Abstract
Two major inconsistencies exist in the current neo-Darwinian evolutionary theory that random chromosomal mutations acted on by natural selection generate new species. First, natural selection does not require the evolution of ever increasing complexity, yet this is the hallmark of biology. Second, human chromosomal DNA sequence variation is predominantly either neutral or deleterious and is insufficient to provide the variation required for speciation or for predilection to common diseases. Complexity is explained by the continuous flow of energy through the biosphere that drives the accumulation of nucleic acids and information. Information then encodes complex forms. In animals, energy flow is primarily mediated by mitochondria whose maternally inherited mitochondrial DNA (mtDNA) codes for key genes for energy metabolism. In mammals, the mtDNA has a very high mutation rate, but the deleterious mutations are removed by an ovarian selection system. Hence, new mutations that subtly alter energy metabolism are continuously introduced into the species, permitting adaptation to regional differences in energy environments. Therefore, the most phenotypically significant gene variants arise in the mtDNA, are regional, and permit animals to occupy peripheral energy environments where rarer nuclear DNA (nDNA) variants can accumulate, leading to speciation. The neutralist–selectionist debate is then a consequence of mammals having two different evolutionary strategies: a fast mtDNA strategy for intra-specific radiation and a slow nDNA strategy for speciation. Furthermore, the missing genetic variation for common human diseases is primarily mtDNA variation plus regional nDNA variants, both of which have been missed by large, inter-population association studies.
Highlights
Resolved by Schrodinger, who pointed out that living organisms were not closed systems, but rather acquire energy from their environment as what he called ‘negative entropy’ [3]
This concept stood until the 1960s, when molecular genetic studies on human nDNA revealed that much of the genetic variation that differentiated human populations is due to differences in the frequency of alleles common to both populations
PPARg and PPARg coactivator gene-1a (PGC-1a) are nuclear transcription factors that play a major role in regulating bioenergetics and mitochondrial biogenesis
Summary
PPARg and PGC-1a are nuclear transcription factors that play a major role in regulating bioenergetics and mitochondrial biogenesis. The importance of these and multiple other loci identified by GWAS implicate mitochondrial bioenergetics in diabetes and obesity and, by extension, mitochondrial functional variation in human regional environmental adaptation Consistent with this supposition, the mitochondria are estimated to generate about 90 per cent of the cellular energy in differentiated tissue cells and the mitochondrial genome encompasses in the order of one to two thousand nDNA genes and thousands of copies of the mtDNA. By transferring structural genes from the oxidative bacteria to the host cell’s DNA, the number of bacterial gene copies was reduced from thousands to two, the pair of homologues in the nDNA This reduced the amount of DNA to be replicated and reduced the complexity of mtDNA transcriptional regulation, with significant savings in energy. The 13 polypeptides of the mtDNA represent an integrated electrical circuit in which each polypeptide must be functionally compatible with the other 12 mtDNA polypeptides of comparable coupling efficiency [27]
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