DNA repair via junk DNA (2)
See also: DNA repair via junk DNA (1)
Reported in Singer (2015) as:
In 2006, Begun found some of the first evidence that genes could indeed pop into existence from noncoding DNA.
Singer’s claim that genes automagically pop into existence is consistent with Masatoshi Nei’s conclusion in: Mutation-Driven Evolution
…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements. (p. 199)
Diethard Tautz suggested that this representation was a “…fact that is often used as additional evidence for the power of de novo evolution.” Apparently, Tautz believes that the magic of gene evolution in viruses can be linked to his claims about the magic of evolution in Evolution: Dynamics of De Novo Gene Emergence
See my August 20, 2015 comment on Singer (2015):
Begun is the senior author of: Origin and Spread of de Novo Genes in Drosophila melanogaster Populations (2014)
…important details of such processes remain obscure and much additional work is required to clarify the dynamics, biochemical and genetic properties, and phenotypic effects of young de novo genes and the processes underlying gene loss in natural populations.
The works by Begun, Tautz, and others who have claimed that the de novo origin of genes that pop into existence can lead to evolution were reported by Carl Zimmer in The Continuing Evolution of Genes
As genes duplicate over millions of years, they can grow into so-called gene families, each containing hundreds of similar genes.
One family, for example, is essential for our sense of smell. These genes encode 390 different kinds of proteins produced in our noses, called olfactory receptors. Each olfactory receptor has a slightly different structure, allowing it to capture a different set of molecules.
My comment: Gene duplication is energy-dependent. The energy-dependent de novo creation of olfactory receptor genes links hydrogen-atom transfer in DNA base pairs in solution from changes in the microRNA/messenger RNA balance to alternative RNA splicings that link natural selection for energy-dependent codon usage from the innate immune system to supercoiled DNA via the physiology of reproduction in all living genera.
Why have some science journalists continued to place the pseudoscientific nonsense touted by theorists into the context of emergence and evolution? Do they ever wonder how gene duplication occurs in the absence of nutrient-energy dependent changes in organized genomes, or where the organized genomes came from?
Inheritable epigenetic changes (“epimutations”) with effects at a distance would then perdure over the number of generations required for “assimilation” of the several regulatory novelties through the occurrence and selection, gene by gene, of specific classical mutations. These mutations would have effects similar to the epigenetic effects, yet would provide stability and penetrance. The described epigenetic/genetic partnership may well at times have opened the way toward certain complex new functions. Thus, the presence of “junk DNA”, through co-determining the (higher or lower) order and the variants of chromatin structure with regulatory effects at a distance, might make an important contribution to the evolution of complex organisms.
Even if ninety percent of the genome does prove to be junk, that doesn’t mean the junk hasn’t played a role in our evolution. As I wrote last week in the New York Times, it’s from these non-coding regions that many new protein-coding genes evolve. What’s more, much of our genome is made up of viruses, and every now and then evolution has, in effect, harnessed those viral genes to carry out a job for our own bodies. The junk is a part of us, and it, too, helps to make us what we are.
*I mean functional in terms of its sequence. The DNA might still do something important structurally–helping the molecule bend in a particular way, for example.
[Update: Fixed caption. Tweaked the last paragraph to clarify that it’s not a case of teleology.]
“How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.”
My comment: Claims that genes pop into existence do not address how the genes are created or how they are incorporated into actual cellular processes. There is only one way for incorporation into cellular processes to occur. The innate immune system must link RNA-mediated cell type differentiation from amino acid substitutions to supercoiled DNA via the nutrient energy-dependent creation of G protein-coupled receptors that link receptor-mediated behavior from natural selection for codon optimality to supercoiled DNA. The supercoiled DNA is the link from non-coding DNA to the epigenetically-effected organized genomes of all living genera.
See for instance:
Junk DNA: A Journey Through the Dark Matter of the Genome (2015) reviewed by Casey Luskin in New Book on “Junk DNA” Surveys the Functions of Non-Coding DNA
The bits of gobbledygook between the parts of a gene that code for amino acids were originally considered to be nothing but nonsense or rubbish. They were referred to as junk or garbage DNA, and pretty much dismissed as irrelevant. … But we now know that they can have a very big impact. (pp. 17-18)
The impact of the amino acids links everything known about molecular epigenetics to RNA-mediated DNA repair. The epigenetically-effected RNA-mediated amino acid substitutions in organized genomes must link the initiation of DNA repair to the maintenance of organized genomes throughout the life history transitions of all living genera. Simply put, the energy-dependent RNA-mediated amino acid substitutions are linked to healthy longevity.
Codon optimality controls differential mRNA translation during amino acid starvation
Our data reveal a previously unappreciated mechanism underlying cellular adaptation to amino acid shortage at the level of mRNA translation.
For spatial control, one may apply photocaged tamoxifen or 4-HT and use ultraviolet light to target a subset of cells within a mixed population34. Hence, our ERT2-based iCas technology expands the toolkit for precise genome engineering in mammalian cells.
Gastric cancer (GC) is the third leading cause of global cancer mortality. Adenosine-to-inosine RNA editing is a recently described novel epigenetic mechanism involving sequence alterations at the RNA but not DNA level, primarily mediated by ADAR (adenosine deaminase that act on RNA) enzymes. Emerging evidence suggests a role for RNA editing and ADARs in cancer, however, the relationship between RNA editing and GC development and progression remains unknown.
My comment: ADAR is Adenosine-to-inosine RNA editing. They fooled you, didn’t they? If you did not think it was something new, you probably are a serious scientist, or more biologically informed than any theorist.
L1-associated genomic regions are deleted in somatic cells of the healthy human brain
My comment: They cite Needleman, S.B. & Wunsch, C.D. A general method applicable to the search for similarities in the amino acid sequence of two proteins. J. Mol. Biol. 48, 443–453 (1970).
A Fear of Pheromones (1971)
What on earth would we be doing with such things? With the richness of speech, and all our new devices for communication, why would we want to release odors into the air to convey information about anything?
I should think we might fairly gauge the future of biological science, centuries ahead by estimating the time it will take to reach a complete comprehensive understanding of odor. It may not seem a profound enough problem to dominate all the life sciences, but it contains, piece by piece, all the mysteries (p. 732).
— Lewis Thomas as cited in The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002)