The Proceedings of the Eighth International Conference on Creationism (2018)

manage to propagate their genes from one year to the next (e.g., the human H1N1 influenza virus, see Carter and Sanford [2012] and Carter [2014]). Alternatively, molecular clocks might work in a broad sense when one is able to average accumulation rates among diverse lineages (e.g., Jeanson 2015a). But when this is done, the rates generally line up with the biblical timeframe and defy evolutionary long ages (Jeanson 2013, 2015b; Tomkins 2015). Also, several authors have called for rate variation during human history, specifically a higher recombination rate within Africans (e.g., Jeanson 2016; see also Hinch et al. 2011) or a higher rate associated with the Flood or early post-Flood period (e.g., Wood 2012, 2013). We have demonstrated that the mutation rates along various branches of the chrYand chM trees are clearly variable, manifesting statistically significant differences among multiple group-pairs. This is a direct challenge to the molecular clock hypothesis, and thus the Out of Africa theory. We conclude that either: 1) Ancestor A1 (chrY) and L0 (chrM) are not the common ancestor of these individuals; or 2) the rate of mutational divergence is not constant among haplogroups; or 3) both. Lastly, the observation that most chrY and chrM mutations are rare is excellent evidence that the human genome is young, irrespective of whether or not the clock is precise. Lineages that have accumulated an inordinate number of mutations may have experienced innately higher mutation (similar to the mutator bacterial strains in the famous LTEE experiment), or those lineages may have had a historical episode of accelerated mutation due to environmental, epigenetic, or demographic factors. Costello et al. (2013) claimed that oxidative damage to DNAleads to artifacts in sequence data. Chen et al. (2017) concluded that the majority of G→T transversions in the 1000 Genomes were erroneous. Thus, there may also be artifacts in the sequencing data, perhaps even tracing back to field collection techniques. Recently, Moorjani et al. (2016) detected violations of the molecular clock hypothesis among ten primate species. They concluded that substitution rates are higher in New World monkeys than they are in Old World monkeys and that these in turn are higher than in apes and humans. In fact, they determined that the rate was about 7% faster in gorillas and about 2% faster in chimpanzees than in humans, using nothing but evolutionary assumptions. But there is also evidence of clock violations within humans. Behar et al. (2012) found statistically significant violations of the molecular clock hypothesis for a select few mitochondrial haplogroups (M, specifically). They noted that even young haplogroups showed significant differences in terms of mutation accumulation rates. Scozzarri et al. (2014) reported a statistically significant molecular clock anomaly in terms of the mutations that led to Y chromosome haplogroup A1b. We could not verify this because none of the 1000 Genomes Y chromosomes were from that haplogroup. Mallik et al. (2016) claimed to discover an approximately 5% increase in the rate of mutation accumulation in non-Africans over Africans, genome-wide. After factoring in the source of DNA (e.g., lymphoblastoid cell-lines, blood, and/or buccal samples) Hallast et al. (2015) concluded that subtle haplogroup-specific effects on Y-chromosome branch length do exist. Finally, Sayres et al. (2014) concluded that purifying selection (and possibly positive selection) has had a strong role in reducing Y chromosome diversity worldwide, but their study included only 16 chromosome sequences. Even though each of these studies suggested that branch lengths vary, Hallast et al. (2015) expected the effect on the time to the most recent common ancestor (TMRCA) calculation would be minor. We disagree. We detected different amounts of mutation accumulation among the various haplogroups, which would normally be attributed to different ages of the founders. However, even haplogroups having a common ancestor (i.e., Y chromosome haplogroups N/O and Q/R) often had different rates of divergence (on the order of 5–10%) from that ancestor. This is a violation of the molecular clock principle. There are various explanations for this, including natural selection, but only a minority of SNVs are expected to be subject to selection (Poznik et al. 2016). Early strong population structure (in evolutionary models) could also have an influence on the shape of the modern phylogenetic tree, but how much of an effect remains an open question (Karmin et al. 2015). Mallik et al. (2016) concluded that themutation rate outside ofAfrica has been historically higher than the mutation rate within Africa, and Henn et al. (2015) claimed that mutational load increases with distance from Africa due to reduced selection. However, there are exceptions among the non-African groups as well. For example, even though N/O and Q/R had an identical founder sequence, these two groups had different average ranks (in terms of divergence from their mutual ancestor). The N/O individuals consistently ranked in the first half of the distribution (less diverged) and the Q/R individuals consistently ranking in the second half of the distribution (more diverged). Therefore, it appears that while the average rate of mutational divergence was more or less constant within haplogroups (Fig. 5), the rate of mutational divergence was variable among haplogroups (Fig. 6). This contradicts evolutionary conclusions regarding the timing of events based on the molecular clock hypothesis. Lenski’s LTEE (Tenaillon et al. 2016) tells us there is a real possibility that mutator strains can emerge when sub-populations are cut off from the outside and restricted in size. We suspect the differences occurred early on in post-Flood human history and were driven by a drastically small population moving into new areas and remaining small. This may help to explain why a few scattered individuals and rare groups have highly divergent haplotypes. The same concept might explain the ancient and highly divergent Homo populations such as Neanderthals, Denisovans, H. erectus , H. floresiensis, and Homo naledi (we do not have DNA sequences for all of these yet, but see Wood 2012). It should be noted that the genomes of ancient Egyptians were much more similar to those of Eurasia than sub-Saharan Africa. Substantial mixing across the Sahara has occurred, but probably not until after the rise of Islam (Schuenemann et al. 2017). In a similar way, the first people in Eurasia (apparently, Neanderthals and Denisovans) were different from those that came later. There is additional evidence that the most ancient people in southern and southeastern Africa were different from the people living there today, with the ancient genomes corresponding to the isolated and more divergent Khoi-San peoples instead of the dominant Bantus (Schlebusch et al. 2017; Skogland et al. 2017). Thus, aDNA can reveal interesting historical demographic shifts, but it is as if the Carter et al. ◀ Y Chromosome Noah and mitochondrial Eve ▶ 2018 ICC 146