Viruses come alive: Tree of life pseudoscience

In summary, the spectrum of protein-coding variation is considerably different today compared to what existed as recently as 200 to 400 generations ago. Of the putatively deleterious protein-coding SNVs, 86.4% arose in the last 5,000 to 10,000 years, and they are enriched for mutations of large effect (Supplementary Fig. 14) as selection has not had sufficient time to purge them from the population.

See also: The palaeolithic diet and the unprovable links to our past

…genetics play a pretty minor role in determining the specifics of our diet. Our physical and cultural environment mostly determines what we eat. Textbook examples include genes associated with lactose tolerance, starch digestion, alcohol metabolism, detoxification of plant food compounds and the metabolism of protein and carbohydrates: all mutations associated with a change in diet.

My comment: That claim was linked to this claim in Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants
Excerpt:

Of the putatively deleterious protein-coding SNVs, 86.4% arose in the last 5,000 to 10,000 years, and they are enriched for mutations of large effect (Supplementary Fig. 14) as selection has not had sufficient time to purge them from the population.

My comment: The claim that selection has not had sufficient time to purge the mutations from the population was placed into the context of beneficial mutations via this report: The palaeolithic diet and the unprovable links to our past.
Excerpt:

Textbook examples include genes associated with lactose tolerance, starch digestion, alcohol metabolism, detoxification of plant food compounds and the metabolism of protein and carbohydrates: all mutations associated with a change in diet.

My comment: Theorists have not yet realized that they can not link virus perturbed protein folding to our past via mutations, natural selection, or evolution. Changes in diet must be linked from our past to ~5-10K years of ecological variation and ecological adaptations via biophysically constrained nutrient-dependent RNA-mediated protein folding and the amino acid substitutions that differentiate all cell types in all individuals of all living genera.

On August 21st, the research team led by Prof. Yigong Shi from School of Life Sciences, Tsinghua University in China published two side-by-side research articles in Science, reporting the long-sought-after structure of a yeast spliceosome at 3.6 angstrom resolution determined by single particle cryo-electron microscopy (cryo-EM), and the molecular mechanism of pre-messenger RNA splicing. Until now, decades of genetic and biochemical experiments have identified almost all proteins in spliceosome and uncovered some functions. Yet, the structure remained a mystery for a long time. The works, primarily performed by Dr. Chuangye Yan, and Ph.D students Jing Hang and Ruixue Wan under Prof. Yigong Shi’s supervision, settled this Holy Grail question and established the structural basis for the related area. This work was supported by funds from the Ministry of Science and Technology and the National Natural Science Foundation of China.

The involved proteins and RNAs assemble into and dissociate from spliceosome in a strict order during splicing, endowing extreme dynamics and flexibility of the spliceosome. These features guarantee the accomplishment of the complex splicing reaction, but at the same time tangling the structural investigations of spliceosome.

Excerpt 2)

…[this] group provided the first structural insight into the molecular mechanism for pre-mRNA splicing: the spliceosome is in essence a protein-directed ribozyme, with the protein components essential for the delivery of critical RNA molecules into close proximity of one another at the right time for the splicing reaction (shown in Figure 2).

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

My comment: Attempts to move forward from our accurate representations of biologically-based cause and effect have been stalled by evolutionary theorists for nearly 2 decades. The theorists seem to want mutations to be the cause of cell type differentiation via natural selection and evolution. It has not been possible to convince them to not put natural selection for anything except food in the primary position that must be considered in the context of Darwin’s “conditions of life.”