Maximum genetic diversity hypothesis

The maximum genetic diversity hypothesis is a scientific hypothesis about the process of molecular evolution, the study of genetic change in populations over time. This difference in the observed rate of mutation means some regions of the genome appear to mutate faster than others, and is theorized to relate to balancing the preservation of vital information relating to a species' function against its ability to mutate and adapt to new environmental niches.
The maximum genetic diversity hypothesis asserts that only slow-mutating genes accurately reflect shared evolutionary history, relationships between species can alternatively be calculated by their "maximum genetic diversity," which is determined by measuring the frequency of mutations in specific corresponding regions of orthologous genes instead of using raw overall genetic similarity. Also due to this grouping into fast and slow, it is proposed that over time complex organisms become genetically fragile and less tolerant to mutation as their genetic diversity decreases, since an increasing proportion of their genome will have become slow-mutating over time.
The hypothesis asserts that this is because increased organismal and social complexity means more of the genome is needed to preserve the expanding instructional manual necessary for complex behavior and function, and so more of an organism's genome must become slow-mutating as the organism increases in complexity, since being slow-mutating preserves and protects those vital instructions.
Furthermore, beyond the fact that the hypothesis is still relatively unknown, it also contradicts the current paradigm in molecular evolution, since the neutral theory's fundamental premises are still nearly ubiquitously utilized in genetic analysis and admixture studies.
Overview
According to the maximum genetic diversity hypothesis, modern evolutionary theory becomes an interplay between short-term microevolution which follows the neutral theory's expectation of random but predictable rate of linear change, and longer-term macroevolution that cannot be timed with the same clock as microevolution since diversification can flow in punctuated fits and starts over long periods of time when a complex species disperses into an array of diverse environmental niches.
As this occurs, the hypothesis predicts that each population will preserve the slow-mutating section of its genome which holds its most fundamental instructions from mutations, but quickly preserve mutations at sites that provide greater environmental fitness depending on the pressures of each unique niche. Support for this supposition is provided by a genetic model that seeks to solve the inconsistencies between the way regions of proteins seem to mutate in unison and the speed at which that happens, which observed that mutations seem to occur in "avalanches" that drastically alter not only specific regions of the genome as commonly assumed, but also only for short periods of time, using modeling to create a model of evolutionary change.
The fact that some genomic regions preserve mutations at different rates than others can be demonstrated when any three species separated by significant evolutionary time are compared two at a time: each pair can have aligned overlapping genomic positions in orthologous proteins where mutations get preserved at a far higher rate than the neutral theory's random drift statistically allows. Calculations using the hypothesis yield results that capture the branching and punctuated nature of speciation, preserve its gradual increasing fractal complexity over time, and are consistent with patterns of speciation deduced from the fossil record. the amount of genetic diversity in populations was accepted to tick steadily at a rate timed by a molecular clock set by the mutation of a hemoglobin protein in most vertebrates, which was first calculated by Emanuel Margoliash. This conclusion, that genetic diversity would accumulate within a population indefinitely over time, was reached because it was assumed that every population's genome would continually accumulate mutations as time passed - and so the more mutations that were observed the more basal and older a population was assumed to be since there was thought to be no upper limit as to how many mutations could accumulate.
Timing this presumably stable and universal rate of mutation and hence diversity using the molecular clock was first theorized by Motoo Kimura, but popularized by Émile Zuckerkandl and Linus Pauling. It was assumed to regulate all genetic variation both within and between species. Subsequently, the neutral theory and molecular clock were used in a variety of settings, most notably in phylogenetics, or the study of how different species change and pass on traits over time. Many measurements that are nearly ubiquitous in population genetics, such as the fixation index, are also based on the molecular clock.
However, since its inception there have been points against the neutral theory and its molecular clock's fundamental assumptions, such evidence that they may be affected by natural selection. Despite this, the molecular clock was assumed to regulate all orthologous genes inherited from a common ancestor, and used to set the historic rate of speciation across the animal kingdom, as well as answer questions around the evolutionary and genetic relationships between species. and the neutral theory fails to note and explain the common occurrence of overlapping mutations: where mutations in independently evolving species occur at orthologous overlapping protein positions at a rate too high to be neutral. - meaning that all mutations on earth were set by that protein and had a biologically universal rate that is constant and steady - the genetic equidistance phenomenon could also be explained by the assumption that mutation-rates are specific to each gene and might vary across species and within populations.
Fast and slow
Because simpler organisms are less likely to be affected at all by any one single-base mutation in their exons, or functionally active coding stretches of their genome, the hypothesis considers them to be more genetically robust than more complex organisms whose genomes are less tolerant to mutation and so are thought to be more fragile. The hypothesis states that the variability in the rate of change causes evolutionary selective pressures to sort alleles into two rough groups: slow-mutating ones involved with an organism's most basic structure and function, and fast-mutating ones that respond quickly in order to increase the odds a beneficial mutation occurs and is preserved.<ref name="handbook2010"/>
The hypothesis posits that when two populations have different genetic diversity levels, it does not necessarily mean that the population with lower genetic diversity is descended from the one with higher genetic diversity as implied by the neutral theory.<ref name"equal2017"/> Under the neutral theory's molecular clock, the most basal or older populations will always have the highest rate of diversity because existing first means more mutations would have had time to accumulate in their genome. However, higher overall genomic diversity may simply be due to having more fast-mutating alleles needed to deal with a wider array of environmental challenges, but since genetic distance can only be measured by slow-mutating genes, raw overall diversity rates alone should not to used to derive genetic relationships since slow-mutating genes may make up a minority of the genome.<ref name"auto"/>
The fact that most broad phenotypic traits are regulated by multiple loci is also incompatible with the neutral theory, since it would be statistically unlikely for enough linkage disequilibrium to form across the genome if mutations were occurring randomly. The hypothesis accounts for this, since phenotypically linked fast-mutating SNPs are recognized to respond to selective pressures more rapidly than the slow-mutating more basal SNPs.<ref name"auto"/> The hypothesis also explains why raw genetic diversity does not flow temporally from basal to more modern as a concrete rule.<ref name"handbook2010"/>
The hypothesis contradicts the fixation index, which assumes the neutral theory applies across the entire genome and only considers fast-mutating autosomal DNA in population genetics analyses.<ref name"riddle2016"/><ref name"handbook2010"/>

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