This theme issue focuses on key evolutionary transitions to understand the interaction of biology, behaviour, culture and environment. This issue is dedicated to Richard Leakey, whose critical discoveries have provided evidence for many of the key phases, and who has inspired much of the work discussed here.
This issue is based on a joint Royal Society and British Academy discussion meeting held in October 2015.
This issue is now available to read online.
…most of the credible models tend to take something that is unique to humans – such as language – and show how all the other bits of being human derive from that.
My comment: The Conversation claims to be “…an independent, not-for-profit, news and information service… on current or relevant issues, as well as the latest research and breakthroughs.
1) …most of the credible models tend to take something that is unique to humans – such as language – and show how all the other bits of being human derive from that.
2) The problem with these theories is that they depend on evolution being a sort of one-step game, where one change produces a great leap forward, one from which other changes cascade. But the record does not support this. We split from our last common ancestor with the chimpanzees 5-6m years ago.
Our results so far suggest that comparisons of CVs across species should yield insignificant results when sufficiently large samples are available and single measures are compared and that CV seems not to be the way to look at the inherent ability of a species to vary.
My comment: Despite the lack of credible models, they claim “We split from our last common ancestor with the chimpanzees 5-6m years ago.” But they conclude that coefficients of variation (CVs) in morphological phenotypes are not the way to examine “…the inherent ability of a species to vary.”
For comparison, see: Biology, Molecular and Organismic (1964)
The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.
Ingram and others found that hemoglobin S differs from A in the substitution of just a single amino acid, valine in place of glutamic acid in the beta chain of the hemoglobin molecule.
…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.
More than 1180 hemoglobin variants in human populations have been referred to as mutations, because that’s what population geneticists called the hemoblogin S variant that protects modern human populations from malaria. See also: HbVar: A database of Human Hemoglobin Variants and Thalassemias
Hemoglobinopathies are the commonest single-gene genetic disorders in humans, resulting from pathogenic genome variants in the human α-like and β-like globin gene clusters (reviewed in 1). Single nucleotide substitutions or indels [INsertions/DELetionS] can lead to several hemoglobin variants owing to amino acid replacements, while molecular defects in either regulatory or coding regions of the human HBA2, HBA1, HBB or HBD genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.
Even when all serious scientists know the difference a single nucleotide substitution and an amino acid substitution can make to the ability of a human population to adapt, pseudoscientists report that the variants are mutations.
To identify new hemoglobin variants and thalassemia mutations not previously documented in the database, we continued to manually scan articles from the specialized journal ‘Hemoglobin’, which frequently publishes new hemoglobin variants and thalassemia mutations, and where applicable, previously undocumented variants have been entered into HbVar.
My comment: If you look for variants you will find all of them are nutrient-dependent and RNA-mediated. If you look for mutations, you will find theories that link virus-driven energy theft from perturbed protein folding biochemistry to the magic of evolution via natural selection. Re: “Richard Leakey, whose critical discoveries have provided evidence for many of the key phases…” They dedicated the issue to the man whose ridiculous claims led many people to look at human evolution in the wrong way.
As far as we can tell, human evolution is like a mosaic of change, made up of many small steps, each of which adds a piece to what it is to be human. Only at the end do we see the full configuration, but had we stopped the clock at any point along that continuum, we would have seen a different mosaic. Human evolution is not one great transition, therefore, but many smaller ones.
My comment: That fact explains why all serious scientists are Combating Evolution to Fight Disease. Each small step requires ecological variation to lead
- from RNA methylation to ecological adaptation via the conserved molecular mechanisms…
- that link the nutrient-dependent pheromone-controlled physiology of reproduction in bacteria…
- to the supercoiled DNA in organized human genomes that protect us from virus-driven energy theft…
- and all pathology in the absence of stress.
The fact that neo-Darwinian theorists failed to link viruses and stress to all pathology is the fact that has led all serious scientists to link energy-dependent changes from angstroms to ecosystems in all living genera via RNA-mediated amino acid substitutions in the context of the physiology of reproduction — three years post publication of Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
“Declines in olfactory function have been shown to be among the earliest signs of brain-related neurodegenerative diseases, but we need more data to better understand this connection,” said Monell olfactory scientist Pamela Dalton, PhD, MPH. “Adding an olfactory assessment to the BHR’s large existing database may yield the best information yet on the predictive relationship of olfactory function to neurodegenerative disease.”
See also: CD36 is expressed in a defined subpopulation of neurons in the olfactory epithelium and Farnesol-Detecting Olfactory Neurons in Drosophila and The phylogenetic utility and functional constraint of microRNA flanking sequences
My comment: Energy-dependent RNA methylation seems likely to be the link from hydrogen-atom transfer in DNA base pairs in solution to microRNA flanking sequences and the de novo creation of G protein-coupled receptors that link the innate immune system from receptor-mediated cell type differentiation and behavior to experience-dependent life history transitions that can be perturbed by virus-driven energy theft. If so, the facts about biophysically constrained energy-dependent RNA-mediated cell type differentiation, healthy longevity, and virus-driven pathology will be very difficult to put back into the context of any ridiculous theories about top-down causation.
See also: my review of this book by George Ellis How Can Physics Underlie the Mind? Top-Down Causation in the Human Context