In a recent posting on his Why Evolution Is True website, "Jim Shapiro continues his misguided attack on neo-Darwinism," Jerry Coyne attacks me again. Let us examine some of his arguments.
1.
"[I]n one of his posts he explicitly uses a creationist trope:The first problem with selection as the source of diversity is that selection by humans, the subject of Darwin's opening chapter, modifies existing traits but does not produce new traits or new species. Dogs may vary widely as a result of selective breeding, but they always remain dogs.Given the fossil evidence of transitional forms ... such a statement is simply embarrassing, and is identical to ones you'll see in the creationist literature.
This "guilt by association" argument (even though ID proponents call me a "crypto-Darwinist") does not make sense; the fossil record has little to say about "selection by humans," which was my subject.
2.
[W]e know of no evidence for mutations occurring nonrandomly or "adaptively", i.e., that the occurrence of mutations is somehow biased in a direction that makes them more likely to be favorable when they arise, particularly when the environment changes in a way that requires favorable mutations to fuel adaptive evolution. There has been some controversy about the occurrence of "adaptive mutation" in bacteria, but that's died out because there's simply no evidence that the phenomenon occurs.
"Adaptive mutation" is in fact alive and well in the sense that selection conditions induce (adaptive) mutagenesis carried out by well-documented natural genetic engineering agents: homologous recombination functions, mutator polymerases, and transposable elements. This has been documented in several species of bacteria and in yeast.
3.
In his latest columns at HuffPo, (Part 1 and Part 2), Shapiro makes the same mistake, assuming that some features of the genome -- the vertebrate immune system in this case -- shows that natural selection is ineffective in molding adaptive traits of organisms, and that the innate nature of the genome has really replaced the conventional view of adaptive evolution.
I did not write about evolution of the immune system. I specifically used well-documented immune cell events to illustrate cell capacities to target and regulate genome changes, sometimes in response to intercellular signals. Neither Coyne nor I know in detail how the immune system evolved. But it certainly is a gross error to use ignorance as the basis for asserting dogmatically, as he goes on to do, that it was "molded by a combination of random mutation and natural selection." This is yet another example of Jerry confusing his preferred theory with empirical evidence. (He repeats this unsubstantiated assertion later in his critique.)
4.
The amazing thing is how the body uses a small number of genes in the B cells to generate a huge variety of protective antibodies ... What happens is that there are two processes, called somatic hypermutation and VJ recombination, that take the DNA sequence of the antibody-producing genes and mutate it, either creating "errors" in the DNA sequence or swapping bits within and among genes by physical recombination. This generates a large number of variable antibody proteins.
There a few minor mistakes and one major omission here. "VJ recombination" is actually "V(D)J recombination." Jerry forgets to mention that it is a highly targeted process of successive DNA breakage and joining events that also includes the synthesis of novel DNA sequences inserted next to the D segments. Perhaps he omitted the D region in his description because the ability of cells to generate new DNA sequences does not fit in his worldview.
In discussing somatic hypermutation, the aspects I highlighted were 1) its activation in immune cells following antigen binding, and 2) its specificity for sequences that encode the antigen-binding regions of the antibody without altering the rest of the molecule. Such inducible, selective, targeted mutagenesis is not included in conventional neo-Darwinian explanations of mutations as "errors" (to use Jerry's terminology).
Finally, Jerry does not even mention the switching of antibody classes ("class switch recombination," or CSR). CSR was the subject that occupied the bulk of my second posting. The reason for this absence appears to be that targeting such natural genetic engineering by intercellular signals is antithetical to the "error" view of genome change.
5.
The key point is that there is no evidence that the evolution of the immune system in this way (by differential reproduction of individuals instead of cells) involved anything other than natural selection among individuals having randomly produced mutant variants of an ancestral immune system.
We will examine what we know about the evolution of adaptive immune systems in vertebrates in the future. There is not space now. Let me simply note here that a number of steps already discernible from genome sequencing are not plausibly explained by "randomly produced mutant variants."
6.
Note especially that in both the contingency loci of bacteria and the hypermutability loci of vertebrates, the mutations that occur are random: variants are produced regardless of whether they'd help the beleaguered vertebrate trying to destroy the antigens or the besieged bacterium trying to avoid antibodies.
Here again, Jerry fails to recognize that variations in "contingency loci" are not in any way random mutations. Instead, they involve well-defined natural genetic engineering systems: 1) targeted homologous recombination of coding cassettes (in eukaryotic trypanosomes as well as in bacteria); 2) site-specific recombination within protein coding sequences ("shufflons"); 3) insertion and excision of DNA transposons; and 4) mutation-prone reverse transcription and cDNA reinsertion to diversify specific variable regions of phage and bacterial coding sequences ("diversity-generating retroelements"). These examples simply reinforce the message of my two immune system blogs, namely that cells of all kinds are fully competent to engineer their genomes in well-defined (i.e., non-random) ways.
7. Although Jerry claims near the end of his diatribe that "all the facts are on my side" (always a dangerous position to hold), I think his omissions and theory-observation conflations argue differently.
Jerry, I think you need to do better next time. Please address my real arguments, not your own mischaracterizations.
Random mutation-driven evolution in my mind has the advantage of explaining the great numbers of organisms that don't make it, either as non-viable individuals or as extinct species.
Actually, Shapiro has also done a magnificent job of presenting the research to why RM + NS do not account for the complexity in nature. That in itself is raising the hairs in the back of Coyne's neck as well as anyone else who has a vested philosophical interest in RM and NS!
Unfortunately for Coyne and others, the cat is now out of the bag!
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http://www.amnh.org/exhibitions/permanent/humanorigins/?src=e_h
Nor is he correct in refuting Jerry Coyne's well reasoned speculation that the evolution of the immune system in humans is the result of Natural Selection and genetic drift. Nearly seven years ago, Intelligent Design advocate biochemist Michael Behe made a similar error while testifying under oath during the 2005 Kitzmiller vs. Dover Area School District trial. In a most dramatic presentation, lead plaintiff attorney Eric Rothschild demonstrated why Behe was wrong.
You're right about diversity. Generating this kind of variability is one of the roles that sexual reproduction plays in higher organisms and the background level of mutation plays in microbial populations.
It is a mistake to confuse the roles that diversity plays in response to recurring changes in the environment and the kinds of innovative change that occurs at moments of extreme evolutionary challenge. Those are periods characterized by extreme events, as witnessed by the mass extinctions we see in the fossil record. What we need to explain are the rapid phylogenetic radiations that follow mass extinctions. Darwin called the expansion of different groups of seed plants "an abominable mystery" because it did not fit his gradualist theory. But today we know that interspecific hybridization and doubling of entire genomes played a key role in this process.
Long held Dogma is almost impossible to over come -my view
Please say more about the fungi. It may be relevant and of interest to other readers of this conversation.
But, on the other hand, go back and read it again. How much could a typical christianist actually understand? I consider myself pretty well educated on evolution; but damn I had to reread and think about a lot of what was presented even to understand the differences.
Or, to put it more tersely: There's a lot of big words!!!
Apologies for too much technical terminology. If you click on the links, you will frequently get simpler or fuller explanations. There is also a list of Scientific American references at http://shapiro.bsd.uchicago.edu/SuggestedReadingsForNonProfessionals.shtml. I hope this clarifies somewhat. You may find some of my earlier postings easier to follow.
Follow the threads with Lyaeus. You will find a reply dealing with the problem of how to engage Creationists effectively. I have just drafted a new blog on the subject and hope to post it at the beginning of next week.
1. What is fundamentally new and needs changing in evolutionary thinking (ThinkCreeps, Lyaeus 10, Akia).
2. What human selection and domestication of plants and animals can and cannot accomplish (Junius Gallio, Keith Roragen, Akia).
3. The nature of real scientific discourse (Lyaeus 10, Akia).
4. How to confront ID proponents and Creationists (Lyaeus 10, Akia).
5. The potential role of gamma radiation in evolutionary change (QuietProfessional).
Not exactly. What I'm saying is that environmental input and other life history events (such as mating with someone outside your normal population group) can activate cellular systems that rapidly restructure the genome. This is the source of much evolutionary change. We know this because many taxonomic splits involve whole genome doubling, which happens when two species hybridize.
Coyne certainly writes much better. For example:
`The onus is on Shapiro to show exactly how the systems of “adaptive genome restructuring” he so admires require us to abandon our notion of adaptation via natural selection.'
I haven't asked Jerry to abandon any of his views. That seems to be hopeless. What I ask others interested in evolution to give up is the notion of random accidental mutation. Now that we know about the molecular mechanisms of DNA change, we know mutation results from the actions of a variety of biochemical systems. DNA biochemistry is non-random in the sense that each system operates in predictable ways, that all systems can be turned on and off by cell regulatory circuits, and that their actions can be targeted by various well-established molecular mechanisms. Once the essentially biochemical and cellular nature of hereditary change is assimilated, many new aspects of evolutionary thinking will adapt themselves quite rapidly.
Take a look further down the comment section. You may have to make a few clicks to continue following the thread. I clarify the origins of maize and also discuss strategies for confronting ID advocates and Creationists. You can tell me whether my statements are pro-evolution. Wolfs, by the way, can be crossed successfully with dogs. So they are members of the same species.
Gamma rays can be a source of chromosome breakage and lead to genome rearrangements. You can read more about this in my two blogs on Barbara McClintock posted last month (somewhat repetitive because of a confusion with HuffPost). Such rearrangements can play a role in evolutionary change in a variety of ways (direct effects on phenotype, effects on mating, or acting as stimulating events for further genome change). Although the locations of gamma ray-induced breaks are indeterminate, they only cause heritable genome change as a consequence of cell-mediated repair, and that change is almost always a chromosome rearrangement, not a localized "gene mutation," as McClintock showed in the 1930s with X ray-induced mutants of maize.
Why embarrassing? You agree my statement is accurate. Darwin, on the other hand, argued that a similar process could create new species. But there is no evidence for speciation by human selection. Should I feel embarrassed to point out something that is not widely known? We can create species by other means, in particular by interspecific hybridization. If non-Darwinian processes (i.e those not considered or treated as unimportant by Darwin) lead to speciation, is that not of interest to people who wish to know more about how evolution actually works?
Your not arguing against religious dogma the way Darwin was, you're arguing the consensus scientific viewpoint of your peers and given the post below that calls Dr. Coyne ignorant, you might consider the weight to which dogmatists will give creedance to your opinion with no vetting at all as a serious objection to populists posts of minority scientific viewpoints such as this is.
Science advances by argument, not by consensus. We should look to empirical evidence rather than academic authority in evaluating scientific claims. I am simply trying to point out where evidence from molecular biology does not agree with the consensus view of how evolution proceeds. There are many new molecular mechanisms of genome change we now know about at the molecular level. Jerry Coyne's blog showed that he is not familiar with them, but they are nonetheless quite relevant to evolution.