As was the case last year, I invite anyone with an interest in the question posed as the title of this blog to consider taking this course, or at least sitting in on our discussion online. We will have an online course blog, where any and all comments, criticisms, suggestions, and other trivia will be roasted and toasted...so long as they are civil. As for accusations that I'm biased, let me say upfront that I (like almost everyone else) have an opinion on the question: I believe (based on my research into this question) that the answer is "Yes" and that the specific context within which the capacity for religious experience has evolved is warfare...but we'll talk all about that this summer.

We may also talk about whether or not God (or gods, or whatever) exist, but that will not be the primary focus of the course, nor will I allow it to become the primary focus of our discussions. This course isn't about the existence or non-existence of God (or Darwin or me). It's about whether or not the ability to believe in things like God (or gods, or whatever) has adaptive consequences. It's a fascinating topic and I hope that enough people will sign up for the course with opposing viewpoints on this subject to make for as interesting a summer seminar as last year's was.

So, watch this space; when the course blog goes up, I will announce it here and provide links to all and sundry. And remember:

"If God did not exist, it would be necessary to invent him." – Voltaire

--Allen

Scientists Say Darwin's 'Tree of Life' Not The Theory Of Everything



ARTICLE: physorg.com

AUTHOR: Lisa Zyga

COMMENTARY: Allen MacNeill

First the news item, followed by some commentary:

****************************************************

There is only one figure in On the Origin of Species, and that is a tree diagram. As Darwin’s model for the theory of evolution, he used the Tree of Life (TOL) to clearly and visually explain the interrelatedness of all living things, implying that from one common ancestor (the root) sprung branches, which produced smaller offshoots as genetic progeny, etc.

In this model, similarities between species reveal a common ancestor, and differences result from (and explain) Darwin’s main catalysts: competition and natural selection, which generate improvement in future generations. As a simile, the TOL served a vital purpose for introducing the theory of evolution to the community in an understandable way. Although there is no external evidence to support the idea that evolution is inclusively hierarchical, many evolutionists believe the TOL provides an accurate general representation of the history of life, which could potentially be completely reconstructed by knowing the relevant data.

In recent times, however, a minority of biologists and evolutionists have questioned the accuracy of the TOL hypothesis, including W. Ford Doolittle and Eric Bapteste. In a recent paper in the Proceedings of the National Academy of Sciences, “Pattern Pluralism and the Tree of Life Hypothesis,” the scientists investigate the shortcomings of the TOL, as well as propose alternative models that would better explain how to classify the history of evolving life forms.

Much of the initial concern over TOL was provoked by biologists studying the complex relationships among prokaryotes, the most primitive life forms that include bacteria and archaea. Prokaryotes have a much simpler DNA structure than eukaryotes (all other life forms). Because of this, prokaryotes often transfer their DNA via processes such as lateral gene transfer as opposed to vertical gene transfer (direct transmission form parent to progeny) which is the basis for the “phylogenetic” (evolutionary relatedness) TOL scheme.

“Surely a tree is the right model for most multi-cellular animals and plants,” Doolittle explained to PhysOrg.com. “Thus the TOL is great for fossils and museums and dinosaurs and most of visible life, over the last billion years. But unicellular eukaryotes and prokaryotes represent the bulk of the biomass and diversity of life on earth, as well as the first two-thirds of its history.”

In their paper, Doolittle and Bapteste highlight research that shows other causes of genetic modification, suggesting that evolutionary history is more complex than described by the TOL. For example, recombination, gene loss, duplication, and gene creation are a few of the processes whereby genes can be transferred within and between species, causing variation that’s not due to vertical transfer. These transfer methods give results that don’t fit on the TOL, including species that cannot be traced to a common ancestor.

While such diverse methods might appear to obviously point to a more complex nonhierarchical evolutionary scheme, Doolittle and Bapteste explain that the TOL thinking persists due to confusion between the roles of “process” and “pattern.” The above methods are processes and are widely accepted by modern evolutionists, whereas the TOL is a pattern that, as Doolittle and Bapteste explain, has been ingrained in biologists’ minds from early education as a single, unifying model. As the researchers explain of the current biology scene, “We may be process pluralists, but we remain pattern monists.”

If this combination of thinking seems to clash, Doolittle and Bapteste suggest that the Western philosophical tradition of thinking in universal patterns has caused biologists to cling to classification without realizing it. The authors point out that many algorithms used to study evolutionary hierarchies impose or extract the TOL structure due to their intrinsic design. TOL is a paradigm that has stuck. But Doolittle sees ways to alter this mentality.

“Sure we can [re-train Western thinking]. That's what ‘postmodernism’ is about,” he said. “I would agree that the need to classify might be built in, but the coupling of this practice to a specific theory about what classifications are ‘natural’ is surely not.

As an alternative to the TOL, the scientists suggest that relationships among life forms may be represented by whatever model fits for a certain purpose, a certain taxonomic group, or a certain scale. In contrast to pattern monism, they call this belief “pattern pluralism.” While parts of evolution certainly are tree-like, other parts may be nets or webs or other complex models. Most importantly, however, there seems to be no “theory of everything” in evolution, no metanarrative to unify all life forms.

“In 2006, our understanding of evolution at the molecular, population genetic, and ecological levels is rich and pluralistic in character,” the scientists conclude, “and does not require (or justify) a monistic view of the phylogenetic pattern.”

As for any blow to Darwin’s ego, the scientists point out that he never wrote about reconstructing the tree in an attempt to relate every living thing, but rather used the model as a general guide.

“I'd like to think he would adjust,” Doolittle said about Darwin. “After all, his theory was developed before there was any understanding of genetics and when bacteria were still believed to be spontaneously generated.”

REFERENCES CITED:
Doolittle, W. Ford, and Bapteste, Eric. “Pattern pluralism and the Tree of Life hypothesis.” PNAS, February 13, 2007, vol. 104, no. 7, 2043-2049.

****************************************************
COMMENTARY:

Ford Doolittle has been saying this for many years, and has been joined by Lynn Margulis, who has argued that the concept of "species" does not apply to prokaryotes.

But, that's not what I want to talk about. What I want to talk about is how "intelligent design theorists" quote-mine and otherwise distort reality to the point of outright lying. Why do I say this? Because former lawyer and professional propagandist, Casey Luskin, has a postat Evolution News, propaganda outlet for the Discovery Institute in which he says

"By invoking insufficient data, horizontal gene swapping, rapid evolution, and other ad hoc explanations, Darwinists reveal that neo-Darwinism is trying explaining away the data; it is not explaining the data. Perhaps the inability to construct robust phylogenetic trees using molecular data stems from the fact that common descent is simply wrong."

And the alternative? Why, magic of course. All of the living forms on Earth today were created, all at once, on Tuesday 25 October 4004 BC at 9 AM...or some other time in the past, exact date unspecified. Because, of course, that is the only alternative to common descent. Either you and your siblings are the offspring of your parents (i.e. common descent) or you aren't, and if the latter is true, then you must all have been created separately, not by your parents, but rather by God...excuse me, the Grand Omnipotent Designer. And with your memories of your childhood already inserted into your minds, so that the jarring discontinuity of your separate creations would not disturb you too much...would lead you, in fact, into the damning conclusion that you were, in fact, the offspring of your parents, and thus consign yourself to everlasting torment in the lake of fire.

Or not. You see, this is what the kind of egregious propagandizing of the folks of the Disco Institute leads to. Not discussion of the science of biology on its merits, on the basis of reason and evidence, but pure assertions without any alternatives at all (not that they want you to read in public, anyway).

I'm tired (our new baby is keeping Leah and me awake at night), and so I'll sign off now. But damn, people like Luskin just make me want to scream sometimes...

"Against stupidity, the gods themselves contend in vain."
- Friedrisch Schiller

--Allen

For First Time, Chimps Seen Making Weapons for Hunting



SOURCE: The Washington Post

AUTHOR: Rick Weiss, Washington Post Staff Writer

COMMENTARY: Allen MacNeill

Friday, February 23, 2007: Chimpanzees living in the West African savannah have been observed fashioning deadly spears from sticks and using the tools to hunt small mammals — the first routine production of deadly weapons ever observed in animals other than humans. The multistep spearmaking practice, documented by researchers in Senegal who spent years gaining the chimpanzees' trust, adds credence to the idea that human forebears fashioned similar tools millions of years ago. The landmark observation also supports the long-debated proposition that females — the main makers and users of spears among the Senegalese chimps — tend to be the innovators and creative problem solvers in primate culture.

Using their hands and teeth, the chimpanzees were repeatedly seen tearing the side branches off long, straight sticks, peeling back the bark and sharpening one end. Then, grasping the weapons in a "power grip," they jabbed them into tree-branch hollows where bushbabies — small, monkeylike mammals — sleep during the day. In one case, after repeated stabs, a chimpanzee removed the injured or dead animal and ate it, the researchers reported in yesterday's online issue of the journal Current Biology.

"It was really alarming how forceful it was," said lead researcher Jill D. Pruetz of Iowa State University, adding that it reminded her of the murderous shower scene in the Alfred Hitchcock movie "Psycho." "It was kind of scary."

The new observations are "stunning," said Craig Stanford, a primatologist and professor of anthropology at the University of Southern California. "Really fashioning a weapon to get food — I'd say that's a first for any nonhuman animal."

Scientists have documented tool use among chimpanzees for decades, but the tools have been simple and used to extract food rather than to kill it. Some chimpanzees slide thin sticks or leaf blades into termite mounds, for example, to fish for the crawling morsels. Others crumple leaves and use them as sponges to sop drinking water from tree hollows.

But while a few chimpanzees have been observed throwing rocks — perhaps with the goal of knocking prey unconscious, but perhaps simply as an expression of excitement — and a few others have been known to swing simple clubs, only people have been known to craft tools expressly to hunt prey.

Pruetz and Paco Bertolani of the University of Cambridge made the observations near Kedougou in southeastern Senegal. Unlike other chimpanzee sites currently under study, which are forested, this site is mostly open savannah. That environment is very much like the one in which early humans evolved and is different enough from other sites to expect differences in chimpanzee behaviors.

Pruetz recalled the first time she saw a member of the 35-member troop trimming leaves and side branches off a branch it had broken off a tree.

"I just knew right away that she was making a tool," Pruetz said, adding that she suspected — with some horror — what it was for. But in that instance she was unable to follow the chimpanzee to see what she did with it. Eventually the researchers documented 22 instances of spearmaking and use, two-thirds of them involving females.

In a typical sequence, the animal first discovered a deep tree hollow suitable for bush babies, which are nocturnal and weigh about half a pound. Then the chimp would break off a branch — on average about two feet long, but up to twice that length — trim it, sharpen it with its teeth, and poke it repeatedly into the hollow at a rate of about one or two jabs per second. After every few jabs, the chimpanzee would sniff or lick the branch's tip, as though testing to see if it had caught anything.

In only one of the 22 observations did a chimp get a bush baby. But that is reasonably efficient, Pruetz said, compared with standard chimpanzee hunting, which involves chasing a monkey or other prey, grabbing it by the tail and slamming its head against the ground.

In the successful bush-baby case, the chimpanzee, after using its sharpened stick, jumped on the hollow branch in the tree until it broke, exposing the limp bush baby, which the chimp then extracted. Whether the animal was dead or alive at that point was unclear, but it did not move or make any sound.

Chimpanzees are believed to offer a window on early human behavior, and many researchers have hoped that the animals — humans' closest genetic cousins — might reveal something about the earliest use of wooden tools. Many suspect that the use of wooden tools far predates the use of stone tools — remnants of which have been found dating from 2.5 million years ago. But because wood does not preserve well, the most ancient wooden spears ever found are only about 400,000 years old, leaving open the question of when such tools first came into use. The discovery that some chimps today make wooden weapons supports the idea that early humans did too — perhaps as much as 5 million years ago — Stanford said.

Adrienne Zihlman, an anthropologist at the University of California at Santa Cruz, said the work supports other evidence that female chimps are more likely than males to use tools, are more proficient at it and are crucial to passing that cultural knowledge to others.

"Females are the teachers," Zihlman said, noting that juvenile chimps in Senegal were repeatedly seen watching their mothers make and hunt with spears.

Females "are efficient and innovative, they are problem solvers, they are curious," Zihlman said. And that makes sense, she added.

"They are pregnant or lactating or carrying a kid for most of their life," she said. "And they're supposed to be running around in the trees chasing prey?"

Frans B.M. de Waal, a primatologist at Emory University, said aggressive tool use is only the latest "uniquely human" behavior to be found to be less than unique.

"Such claims are getting old," he said. "With the present pace of discovery, they last a few decades at most."

COMMENTARY:

Yet another supposedly significant difference between humans and non-human animals falls by the wayside. It would be really interesting to know when this behavior first began, and where (and by whom). Based on what we already know about chimp learning behavior, it is very likely that a young female first tried this technique, possibly modeling it on the already well-developed technique of using a twig stripped of its branches to "fish" for termites in termite mounds. Also, it is likely that the technique has spread via imitation, rather than by directed learning. Chimps (like many other primates) are very good at imitative learning, but apparently do not actually "teach" each other how to do things...but maybe this will also be observed at some point in the future.

Furthermore, it is clear that the female chimps fashioning these spears are doing so intentionally: they perform a specific, learned behavior with the intent to use it to extract food (i.e. bushbabies) from locations that would otherwise be inaccessible. A clear case of "design" in a non-human animal, and clearly learned/based on experience (i.e. not innate/hard-wired). Anyone who argues that "design" or "intentionality" does not exist in nature is either deliberately self-deceived or stupid.

Does this mean that "design" is an intrinsic property of nature, however? Not at all; rather, it shows that "design" (i.e. intentional behavior) can be an emergent property of a particular class of natural entities. We know that we are capable of intentional behavior, and now we have solid evidence that chimps are as well. However, none of this is evidence for the kind of "intrinsic design" that "intelligent design theorists" propose as an explanation for the origin of complex adaptations. Rather, it is evidence for the kind of "emergent design" that Ernst Mayr explained as fully compatible with evolutionary theory more than thirty years ago.

--Allen

More on Steve Fuller and "Social Epistemology"

SOURCE: Cornell IDEA Club

AUTHOR: Allen MacNeill

The debate begun in my previous post continues...

A poster to the Cornell IDEA Club listserve wrote:

"Fuller '... deserves to have his ideas discussed instead of lambasted.'"

Okay, here's something to discuss (a direct quote from Fuller):

"In this respect, 'our' side pulled its punches in the Science Wars when it refused to come out and say that the scientific establishment may not be the final word on what science is, let alone what it ought to be." [emphasis mine]

In that one sentence alone is encapsulated nearly everything that most practicing scientists find so deeply objectionable about Steve Fuller and his ilk. Let's take it apart:

"'our' side"

What precisely does Fuller mean by this? "Our side" in what way? "Our side" in the evolution/ID debate? The natural science/social science debate? The science/sociology debate? The "culture wars" that Phillip Johnson says ID is part of? What does it mean to say you're on a "side"?

When I debate with other scientists about scientific subjects, those debates can be pretty heated, but generally we're all on the same "side": the "side" of empirical verification/falsification of explanations of natural phenomena. In other words, we're all on the "science side," the side that does what it does based on the premise that such explanations should be grounded in observation of nature and the investigation of natural causes for natural phenomena.

I don't think that's what Fuller means by "our side." Sociologists in general, and "social epistemologists" in particular have as a basic starting assumption that all explanations of all phenomena (natural or otherwise) are ultimately socially constructed.

Now, I have no problem with that idea per se, as I believe as well that such explanations are indeed socially constructed. What I and other scientists have a problem with is the seemingly inevitable logical extension of that idea which most sociologists (and I would put Fuller in this camp) seem prone to: that nature itself is therefore "socially constructed." That's what "social epistemology" means, isn't it? That what we know about reality (i.e. epistemology) is socially constructed, and that therefore we can't actually know anything about nature at all outside of our social construction of it.

But this is precisely what science was and is supposed to be about: the discovery and understanding of what nature is, independent of our opinions and "social constructions." That's why statistical analysis was developed, to remove as much as possible our subjective/socially constrained interpretation of what our observations mean vis-a-vis our explanations about how nature works. That's why we have "double-blind" experimental protocols, and why we argue so vehemently over the validity of data and what it means for theories: because, in the end, all scientists agree that this is the best we can do at understanding how nature works.

But Fuller and his cohorts do not agree; they think that real scientific objectivity (and hence the entire scientific enterprise) is impossible, and that since all scientific explanations are "socially constructed," it all comes down to "sides" and "debates" and, most of all, WINNING. It call comes down to politics, in other words.

"Science Wars"

Here it is in a nutshell. Wars between whom, precisely? Between scientists, who believe that they really are able to say something about the nature of nature, and non-scientists, who believe that it's all really about political power and "hegemony" and "patriarchy" and winning. What happens when you fight a "war", including a "culture war"? Somebody WINS.

"the scientific establishment"

More tired 1970s radical political rhetoric, all dressed up in "scienciness" (like "truthiness" only more "scientific") to impress the gullible and gratify the "politically correct". Yes, I'd be the first to admit that there are "science establishments" - I live and work in one of them. But that's not what Fuller is talking about here. He's talking about the capital E Establishment: the "bad guys" on the other "side", the scientists who believe that they are describing physical reality, when what they are really doing is "oppressing" the poor and downtrodden of the world, the victims of "patriarchy" and "political hegemony" and their advocates, the "social epistemologists", who tell them that there is no objective reality outside of social discourse, and debates are all about WINNING and not about refining our understanding about how nature works.

His mention of the Sokal affair is also telling in this respect. The Sokal affair decisively exposed the intellectual bankruptcy at the heart of sociology and "social epistemology" - the belief that everything is socially constructed. Not just our understanding of reality, but reality itself.

"the final word on what science is"

Hmm, well, what does this tell us about Fuller et al? Who should have the "final word" about anything? The people doing it, or the people criticizing it? Who is the real subject - the monster or the critics (as Tolkein so eloquently put it)? True, scientists sometimes don't completely understand why they do things the way they do (i.e. some of them follow instructions, like an apprentice emulates a master), but this does not mean that scientists don't really understand why we do what we do and need somebody like Fuller to tell us.

Why not? Because social "scientists" like Fuller (and like ID "theorists") don't do natural science. They "interpret" or "criticize" or "analyze" what natural scientists do, but they don't do what natural scientists do. If they did, Alan Sokal's trick would not have worked, but instead it sucked them all in, so deep that some of them still don't realize how completely their intellectual bankruptcy was exposed by the "Sokal affair."

"let alone what it ought to be"

And there it is, right there in plain English. The people who DO science are probably the last people who should have anything to say about how science ought to be practised, right? Because, of course, we're all "blinded by science" and don't understand that it isn't about objective analysis of nature, it's about "social construction of reality" which ultimately is about politics (from the Greek polis, for "people"), which is about WINNING.

So, yes, I find it fascinating that ID advocates, the vast majority of whom are deeply committed Christians, can find common cause with Fuller and other "social epistemologists." Christian belief, as I understand it, is ultimately based on unshakable faith in the truth of the Word: the logos of the gospel of John. But, to somebody like Fuller, the Word is just another form of "social discourse", just part of a political struggle of which the ultimate point is WINNING. Why does Phillip Johnson call what he's doing part of a "culture war?" Why does William Dembski and Robert Crowther and Stephen Meyer and Jonathan Witt and Benjamin Wiker (but, significantly, not Michael Behe nor Gullielmo Gonzales, both natural scientists) agree with Johnson? Because that's what they're doing, they're fighting a war, and as I said in my last post, wars aren't about truth, they're about WINNING. Truth be damned, so long as your side WINS. "Lying for Jesus" is justified, and no amount of distortion of experimental results or character assassination or egregiously twisted and vicious propaganda is too much, so long as your side WINS.

Isn't the quotation from Fuller that stands at the top of this post an indication that he sees what he and other "social epistemologists" do is ultimately all about winning? Seems like it to me...

--Allen

On the "Darwin Fetish" and Other Political Oxymorons




SOURCE: Cornell IDEA Club

AUTHOR: Allen MacNeill

The IDEA Club at Cornell has recently been discussing the following quote by Steve Fuller, a sociologist and one of the "experts" who testified in support of "intelligent design" at the Dover trial in Pennsylvania last year:

"If you want to stop use of the word 'Darwinist' to capture modern evolutionary theory, then you should encourage people like Dawkins, Jones, Wilson, Watson, Ridley and (were he alive) Gould to stop talking about 'Origin of Species' etc. as if they were books of some secular Bible. This kind of thing doesn't happen in physics. The world-view implications of physics can be discussed, while giving due respect to Newton, Einstein, etc., without trying to find bits of their texts that anticipate or legitimise what the author wants to say today . From a sociological standpoint, the Darwin fetish is very weird, and doesn't seem to be related to any claims that creationists or ID people are making. Marx and Freud are the only figures who have been treated this way in recent memory – and you've seen what's happened to them…"

Here's my take on all of this:

It sounds to me like Fuller is objecting to the idea that biologists, especially evolutionary biologists, cite Darwin as a published authority when writing (and talking and teaching) about their own work. However, this is exactly what you're supposed to do in science: back up your assertions with citations whenever your assertions are not completely original. Fuller, who is not a natural scientist but rather a sociologist, doesn't seem to understand this basic fact. Indeed, he seems to think that citation is somehow illegitimate in science, even that it may indicate some kind of slavish adherence to dogma, rather than simply an attempt to ground one's own work in previous work on the same subject.

If I were to cite W. D. Hamilton on the subject of kin selection, for example, does that mean that I have some kind of "Hamilton fetish?" What if everyone who works on kin selection does the same thing; does this mean that we're "deifying Hamilton?" No, the whole idea is absurd; citation is both an accepted and indeed required part of standard science writing, teaching, and speaking.

It goes deeper than this, of course. The reason that Fuller was chosen as one of the "experts" in defense of "intelligent design" at the trial in Dover, PA was because Fuller (like many sociologists today) is a "post-modernist." This means that, like post-modernism's founders such as Foucault and Derrida, Fuller believes and promotes the idea that "all knowledge is reducible to 'discourse'" in which politics is the ultimate force, and political victory over one's intellectual opponents is the ultimate goal. Fuller and others like him argue that there is no such thing as "objective knowledge" at all, only competing ideologies. According to this view, science is just another way for the "dominant white patriarchal class to extend its hegemony" by forcing others to believe in its politically motivated view of reality, and that all intellectual debates are really just part of the ongoing class struggle for political power.

It surprises me, therefore, that "intelligent design" supporters would cite Fuller and promote his ideas, which are of course ultimately based on Marxist (and therefore atheist) theories. Politics indeed makes for strange bedfellows, and to see Christian supporters of ID cite Fuller and others like him as authorities and supporters of their world view strikes me as laughable and ultimately self-defeating.

Yet at the same time, it doesn't surprise me, because that's what "intelligent design theory" started out as and has remained: not science, not the legitimate search for knowledge derived from empirical analysis of nature, but rather politics, pure and simple. This is why IDers don't publish in scientific journals, but rather push their agenda in the media, the courts, and in elections. ID isn't science, it's politics, conducted by press release and lawsuit, and its goal isn't the expansion of knowledge or understanding, it's winning by whatever means possible: distortion, misrepresentation, mischaracterization, even character assassination and outright lying are sanctioned, so long as they promote the ultimate goal: the victory of ID (and therefore the forces of "good," i.e. Christianity) over evolution (and therefore the forces of "evil," i.e. evangelical atheism).

How else to explain such masterpieces of political propaganda as Phillip Johnson's The Wedge of Truth or Benjamin Wiker's Moral Darwinism? The former was written by the acknowledged founder of "intelligent design theory," and the latter was published with a foreword by William Dembski in which he lavishly praises Wiker for getting down to the real issues in the evolution/intelligent design debate. IOW, it's not about knowledge, it's all about winning folks, and cultural warfare (Johnson's term) is just politics by other means. And in cultural warfare as in war in general, the first casualty is the truth...

--Allen