Salvador's Redundancy
[Update: This discussion is continued here and here.]
When we last met Salvador Cordova, the energetic proponent of intelligent design (ID) creationism, he was saying spectacularly silly things about the robustness of biological systems over at evolgen. Now he's at it again:
What about the rest of the post? Interestingly, we learn where Salvador got his misconceptions on nematode vulval development. He quotes the following passage from Michael Denton:
So what of the more general claim that redundancy and robustness pose difficulties for evolutionary biologists? As I've argued before, this is a delusion. Redundancy arises readily from a common evolutionary mechanism: gene duplication. And robustness is an exciting active area of research in evolutionary biology. As regular readers of this blog will know, even I work on it.
I should end by quoting a comment made by Mark Perakh to Jason's post:
When we last met Salvador Cordova, the energetic proponent of intelligent design (ID) creationism, he was saying spectacularly silly things about the robustness of biological systems over at evolgen. Now he's at it again:
"Intelligent design will open doors to scientific exploration which Darwinism is too blind to perceive. The ID perspective allows us to find designed architectures within biology which are almost invisible to natural selection. Thus, the ID perspective is a far better framework for scientific investigation than the Darwinian perspective. What do I mean, and how will I justify my claim?"Give the man credit: this opening paragraph has flair. But does the rest of the post deliver? Sadly, it's just the same argument that redundancy and robustness are somehow a problem for evolutionary biology. Bizarrely, he chooses to illustrate his point with a press release from Laurence Hurst about his latest paper in Nature. He quotes the following passage with approval:
"Previous attempts to work out the minimal genome have relied on deleting individual genes in order to infer which genes are essential for maintaining life [...] This knock out approach misses the fact that there are alternative genetic routes, or pathways, to the production of the same cellular product [...] Using the knock-out approach you could infer that both genes are expendable from the genome because there appears to be no deleterious effect in both experiments."The point being made is uncontroversial to any biologist who knows her genetics. So what does Salvador conclude from this? Incredibly this is what he writes:
"Knockout experiments have also been used to argue 'junk DNA' is junk. This is out rightly bad science, but it persists because of Darwinist’s eagerness to close their eyes to design and paint various artifacts in biology a the product of a clumsy blind watchmaker rather than an intelligent designer."This is wrong on so many levels that it's hard to know where to begin. Jason Rosenhouse did a good job debunking this, but I'll make a couple more points. First, where did this connection to "junk" DNA come from? I suspect it arose from the discussion on evolgen. My colleague Dan Graur made the point that experiments where large portions of "gene deserts" (long stretches of nongenic DNA without apparent function) were deleted support the hypothesis that they truly are "junk" DNA. The "Darwinist's eagerness" is entirely in Salvador's imagination. Second, Salvador seems to be suggesting that Darwinists have been getting the wrong end of the stick about knockout experiments. So who is this Hurst fellow? Surely, he must be a rising star at the Discovery Institute. Actually, you'll be shocked to find that that is not the case: Laurence Hurst is one of the brightest young British evolutionary biologists, a disciple of Darwin if ever I've met one. Indeed, the abstract of the paper the press release was about leaves us in no doubt as to what Hurst and his colleagues were doing (I've highlighted a few key concepts in bold):
It is possible to infer aspects of an organism's lifestyle from its gene content. Can the reverse also be done? Here we consider this issue by modelling evolution of the reduced genomes of endosymbiotic bacteria. The diversity of gene content in these bacteria may reflect both variation in selective forces and contingency-dependent loss of alternative pathways. Using an in silico representation of the metabolic network of Escherichia coli, we examine the role of contingency by repeatedly simulating the successive loss of genes while controlling for the environment. The minimal networks that result are variable in both gene content and number. Partially different metabolisms can thus evolve owing to contingency alone. The simulation outcomes do preserve a core metabolism, however, which is over-represented in strict intracellular bacteria. Moreover, differences between minimal networks based on lifestyle are predictable: by simulating their respective environmental conditions, we can model evolution of the gene content in Buchnera aphidicola and Wigglesworthia glossinidia with over 80% accuracy. We conclude that, at least for the particular cases considered here, gene content of an organism can be predicted with knowledge of its distant ancestors and its current lifestyle.Isn't it strange how ID, with its "far better framework" keeps opening "doors" in blog posts, while the Darwinists keep publishing papers in Nature, despite having their eyes closed.
What about the rest of the post? Interestingly, we learn where Salvador got his misconceptions on nematode vulval development. He quotes the following passage from Michael Denton:
"The development of the female sexual organ, the vulva, in the nematode provides perhaps the most dramatic example to date of redundancy exploited as a fail-safe device at the very highest level. A detailed description of the mechanism of formation of the nematode vulva is beyond the scope of this chapter, suffice it to say that the organ is generated by means of two quite different developmental mechanism, either of which is sufficient by itself to generate a perfect vulva."Since Salvador seems to have missed my earlier discussions of this example (here and here), I'll repeat it. Here's a good review of vulval development in the nematode Caenorhabditis elegans, by the leader of the field. The abstract gives an overview:
A single cell of the somatic gonad, the anchor cell, organizes the development of the vulva from epidermal precursors as well as the physical connection of the epidermis with the uterus. WNT signaling acting via the HOX gene lin-39 renders six epidermal precursor cells competent to respond to other developmental signals. The anchor cell induces nearby epidermal precursor cells to generate vulval cells via an epidermal growth factor (EGF) signaling pathway. The precise pattern of vulval precursor cell fates involves the graded action of the EGF signaling and LIN-12 (Notch) mediated lateral signaling. EGF promotes the primary fate while LIN-12 promotes the secondary fate. Both EGF and LIN-12 prevent precursor cells from adopting the tertiary fate, which generates non-specialized epidermis.So what about those "two quite different developmental mechanisms, either of which is sufficient by itself to generate a perfect vulva"? Well, the thing is, the two signaling pathways are not redundant. Of course there is redundancy in the network (I've discussed one kind here), as there is in almost all biological networks known -- it's just that there are no "independently successful redundant developmental pathways" for making a vulva, to use Salvador's earlier description. This shows a recurrent pattern in ID literature, and other pseudoscience -- grandiose claims based on sloppy scholarship, selective quotation and ignoring reality.
So what of the more general claim that redundancy and robustness pose difficulties for evolutionary biologists? As I've argued before, this is a delusion. Redundancy arises readily from a common evolutionary mechanism: gene duplication. And robustness is an exciting active area of research in evolutionary biology. As regular readers of this blog will know, even I work on it.
I should end by quoting a comment made by Mark Perakh to Jason's post:
It would be entertaining to watch a debate between Salvador Cordova and Michael Behe, wherein Salvador would defend his thesis that biological entites possess redundancy which points to design, while Behe would defend his thesis that biological system are irreducibly complex, hence possess no redundancy, which points to design. A moderator (say, Dembski) would dance between them reconciling these two mutually incompatible arguments by means of writing lengthy equations and inventing new terms, say of "irreducibly complex redundancy," as a corollary to a newly discovered Fifth law of thermodynamics: the law of conservation of redundant irreducible complexity. A lot of fun watching Cordovas and his ilk pretending to have (redundant) brains.In other words, anything is considered evidence for an intelligent designer by these people, no matter how inconsistent. Now, that is what I call a framework!
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