… we propose as a working model that syncytins have been captured primarily as a placental gene, but that some expression in the muscle is taking place (possibly as a consequence of regulatory processes and transcription factors shared by placenta and muscle), and that a “collateral” effect of the capture of such genes -with a clear-cut fusogenic activity- is an add-on contribution to myogenesis in males of placental mammals.
Reported as: Virus Pumps Up Male Muscles—in Mice
In 2000, scientists discovered that syncytin, a protein that enables the formation of the placenta, actually originated as a viral protein that humans subsequently ‘borrowed’. That original viral protein enables the retrovirus to fuse with host cells, depositing its entire genome into the safe harbour of the cytoplasm. Syncytin has changed little from this ancestral protein form; it directs certain placental cells to fuse with cells in the mother’s uterus, forming the outer layer of the placenta.
My comment: This representation is a damning example of “Just So” story-telling that puts everything known about virus-driven energy theft and all pathology into the context of conserved molecular mechanisms linked to sexually dimorphic phenotypes via energy-dependent biophysically constrained cell type differentiation. The nutrient energy-dependent de novo creation of genes is the only known link from the early form of syncytin to the biophysically constrained form that enables the formation of cell types for the placenta.
The fact that male muscle development also is energy-dependent and virus-driven energy theft is linked to atrophy also attests to the fact that virus-driven entropy of mammalian organized genomes was contrained by energy-dependent changes that link angstroms to ecosystems in all living genera via the physiology of reproduction.
“We were mining the DNA record for information about how evolution works,” says [Sean B.] Carroll, professor of molecular biology and genetics at UW-Madison and vice president for science education at the Howard Hughes Medical Institute (HHMI).
My comment: Nei (2013) claimed that this is how evolution works:
…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.
What they found surprised them and challenged all of their initial hypotheses: Rattlesnakes have quickly evolved a great variety of differences through the loss of genes, resulting in varying venom gene numbers and types.
My comment: (see A third of Americans don’t believe in evolution)
Ecological adaptation occurs via the epigenetic effects of nutrients on alternative splicings of pre-mRNA which result in amino acid substitutions that differentiate all cell types of all individuals of all species. The control of the differences in cell types occurs via the metabolism of the nutrients to chemical signals that control the physiology of reproduction.
These facts do not refute evolution; they simply refute the ridiculous theory of mutation-initiated natural selection that most people here were taught to believe is the theory of evolution.
That theory is far too ridiculous to be anything but a joke in the context of biological-based increasing organismal complexity. But here, we have lots of jokers, don’t we? The proof of ecological variation that appears to refute the theory of evolution, which actually refutes itself, is that ecological adaptations occur too fast for mutations to compete with them as a source of anything but diseases and disorders.
In most species studied, genes that are no longer necessary usually linger a long time in the genome, eventually degrading. For instance, in the human genome we still see the remnants of the large olfactory receptor gene family that gave our evolutionary ancestors a keen sense of smell, even though humans no longer rely on them.
The researchers can’t say for certain why snakes got rid of some of their weapons, but ecologically, they say it’s likely related to the individual circumstances each species found itself in over time.
My comment: The researchers are not sure of anything that they placed into the context of evolution because no experimental evidence of biologically-based cause and effect supports claims that cannot be placed into the context of ecological variation and energy-dependent ecological adaptations.
They cite: 28. Lynch, V.J. (2007). Inventing an arsenal: adaptive evolution and neofunctionalization of snake venom phospholipase A2 genes. BMC Evol. Biol. 7, 2.
V.J. Lynch is a co-author of Ancient Transposable Elements Transformed the Uterine Regulatory Landscape and Transcriptome during the Evolution of Mammalian Pregnancy (2015)
Taken together, our data suggest that novel gene regulatory networks and cell-type identities can evolve through large-scale genome-wide changes rather than gradual gene-by-gene changes (Goldschmidt, 1940). TEs may play a particularly important role in this process because they provide a mechanism to coordinately regulate the expression of numerous genes to the same stimuli upon their integration into multiple locations in the genome, alleviating the need for the de novo evolution of cis-regulatory elements capable of directing stereotyped responses to the same stimuli one gene at a time across the genome (Britten and Davidson, 1969, Davidson and Britten, 1979, Feschotte, 2008, McClintock, 1984).
Günter P. Wagner is the senior author. The results were Reported as: Ancient ‘genomic parasites’ spurred evolution of pregnancy in mammals
“For the first time, we have a good understanding of how something completely novel evolves in nature, of how this new way of reproducing came to be,” said study author Vincent Lynch, PhD, assistant professor of human genetics at the University of Chicago. “Most remarkably, we found the genetic changes that likely underlie the evolution of pregnancy are linked to domesticated transposable elements that invaded the genome in early mammals. So I guess we owe the evolution of pregnancy to what are effectively genomic parasites.”
Sean B. Carrol has at least one good reason to cite the Lynch (2007) and one good reason to avoid citing the 2015 paper that was co-authored by Lynch under the senior authorship of Günter P. Wagner.
The best reason to ignore the claims from 2015 is this claim in Examining the Modularity Concept in Evolutionary Psychology: The Level of Genes, Mind, and Culture (2003) Published online in 2005.
Wagner and Wagner (2003) wrote:
Several studies (reviewed in Kohl, Atzmueller, Fink & Grammer, 2001) show pheromone perception to influence general social and sexual cognition and associated social interactions, where the hormonal status of men and women provides the link between olfactory-cognition and the visual cognitive analysers.
My comment: Kohl, Atzmueller, Fink & Grammer (2001) is our award-winning review Human pheromones: integrating neuroendocrinology and ethology.
If Sean B. Carrol cited the 2015 publication, others could link claim from 1940 to 2001, and from 2003 to Lynch (2007). That would reveal the misrepresentations that Sean B. Carrol has continued to make for more than 15 years (since 2001).
When experts like Sean B. Carrol selectively include references to older but not to newer published works that refute their claims about evolution, they reveal the tactics theorists often use to keep people focused on their ridiculous theories until everyone finally realizes how ridiculous the theories have always been.
For example, the theories based on de Vries 1902 definition of mutation as a sudden jump in energy have been replaced by what is known about energy-dependent RNA-mediated cell type differentiation in all living genera. There are no theories about captured genes and no working model that links anything but the fixation of RNA-mediated amino acid substitutions to the de novo creation of genes. The working model of gene creation also links virus-driven energy theft from loss of function to loss of genes. Sean B. Carrol and others like him may want to pretend there is another model for that, but there isn’t. Genes cannot be “captured” outside the context of the physiology of energy-dependent reproduction and the transgenerational epigenetic inheritance of morphological and behavioral phenotypes.
See also these other publication from the Wagner lab: Publications
In the context of those works, see: Excess of Deleterious Mutations around HLA Genes Reveals Evolutionary Cost of Balancing Selection, which was reported as: Hereditary diseases are the price of protection against infections.
A special form of selection preserves this variation within the group of immune proteins: scientists describe it as balancing selection. It arises, for example, when several alternative variants of a gene confer a survival advantage, and are therefore not eliminated by selection.
My comment: The consistent misrepresentations by theorists who claim that natural selection eliminates mutations have forced them to invent a special form of selection. The special form of selection must now preserve biophysically constrained cell type differentiation in the context of the physiology of reproduction and healthy longevity. That is what energy-dependent natural selection for codon optimality does. Codon optimality links the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
The confusion about what must be selected is also readily apparent in the new transposon theory of aging.
As cells get older, prior studies have shown, tightly wound heterochromatin wrapping that typically imprisons transposons becomes looser, allowing them to slip out of their positions in chromosomes and move to new ones, disrupting normal cell function.
My comment: The unwinding of tightly wound heterochromatin is linked from virus-driven energy theft to the release of the transposons. That allows the transposons to cause all age related pathology. Only the nutrient energy-dependent biophysically constrained chemistry of RNA-mediated protein folding has been linked to supercoiled DNA. And, only supercoiled DNA prevents virus-driven energy theft from leading to the entropy of organized genomes that is manifested in mutation-driven pathology. The ridiculous concept of Mutation-Driven Evolution cannot be considered in the context of what is known about chromatin remodeling and supercoiled DNA.
… viral latency is responsible for life-long pathogenesis and mortality risk…
My comment: Supercoiled DNA biophysically constrains viral latency. Stress-induced viral replication unwinds tightly would heterochromatin, which is how the release of transposons in linked from mutations to all pathology.