Retrotransposons (also called transposons via RNA intermediates) are genetic elements that can amplify themselves in a genome and are ubiquitous components of the DNA of many eukaryotic organisms.
Target site biases observed among retroviruses and retrotransposons are thought to be the consequence of interactions between the retroelement integration complex and chromosome-localized proteins.
My comment: Clearly, the way to make scientific progress is to examine the consequences of these interactions. It is past time to abandon claims about mutations and evolution that have failed to be supported by experimental evidence of biologically-based cause and effect in the context of the nutrient-dependent physiology of reproduction and ecological adaptations in all living genera. The balance of nutrient-dependent microRNAs and viral microRNAs can be linked to nutrient-dependent healthy longevity or to virus-driven pathology. But the contribution of microRNAs to the microRNA/messenger RNA balance and nutrient-dependent DNA repair or virus-driven pathology is missing in everything presented below.
Abstract conclusion: “Capped and polyadenylated ORF0 mRNAs are present in the cytoplasm, and endogenous ORF0 peptides are identified upon proteomic analysis. Finally, ORF0 enhances LINE-1 mobility. Taken together, these results suggest a role for ORF0 in retrotransposon-mediated diversity.”
My comment: Retrotransposon-mediated diversity.is nutrient-dependent and biophysically constrained. The diversity is constrained by the RNA-mediated amino acid substitutions that differentiate cell types in the context of the physiology of vertebrate and invertebrate reproduction.
Note: The Gage lab concentrates on the adult central nervous system, and unexpected plasticity and adaptability to environmental stimulation that remains throughout the life of all mammals.
Rusty Gage may be the best person to ask about RNA-mediated retrotransposon-mediated diversity in the context of what is currently known about the honeybee model organism and the links from its life history transitions to humans. For example: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults.
If nutrient energy-dependent base pair changes and RNA-mediated amino acid substitutions do not link RNA-directed DNA methylation to cell type differentiation in species from microbes to human via chromosomal rearrangement and the physiology of reproduction, there may be another model for comparison to mine. If there is, Dr. Gage probably knows where to find information on the comparable model of biologically-based cause and effect.
Evolutionarily speaking, this represents a way to generate entirely new molecules that could be beneficial to a species. On the other hand, the reshuffling of an existing ORF0 sequence during a jump could result in a disease-causing mutation.
My comment: It is not surprising to me that they claim this link from the epigenetic landscape to the nutrient-dependent physical landscape of primate DNA exemplifies a form of evolution that must be placed into the context of disease-causing mutations. Serious scientists learned only recently that the generation of any new molecules must be linked from base pair changes to their function without the pseudoscientific nonsense about the evolution of new proteins and/or new genes.
But see for comparison from Dobzhansky (1973)
…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla. ( p. 127)
My comment: The link from base pair changes to RNA-mediated amino acid substitutions in the cell types of 3 primate species appears to require just one amino acid substitution in the hemoglobin molecule of three primate species.
…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.
See also: Speedy evolution affects more than one species
The fruit flies in question evolved into new species when they began laying their eggs and mating on apple trees, as opposed to their native hawthorn tree hosts. Three different kinds of parasitoid wasps were collected from a number of different fly host plant environments in the wild.
Analyses in the lab showed that all three of the different kinds of wasps had diverged from others of the same kind, both genetically and with respect to host-associated physiology and behavior.
“In a sense,” Smith said, “they have caught an entire community of parasitoids actively ecologically diverging in response to a historically documented host plant shift of their fly host.”
My comment: They report ecological variation and nutrient-dependent adaptations controlled by the physiology of reproduction in all living genera, in the context of fruit fly evolution. To the biologically uninformed this links the evolution of the flies to the evolution of other species. To anyone who understands anything about the biophysically constrained chemistry of nutrient-dependent protein folding, they place ecological divergence into the context of a magic trick.