by Marcia Malory
Excerpt: “The researchers found that over time, mutations in the gene that codes for uricase made the enzyme progressively less effective. Finally, about 17 million years ago, apes developed a mutation that causes us not to produce any uricase at all.
The team noticed that the greatest reduction in uricase’s effectiveness took place when the Earth was cooling. From this, they hypothesized a connection between the decreasing ability to metabolize uric acid and an increasing scarcity of fruit.”
My comment: Climate change leads to changes in nutrient availability and natural selection of food via odors that epigenetically link the natural selection of food to metabolism of nutrients to the species-specific pheromones that control the physiology of reproduction in species from microbes to man. No experimental evidence suggest that ecological variations in the food supply cause mutation-initiated natural selection, which is why the concept of natural selection for anything except food is falling out of favor with informed biologists. Predictably, we will next see the concept of mutation-driven evolution fall out of favor since all experimental evidence continues to provide support for species diversity that results from ecological adaptation.
by Ed Yong
Excerpt: “Uricase is an ancient invention, one that’s shared by bacteria and animals alike. But for some reason, apes have abandoned it. Our uricase gene has mutations that stop us from making the enzyme at all. It’s a “pseudogene”—the biological version of a corrupted computer file.”
My comment: We are biological creatures; not computers. For example, we must eat. Kratzer et al (2014) tested the alternative hypothesis associated with eating because mutations perturb protein folding. If they accumulate and perturb protein folding required for functional intercellular signaling, mutations are eliminated from the DNA of organized genomes in species from microbes to man. Also, mutations involved in gene expression are susceptible to compensatory changes that up-regulate expression of other genes. That masks epigenetic cause and effect, which is exemplified in the fact that “pseudogenes” are ever-present in the genome.
The pseudogenes are not eliminated from organized genomes. They remain in case their reactivation is required for more efficient nutrient-dependent intercellular signaling that may be required for organism level thermoregulation in ever-changing ecologies. For example, olfactory receptor pseudogenes are not mutations that can be compared to “—the biological version of a corrupted computer file.” The experience-dependent de novo creation of olfactory receptor genes exemplifies the flexibility that all genomes must maintain to respond to conditions of nutrient stress and social stress.
Some scientists and many science journalists fail to report results in terms of what is currently known about how the epigenetic landscape becomes the physical landscape of DNA. Either they don’t know anything about current metabolic insights, or they choose to misrepresent cause and effect in the context of mutation-driven evolution. The misrepresentations of pseudogenes as corrupted computer files is akin to reporting science as if it were pseudoscience.
For comparison, the concluding paragraph of the discussion section in their publication, the co-authors state [subscription required]: “In total, we have shown that ancient mutations decrease uricase activity over evolutionary time, and this progressive decrease is correlated with physiological function and (potential) adaptation.” The ecological adaptation is more efficient use of fructose (fruit sugar). Since no mutations were fixed in the genome, the correlation among 1) the presence of pseudogenes; 2) physiological function; and 3) adaptation, exemplifies one of many nutrient-dependent pheromone-controlled ecological adaptations, which are detailed in the context of the metabolic insights in my model.