ual’s lineage. This is accelerated by a bottleneck every generation, where the number of mitochondria is reduced to approximately 100 during oogenesis (Li et al. 2018). Still, it takes several generations for a mutant lineage to become ‘fixed’ within a family line, meaning mitochondria are often found in a diploid state on the level of the individual. Given this discrepancy, the population model of Carter (2019b) was further modified to include a similar style of probability selection as performed in Mendel. It was not trivial to achieve a population model that showed a significant reduction in deleterious mutations without causing extinction, and this is only amplified by the lack of recombination within the mitochondrial genome. The most effective method was to reduce the mutation rate while increasing the average mutation effect, but this quickly became non-biological, e.g., the mutation rate had to be set below 0.005. This is about two orders of magnitude below genealogical estimates (Fig. 9). IV. DISCUSSION Nearly all mutations, by evolutionary necessity, must be selectively neutral. Yet nearly all mutations are also expected to be deleterious (Sanford 2014). This is only becoming more obvious as additional functions are found for multiple genomic elements (Carter 2022b). Here, it was shown that selection can only remove a small number of the mutations that are bound to occur in any genome. This is not surprising, given what is already known (Carter 2019a). And yet, the sheer number of new mutations in a population means that some mutations will be retained. In fact, a reasonable estimate of the mutation load of any given individual is obtained by simply multiplying the mutation rate by the number of generations that have elapsed. Thus, the formulas of standard population genetics are directly applicable to the question of the timing of Y Chromosome Adam and Mitochondrial Eve, with the caveat that selection will remove some small percentage of mutations. Genetic drift is almost irrelevant when considering the mutation load of any given individual. Thus, due to selection, the long-term, phylogenetic mutation rate will be slightly less than the short-term, genealogical mutation rate. The degree of separation between these two rates depends on many factors, only some of which were modeled here. Yet, there is only so much that selection can do. Reproductive output is limited, and most mutations are expected to be lower than the selection threshold anyway. Thus, the question comes down to 1) the real mutation rate and 2) the relative proportions of selectively neutral vs. non-neutral mutations. Yes, selection can remove a certain proportion of deleterious mutations, but if the rate at which these occur is relatively low, there is nothing for selection to act upon. To see a significant difference between the genealogical mutation rate and the phylogenetic mutation rate, the proportion of deleterious alleles would need to be much higher than theory allows. Selection is also more efficient in smaller populations, but so is fixation, which increases the risk of extinction. Yet, even in the smallest populations with high rates of deleterious alleles, the ratio of observed to expected fixed deleterious alleles was greater than 0.9. There is no way to remove a higher proportion of deleterious mutations, and those populations all went extinct! Several anti-creationists have made the mistake of assuming that, since most mutations are lost, the phylogenetic mutation accumulation rate is necessarily much slower than the genealogical mutation rate. This exemplifies a gross misunderstanding of the mathematics Figure 9: The accumulation of mutations in a haploid mitochondrial model. As above, these are the results of a single model run, but with a mutation rate of 0.005 and a population size of 10,000. Data were plotted every 100 generations. CARTER Genealogical vs. phylogenetic mutation rates 2023 ICC 177
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