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Inconvenient Truths: Why Are Self-Styled Defenders of Evolution so Resistant to Lessons From Molecular Genetics?

12/04/2012 01:56 pm ET | Updated Feb 03, 2013

Last week, on his very popular blog, WhyEvolutionIsTrue.wordpress.com, Jerry Coyne ridiculed Nicholas Wade's NYT article discussing the negative consequences resulting from the anti-religious tone of most orthodox defenses of evolution.

Wade's article was far from ideal. He failed to distinguish clearly between the overwhelming empirical evidence for evolution and the inevitably limited theories advanced to explain how it occurs. But Wade was taken to task chiefly for making the eminently reasonable argument that the pro-evolution side would be more effective if it showed greater respect for people with religious beliefs.

In the course of the discussion, Ben Goren posted the following scientific challenge on the blog:

"I am unaware of even a single example of biological complexity which defies explanation within the modern Darwinian framework. Perhaps you could offer up such an example...?"

I decided to respond and provide a few examples of evolutionary change where we have enough molecular evidence to know that they did not occur by the gradual accumulation of random mutations:

1. Multiple antibiotic resistance in bacteria;
2. Origin of the eukaryotic cell;
3. Origin of photosynthetic eukaryotic lineages;
4. The "abominable mystery" of rapid angiosperm evolution.

Ben's reply to my intervention illustrates how little some followers of TheWhyEvolutionIsTrue blog care about the molecular analysis of evolution. He seemed to have no idea that bacterial antibiotic resistance evolves by horizontal transfer of plasmids and the accumulation of multiple resistance determinants by transposition and site-specific recombination. (He did not address any of the other three examples I gave.)

Instead of a reasoned answer, I got the following:

Your list indicates to me that you are suffering from some significant misconceptions and / or a lack of understanding of what the Theory of Evolution by Random Mutation and Natural Selection actually is.


Just addressing your first case, for example... well, antibiotic resistance is a textbook example of evolution in practice, and one that Darwin himself likely would have predicted (and certainly not been surprised by).

The idea of Darwin predicting conjugative plasmids, transposons and integrons was indeed novel to me. All Ben seemed able to envision is random mutation to antibiotic resistance. He was unaware that such mutations are irrelevant to the real world evolution and global spread of multiple antibiotic resistance determinants.

I pointed Ben to two of my blogs on the subject. After reading one of them, his response was as follows:

Jim, I just read your first blog entry. And, I'm sorry, but I don't see any significant difference between you and Behe on this.

Ben ignored the history I outlined of research on the evolutionary case in question. Evidently, it was more important for him to equate me with Intelligent Design advocate Michael Behe. I guess he made that connection because I wrote that we still lack a complete scientific explanation for well-documented evolutionary relationships between bacterial flagella, DNA transfer apparatus, and protein injection complexes used in pathogenesis.

Where did Ben's resistance to considering the theoretical implications of molecular analysis come from?

Why did he find it unacceptable for me to indicate specific unresolved evolution issues, as I did in the superbug blog? To quote Ben:

Again, all you're doing is pointing at something you don't understand and lack the imagination to guess at a reasonable understanding, and throwing up your hands and insisting that everybody else should quit as well and join you in your ignorance.

A second commentator, Torbjörn Larsson, argued that horizontal DNA transfer posed no challenge to the neo-Darwinian theory: "In other words the generic gradualism of Darwin mentioned in the article isn't rejected by the observed degree of horizontal gene transfer."

But Torbjörn's claim does not make sense scientifically. Horizontal transfer is not the gradual Darwinian accumulation of changes. Horizontal transfer episodes rapidly incorporate complex evolved DNA structures into new genomes by coordinated molecular events.

There is no way we can reasonably apply the term "random mutation" to a DNA transfer process that utilizes dedicated surface structures for bringing two cells together, assembles a multi-protein DNA transport pore connecting the cells, and initiates DNA transfer replication at a specific site on plasmid DNA.

The well-established molecular details of horizontal transfer in the evolution of bacterial antibiotic resistance are difficult to reconcile with neo-Darwinism.

Is it possible that Ben, Torbjörn and their friends fear that readers will start to entertain doubts about evolutionary orthodoxy when they learn what molecular genetics and the DNA record have to teach us about the molecular nature of variation? The molecular data show that orthodox neo-Darwinian theory is far from providing realistic explanations for well-documented cases of genome sequence evolution.

In preparing for a public lecture early next year on what DNA teaches us about evolution, I made a list of take-home lessons to use as an introduction:

1. Evolution is complex, not reducible to simple formulas;
2. Evolutionary thinking has a long history full of ongoing discoveries;
3. Cell mergers are an important source of abrupt evolutionary novelty;
4. Horizontal DNA transfer is an important source of rapid evolutionary novelty;
5. Cells actively repair and restructure their genomes (the genome as a RW memory system);
6. Proteins evolve by swapping segments, not by changing one amino acid at a time;
7. Mobile genetic elements can rapidly modify genome function at multiple locations and establish genomic networks;
8. Inter-specific hybridization and whole genome duplications are further sources of rapid evolutionary innovation;
9. Genome restructuring (natural genetic engineering) is regulated and activated by stress, cell fusions and inter-specific hybridization.

I would like to understand where Ben and Tobrjörn find a basis for the certainties they express about what kind of evidence to accept. So, can someone please answer two questions for me?

A. What do my nine take-home statements have to do with supernaturalism outside the bounds of science?
B. Where have these statements been convincingly incorporated into Ben's all-encompassing "Theory of Evolution by Random Mutation and Natural Selection"?