I’ve read your blog about the Lenski experiment “Microbes: living …

Comment on Dr. Richard Lenski’s “Unicorns” by Sean Pitman.

I’ve read your blog about the Lenski experiment “Microbes: living in the past”. However, I think you’re mistaken. You wrote:

The adaptations arose [in the Lenski experiment] due to the de novo creation of olfactory receptor genes under conditions that would otherswise lead to death by starvation.

This simply isn’t true. No new receptor genes evolved at all – olfactory or otherwise. The very same genes stayed exactly the same. The only thing that changed is the location of the very same genes within the genome. Also, the bacteria were not starving. They simply started using citrate as an additional source of energy to the nutrients that they were already being provided with – over the course of the decades that Lenski has been running this particular experiment. I see no evidence for epigenetic factors in play here or thermodynamic instability before or after the changes in function.

Sean Pitman

Sean Pitman Also Commented

Dr. Richard Lenski’s “Unicorns”
There was no change in the citrate receptor or transport protein, or any other protein. No structural change took place at all. You simply don’t understand the Lenski experiment. All that happened was that the gene that codes for the citrate transport protein, which already existed and was active under anoxic conditions, was turned on in an oxygenated environment by being placed next to an active promotor. That’s it. There’s simply no new receptor being made here. No new gene or protein – olfactory or otherwise.

Dr. Richard Lenski’s “Unicorns”
It doesn’t matter what stressors may or may not contribute to protein biogenesis. The fact remains that whatever else might contribute to mutagenesis, novel proteins are dependent upon novel genetic mutations. In this particular Lenski experiment, no novel protein was produced. However, there was a novel genetic mutation that gave rise to the new functional abilities of the E. coli bacteria. This genetic mutation simply allowed a protein-coding gene to be turned on in a different type of environment by moving a gene to a different location within the genome. Statistically, this isn’t a problem given the number of bacteria in the steady-state population over the course of a few tens of thousands of generations. It’s very predictable in fact – statistically. What is not statistically tenable, however, is the evolution of a qualitatively novel protein-based system of function that requires more than 1000 specifically arranged residues. Such a feat is not statistically feasible – and Lenski should know better than to suggest otherwise.

Dr. Richard Lenski’s “Unicorns”
@Bob Helm:

Most of this information, in this particular article, has already been published by others in various journals. The only thing I contributed here of any uniqueness is the concept of changes in the ratio of beneficial vs. non-beneficial sequences in sequence space at various levels of functional complexity.

When I submitted the technical argument for sequence space to Origins (a few years ago), they told me that it was too technical for their readership to understand. I should probably try again to submit a toned down version for more general readership.

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Again, this paper doesn’t present an actual mechanism for harming the human immune system as already explained to you. Let me know what the authors say – if they ever respond.

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I thought you’d appreciate it – given the irony of it. After all, this is just basic science here. The authors here are not claiming something novel that has no mechanistic basis. There are many other places where you can read up on the mechanism of how the spike proteins are presented on the surfaces of the muscles cells where they are produced (Link, Link, Link, Link).

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