Answering two questions from Vincent Torley

Vincent Torley read a post by Jerry Coyne where Jerry wondered if Intelligent Design Creationism was in trouble because the Discovery Institute has lost Bill Dembski and Casey Luskin [Is the Discovery Institute falling apart?].

Torley disagrees, obviously, but he focuses on a couple of the scientific statements in Jerry Coyne's post and comes up with Two quick questions for Professor Coyne.

I hope Professor Coyne won't mind if I answer.

Before answering, let's take note of the fact that Vincent Torley has been convinced by the evidence that most of our genome is junk. I wonder how that will go over in the ID community?

Here's question #1 ...

So my first question is: if (i) Nature contains systems which accomplish a feat (namely, coding for complex structures) in a manner which is far better than what our best computer scientists can do, and (ii) despite diligent searching, scientists have failed to observe any cases in Nature of unguided processes generating a new code from scratch, then why isn’t it reasonable to infer (at least provisionally) that these systems were designed by a super-human Intelligence? You tell me, Professor.

Both of the premises are wrong. I've yet to see any natural system that's as good as what computer scientists can do. Most of the genes that code for complex structures are inefficient and error-prone. Natural systems look like they were designed by a tinkerer who cobbles together odds and ends that just happened to be in reach. They look like they evolved haphazardly. Any intelligent scientist could do better and, in some cases, they have done better by genetically modifying organisms to make them more efficient.

This is an important point. Intelligent Design Creationists never see the big picture so they lack perspective—a fault shared by many non-creationists as well. It's simply not true that complex biological structures are complex because they are very sophisticated and efficient. In many cases, they are complex by accident and it's easy to make better, more simple, systems that can do the same job.

The second premise of Vincent Torley's question is also wrong. We have lots of examples of unguided processes generating new code from scratch. This includes de novo genes. See

Kaessmann, H. (2010) Origins, evolution, and phenotypic impact of new genes. Genome research, 20:1313-1326. [doi: 10.1101/gr.101386.109]

Here's a quotation from the abstract of the Kaessmann review,

Thus, it was shown that novel genes also regularly arose from messenger RNAs of ancestral genes, protein-coding genes metamorphosed into new RNA genes, genomic parasites were coopted as new genes, and that both protein and RNA genes were composed from scratch (i.e., from previously nonfunctional sequences).

This is another case where a little knowledge is a dangerous thing. Vincent Torley and his friends have convinced themselves that the evolution of de novo genes has never been observed. None of them bother to read the scientific literature to see if their stories are correct.

See also:

Carvunis, A.-R., Rolland, T., Wapinski, I., Calderwood, M.A., Yildirim, M.A., Simonis, N., Charloteaux, B., Hidalgo, C.A., Barbette, J., Santhanam, B., Brar, G.A., Weissman, J.S., Regev, A., Thierry-Mieg, N., Cusick, M.E., and Vidal, M. (2012) Proto-genes and de novo gene birth. Nature, 487:370-374. [doi: 10.1038/nature11184]

Long, M., Betran, E., Thornton, K., and Wang, W. (2003) The origin of new genes: glimpses from the young and old. Nat Rev Genet, 4:865-875.

Long, M., VanKuren, N. W., Chen, S., and Vibranovski, M. D. (2013) New gene evolution: little did we know. Annual review of genetics, 47:307. [doi: 10.1146/annurev-genet-111212-133301]

Näsvall, J., Sun, L., Roth, J. R., and Andersson, D. I. (2012) Real-time evolution of new genes by innovation, amplification, and divergence. Science, 338:384-387. [doi: 10.1126/science.1226521 ]

Neme, R., and Tautz, D. (2013) Phylogenetic patterns of emergence of new genes support a model of frequent de novo evolution. BMC genomics, 14(1), 117. [doi: 10.1186/1471-2164-14-117]

Schlötterer, C. (2015) Genes from scratch–the evolutionary fate of de novo genes. TRENDS in Genetics, 31(4), 215-219. [doi: 10.1016/j.tig.2015.02.007]

Tautz, D., and Domazet-Lošo, T. (2011) The evolutionary origin of orphan genes. Nature Reviews Genetics, 12(10), 692-702. [doi: 10.1038/nrg3053]

Wu, D.-D., Irwin, D.M., and Zhang, Y.-P. (2011) De novo origin of human protein-coding genes. PLoS Genet, 7:e1002379. [doi: 10.1371/journal.pgen.1002379]

Given that both of his "facts" (premises) are wrong, Vincent Torley's question becomes irrelevant. But let's answer it anyway. He asks,

... why isn’t it reasonable to infer (at least provisionally) that these systems were designed by a super-human Intelligence? You tell me, Professor.

It's not reasonable because it raises far more questions than it answers. If Torley's facts were correct (they aren't), it would still be much more reasonable to infer that that new coding information arose by unknown natural processes than to speculate that there are unknown supernatural beings who could have done the job.

In other words, "we don't know" is still a more reasonable answer than "gods did it" because by inferring gods you just shift the questions to another level, e.g. who made the gods?

The problem here is that Torley's question does not reflect his actual logic. Creationists begin with the "knowledge" that omnipotent supernatural beings actually exist and that he/she/it/them is/are responsible for creating us and the universe. That makes it much more "reasonable"—in their eyes— to infer that gaps in our scientific knowledge can be filled by their gods.

Vincent Torley's second question is no better,

So my second question for you is: will you concede that neo-Darwinism is unable to account for the origin of the epigenetic information needed to create novel body-plans (which must have occurred before the Cambrian explosion took place), and that natural selection therefore doesn’t explain all cases of apparent design in nature, falsifying your previous claim that it’s the “only game in town” for producing adaptations?

Incidentally, are you aware of any good evidence that epigenetic information is not divine in origin? If so, please elaborate.

Torley is using the broad definition of epigenetics: "the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself." That includes things like the regulation of the lac operon in E. coli and developmental regulation of transcription factor genes in Drosophila melanogaster. It also includes regulatory mechanisms that involve methylation of DNA and modification of histones during the transition from 'open' to 'closed' chromatin configurations.

We know how the transcription of genes is regulated by transcription factors and there's nothing mysterious going on. It's easy to envisage how such regulatory mechanisms can arise by purely naturalistic means. There's nothing about our understanding of evolution, biochemistry, genetics, and molecular biology that precludes the origin of such epigenetic information. It's silly to say that "neo-Darwinism" (whatever that is) is unable to account for the evolution of gene regulation by repressors and activators [see The Extraordinary Human Epigenome].

We know that novel body plans can be created by simply altering the expression of pre-existing genes. That's the main discovery of developmental biology in the 70s and 80s. There's no mystery there, either.

Same with modifications of DNA and histones in eukaryotes. These modifications are associated with a mode of control and regulation at the level of chromatin structure. Much of the eukaryotic genome is effectively silenced by a tight association with nucleosomes (histones) in a three-dimensional structure called the 30nm chromatin fiber (and higher order structures).

The 30nm fiber exists in dynamic equilibrium with an open conformation called the 'beads-on-a-string' structure (see the electron microscope structures below). Transcription factors can recognize and bind to their binding sites in the open conformation but not the closed one. If the transcription factor binds to a functional promoter region then the adjacent gene will be transcribed.

As genomes expanded during the evolution of eukaryotes, it became selectively advantageous to shut down much of the genome that wasn't immediately required for viability. But the gradual evolution of more and more tightly binding nucleosome structures came at the cost of accidentally turning off genes that were needed. Thus, mechanisms for maintaining an open conformation around active genes evolved simultaneously with the evolution of heterochromatin and 'closed' structures. Those mechanisms involved modifying the histones bound to active genes so that they could not associate with each other to form the 30nm chromatin fiber.

The modifications vary from species to species but many of them involve attaching acetyl groups to the ends of individual histone proteins in the nucleosome. When the open configuration needs to revert to the closed configuration the acetyl groups are removed by deacetylation. Thus, the opening and closing of chromatin domains can be triggered by the binding of transcription factors near a promoter.

This mode of regulation at the level of chromatin structure can also be controlled by methylation of DNA at cytosine residues. When transcription of a gene is required, the sequences in the promoter region can be methylated at certain sites and this inhibits formation of the closed structure. Methylation is also reversible so that when the gene is turned off the methyl groups are removed.

Some genes will need to be active for many cell generations so a given promoter region will contain modified histones and methylated DNA for a long time. Some genes will transiently revert to the closed configuration only to be re-activated. (Everything in biology exists in a transient state of dynamic equilibrium.) Thus, epigenetic modifications are 'inherited' from generation to generation.

If the genes are active in germ cells then the activation can be passed to another generation in multicellular species. This is not conceptually different from E. coli cells that "inherit" active transcription of the lac operon or repression of prophage genes. None of those discoveries from the 60s and 70s caused anyone to question our understanding of evolution just like none of the discoveries of other levels of control ( = more epigenetics) in the 80s caused any concern.

The only people who get excited about the evolutionary implications of epigenetics are biologists who don't understand biochemistry, genetics, evolution, and molecular biology and creationists who don't understand any of those subjects and who are looking for god in the gaps of their knowledge.

As for the claim that natural selection can account for all cases of apparent design in nature, that's an exaggeration promoted by Jerry Coyne. It's not far from the truth but there may be non-selective processes that play an important role in adaptation.

But that's not what Vincent Torley is referring to. He's not just questioning whether natural selection can explain all cases of apparent design but whether any kind of evolution can explain it. Torley thinks he's proved the negative; namely, that epigenetic phenomena cannot be explained by naturalistic means. Therefore, gods must have done it.

His claim is absurd. His questions are absurd.

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Image credit for histones & chromatin figures: Moran, L.A., Horton, H.R., Scrimgeour, K.G., and Perry, M.D. (2012) Principles of Biochemistry 5th ed., Pearson Education Inc. pages 590 and 591 © Pearson/Prentice Hall