of population genetics. In fact, the rate of change within a species (the fixation rate) has little to do with the rate of change within the individuals inside the population (the mutation rate). The fixation rate is extremely slow in large populations, but individuals are always accumulating mutations. An individual carries the new mutations they were born with plus whatever mutations they inherited from their ancestry. Because of this, the timing of the Y chromosome and mtDNA common ancestors are independent of the fixation rate; they only depend on the mutation rate. There is a fine balance between mutation, selection, and long-term survival. Generally, selection is invoked as a means of both advancing a species (e.g., positive selection) and protecting a species against decay (e.g., purifying selection). Yet, selection is limited in its power (due to epistasis, epigenetics, and other sources of ‘noise’) and speed (due to limits of reproductive output, see ReMine 2005). Genetic drift also fails to account for the discordance between the genealogical and phylogenetic mutation rates. The evolutionary community is not unaware of these difficulties, yet they persist in their belief that, given enough time, the genealogical and phylogenetic mutation rates will diverge significantly. In computer models, there are ways to maximize the difference (e.g., by lowering the base mutation rate and increasing the negative effects of deleterious mutations), but the question of biological reality always looms over the results. The constraints of biology severely limit evolutionary models, to the point where basic mathematics argues strongly against all long-term evolutionary ideas. The problem is amplified for haploid compartments like mitochondria and Y chromosomes. Recombination has a real, measurable, long-term benefit in helping to remove deleterious alleles. Haploid systems do not undergo recombination. Thus, mutations accumulate in a ratchet-like way (Rupe and Sanford 2013) and all lineages will be picking up deleterious mutations over time. The net effect is a downward trend. Worse, the negative effects of mutations cannot be masked by alternate alleles, as in haploid systems. Due to these factors, attempts to model the separation of neutral and deleterious alleles over time (e.g., Fig. 9), were hampered. Many model settings resulted in population extinction before the proscribed 10,000 generations (300,000 years) was reached, and this was after the mutation rate was reduced to 0.005 (one new mutation in every 200 births, with half of being perfectly neutral) or less. Note the declining fitness trend line in Fig. 9 and the fact that the x-axis is in years, not generations. The population in this model did not make it to 300,000 years. It was possible to reduce the average effect of deleterious mutations, but this would lead to even less removal of these mutations over time. It was also possible to reduce the mutation rate, but that would diverge even further from biological reality. In the end, causing a divergence between the genealogical and phylogenetic mutation rates is a non-trivial matter. There is no reason to suspect the two would be significantly different over long timespans. Hence, the genealogical rate stands as a valid method of computing ancestral events and both Mitochondrial Eve and Y Chromosome Adam must have lived in the recent past. Several skeptics have attempted to argue that there is no ‘perfect’ fitness, as evolution is considered to be a continual process of mutation and selection over millions of generations. Thus, they claim, it is incorrect to start all individuals with no deleterious or beneficial alleles. However, in these models, ‘fitness’ is arbitrary. It is simply a measure of the relative reproductive potential of any individual with respect to the other individuals alive at the time. Yes, tracking changes in fitness allows us to see long-term trends, but reproductive potential is always in terms of the contemporaneous population. Also, given long run times, sufficient mutational ‘burn in’ occurs, such that the population contains a range of fitness scores, similar to what is assumed in evolutionary models. Note also that lethal mutations were not taken into account in this study. By default, any mutation that causes death, that prevents pregnancy, or that causes severe malformations or intellectual disability, will be filtered out of the population instantaneously. These mutations reduce reproductive output but are never subject to selection in the way that it is modeled here (e.g., via an annual risk of death). The mutation rate per generation is approximately 60 in the nuclear genome, 1 in the Y chromosome, and 0.5 in the mitochondrial genome. Every one of these estimates puts Adam and Eve within a biblical time frame, even if we were to reduce the mutation rates by an order of magnitude. Natural selection cannot remove most of these mutations, so the burden of proof is on the evolutionary community to explain the discordance between the genealogical and phylogenetic mutation rates. V. CONCLUSIONS In conclusion, the short-term, measurable, genealogical mutation rate is a serious challenge to evolutionary history. The long-term mutation accumulation rate should equal the base mutation rate less the proportion of deleterious alleles that can be removed by selection. Yet, even if selection were 100% efficient at removing all deleterious alleles, it would have no effect on neutral alleles. Given that most alleles are selectively neutral, only a small proportion of all mutations can be removed. It would take very little time to accumulate the number of differences seen in extant Y and mitochondrial chromosomes. The amount of diversity seen in human autosomes could also be explained in a biblical timeline. When one considers that much of that diversity was probably created by God and placed directly into Adam and/or Eve, it would be trivial to explain what remains. ACKNOWLEDGEMENTS I would like to thank John Sanford for making Mendel’s Accountant available and for years of guidance. Bruce Potter was very helpful on the technical side. REFERENCES Ballantyne, K.N., A. Ralf, R. Aboukhali,, N.M. Achakzai, M.J. Anjos, Q. Ayub, J. Balažic, J. Ballantyne, D.J. Ballard, B. Berger, C. Bobillo, M. Bouabdellah, H. Burri, T. Capal, S. Caratti, J. Cárdenas, F. Cartault, E.F. Carvalho, M. Carvalho, B. Cheng, M.D. Coble, D. Comas, D. Corach, M.E. D’Amato, S. Davison, P. de Knijff, M.C. De Ungria, E. Decorte, T. Dobosz, B.M. Dupuy, S. Elmrghni, M. Gliwiński, S.C. Gomes, L. Grol, C. Haas, E. Hanson, J. Henke, L. Henke, F. Herrera-Rodríguez, C.R. Hill, G. Holmlund, K. Honda, U.D. Immel, S. Inokuchi, M.A. Jobling, M. Kaddura, J.S. Kim, S.H. Kim, W. Kim, T.E. King, E. Klausriegler, D. Kling, L. Kovačević, L. Kovatsi, P. Krajewski, S. Kravchenko, M.H. Larmuseau, E.Y. Lee, R. Lessig, L.A. Livshits, D. Marjanović, M. Minarik, N. Mizuno, H. Moreira, CARTER Genealogical vs. phylogenetic mutation rates 2023 ICC 178
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