Mu, Part 4:

Evidence linking the Denisovan-Neanderthal-Y-Adam meta-group exists in the form of two genes related to pigment - BNC2 and UGT1A1;

>http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0134548#pone.0134548.ref058
>The microsatellite length in two Neandertal individuals [57] and one Denisovan [58] are similar to present-day humans outside of Africa in having a TA repeat of length 6 in the promoter of UGT1A1

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478293/
>BNC2 seems to be a strong candidate for adaptive introgression, as shown in two genome-wide archaic ancestry analyses23, 47. Sankararaman et al.47 applied the CRF model to detect introgressed segments, and then inferred selection based on departures from a null model of neutrally introgressed alleles. Vernot and Akey23 also found the introgressed region using S*, then confirmed its ancestry by matching it with the Neanderthal genome, and finally inferred selection by observing that the region has high differentiation between Europeans and Asians, as measured by FST.
>A BNC2 SNP is associated with skin pigmentation76 and freckling in Europeans77, and the archaic haplotype is present at 70% frequency in Europeans, while it is absent in Asians. Interestingly both studies also found a strong adaptive introgression signal in a cluster of keratin genes on chromosome 12 in both Asians and Europeans
>Ding et al.78 identified an introgressed haplotype of Neanderthal origin in Eurasians carrying a loss-of-function variant (Val92Met) in the gene MC1R
>This gene is known to affect hair color in mice79 and is associated with red hair, freckles and type I/II fair skin type in humans80
>Ding et al.78 identified an introgressed haplotype of Neanderthal origin in Eurasians carrying a loss-of-function variant (Val92Met) in the gene MC1R, which encodes a melanocyte stimulating hormone receptor. This gene is known to affect hair color in mice79 and is associated with red hair, freckles and type I/II fair skin type in humans80, 81. The region, however, shows no significant departures from neutrality at the introgressed region in Europeans or East Asians, using either Tajima’s D52, Fu and Li’s test82, or iHS49, presumably because the frequency of the archaic haplotype only ranges from 5–22%. In addition, the lossof- function mutation (Val92Met) is not actually seen in the high-coverage Neanderthal genome4, despite being almost exclusively observed within haplotypes inferred to be introgressed from Neanderthals in Eurasian populations. The variant is also present in 3 African HapMap samples83, which weakens the argument for introgression into Eurasians, unless the variant was later introduced into Africans via admixture from Eurasians. Intriguingly, the same variant is found at very high frequencies in Taiwanese aborigines (60–70%

>https://www.ncbi.nlm.nih.gov/m/pubmed/24916375/
>Human skin color is influenced by an intergenic DNA polymorphism regulating transcription of the nearby BNC2 pigmentation gene
>while the activity of this enhancer element depends on the allelic status of rs12350739. When the rs12350739-AA allele is present, the chromatin at the region surrounding rs12350739 is inaccessible and the enhancer element is only slightly active, resulting in low expression of BNC2, corresponding with light skin pigmentation. When the rs12350739-GG allele is present however, the chromatin at the region surrounding rs12350739 is more accessible and the enhancer is active, resulting in a higher expression of BNC2, corresponding with dark skin pigmentation

Higher BNC2 expression is correlated with scoliosis;

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573260/
>We identified a functional SNP, rs10738445 in BNC2, whose susceptibility allele showed both higher binding to a transcription factor, YY1 (yin and yang 1), and higher BNC2enhancer activity than the non-susceptibility allele. BNC2overexpression produced body curvature in developing zebrafish in a gene-dosage-dependent manner
>Our results suggest that increased BNC2 expression is implicated in the etiology of AIS

>https://www.ncbi.nlm.nih.gov/m/pubmed/23052946/
>We identified two new skin color genes: genetic variants in UGT1A were significantly associated with hue and variants in BNC2 were significantly associated with saturation

However, neither Denisovans nor neanderthals had the A allele of the SLC24A5 gene;

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525967/table/T7/?report=objectonly
>PCMs covered by both the Denisovan sequence and the Neanderthal sequence
>Increased skin pigmentation, association with
>SLC24A5 A > G:GGG

The oldest remains containing the A allele of SLC24A5 date to 13kYBP;

>http://www.nature.com/articles/ncomms9912
>We extend the scope of European palaeogenomics by sequencing the genomes of Late Upper Palaeolithic (13,300 years old, 1.4-fold coverage) and Mesolithic (9,700 years old, 15.4-fold) males from western Georgia in the Caucasus and a Late Upper Palaeolithic (13,700 years old, 9.5-fold) male from Switzerland
>While we detect Late Palaeolithic–Mesolithic genomic continuity in both regions, we find that Caucasus hunter-gatherers (CHG) belong to a distinct ancient clade that split from western hunter-gatherers ∼45 kya, shortly after the expansion of anatomically modern humans into Europe and from the ancestors of Neolithic farmers ∼25 kya, around the Last Glacial Maximum
>Kotias and Satsurblia, the two CHG, are genetically different from all other early Holocene (that is, Mesolithic and Neolithic) ancient genomes1,2,3,4,5,6,8,9,10, while Bichon is similar to other younger WHG
>Thus, WHG split first, with CHG and EF separating only at a later stage
>G-Phocs dates the split between WHG and the population ancestral to CHG and EF at ∼40–50 kya
>The split between CHG and EF is dated at ∼20–30 kya emerging from a common basal Eurasian lineage1 (Supplementary Fig. 2
>Like EF, but in contrast to WHG, CHG carry a variant of the SLC24A5 gene17 associated with light skin colour (rs1426654
>Both WHG and CHG have a high frequency of ROH and in particular, the older CHG, Satsurblia, shows signs of recent consanguinity, with a high frequency of longer (>4 Mb) ROH
>A clear distinction is visible between either WHG and CHG who display an excess of shorter ROH, akin to modern Oceanic and Onge populations, and EF who resemble other populations with sustained larger ancestral population sizes
>Continuity in the Caucasus is also supported by the mitochondrial and Y chromosomal haplogroups of Kotias (H13c and J2a, respectively) and Satsurblia (K3 and J), which are all found at high frequencies in Georgia today
>EF share greater genetic affinity to populations from southern Europe than to those from northern Europe with an inverted pattern for WHG1,2,3,4,5. Surprisingly, we find that CHG influence is stronger in northern than Southern Europe (Fig. 4a and Supplementary Fig. 3A) despite the closer relationship between CHG and EF compared with WHG, suggesting an increase of CHG ancestry in Western Europeans subsequent to the early Neolithic period
>We investigated this further using D-statistics of the form D(Yoruba, Kotias; EF, modern Western European population), which confirmed a significant introgression from CHG into modern northern European genomes after the early Neolithic period
>In modern populations, the impact of CHG also stretches beyond Europe to the east. Central and South Asian populations received genetic influx from CHG
>admixture f3-statistics, which show many samples as a mix of CHG and another South Asian population
>Given their geographic origin, it seems likely that CHG and EF are the descendants of early colonists from Africa who stopped south of the Caucasus, in an area stretching south to the Levant and possibly east towards Central and South Asia

The last common ancestor of H, J and K was HIJK. As I said in Parts 1-2, haplogroup BT is found in Europe dating back to 30k-31kYBP, CT to 31k-33k, I to 31k-34k, C to 36k-38k, F to 37k-41k, and K to 42k-47k.

To repeat the dates of origin for relevant haplogroups;

F = GHIJK, (45-60kYBP - not found in any modern men or ancient remains)
 GHIJK = HIJK, (45-50kYBP - not found in any modern men or ancient remains)
  HIJK = IJK, (45-50kYBP - not found in any modern men or ancient remains)
   IJK = IJ, K, (42.4k-46.4k - Iran, c.2012)
    IJ = I, J (15.3k-30k - Southwest Asia)
     I = I1, (11k-30k - Northern Europe,) I2, (28-30k - Peloponnesus,)
     J = J1, (4k-24k - Yemen,) J2, (4k-24k - Azerbaijan,)
    K = K2, (47k - Found in Africa, Eurasia and Oceania)
     K2 = K2a (45k - Omsk,) K2b, (50k - Papua New Guinea, Philippines)
      K2a = K2a1 (30-45k - India, Malaysia,)
       K2a1 = NO, (45k - Southern China, Southeast Asia,)
        NO = NO1,  (45k - Southern China, Southeast Asia,)
         NO1 = N (14.6k-24.2k - Southeast Asia,) O (28-39k - Southeast Asia,)
      K2b = P (35k - Maritime southeast Asia,)
       P = P1 (35k - Papua New Guinea,)
        P1 = Q (17.2k-31.7k - Borneo,) R (27k - Borneo,)
         R = R1 (27k - Borneo,)
          R1 = R1a (22-25k - Bactria,) R1b (22-25k - Borneo,)

If EF and CHG both have the A allele of SLC24A5 and diverged from one another 40k-50kYBP, this would be precisely the date of origin for haplogroup K and H;

>https://isogg.org/tree/ISOGG_HapgrpH.html
>The founder of haplogroup H probably lived about 30,000-40,000 years ago
>https://isogg.org/tree/ISOGG_HapgrpK.html
>Y-DNA haplogroup K is an old lineage established approximately 40,000 thousand years ago whose origins were probably in southwestern Asia

Y-haplogroup IJK is fouhd in Europe from 30kYBP, and HIJK from 15kYBP - both ancestral to H, I, J and K. If K was found in Europe circa 47kYBP, than IJK must be older than K, and HIJK must be older than IJK. On this chart;

>http://www.nature.com/articles/ncomms9912/figures/2

the split between the SLC24A5-A allele remains 13kYBP in Georgia and EF and the SLC24A5-G allele remains of the WHG potentially happened 75.8kYBP, thus producing a range of 45k-75kYBP. This would be fall within the range both of the evolution Y-haplogroup F in Melanesia at 55.6kYBP, and and close to it's appearance in Europe at 41kYBP;

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105016
>The MA-1 mitochondrial genome belongs to haplogroup U, which has also been found at high frequency among Upper Palaeolithic and Mesolithic European hunter-gatherers10–12, and the Y chromosome of MA-1 is basal to modern-day western Eurasians and near the root of most Native American lineages5
>Gene flow from the MA-1 lineage into Native American ancestors could explain why several crania from the First Americans have been reported as bearing morphological characteristics that do not resemble those of east Asians
>Upper Palaeolithic Siberian genome reveals dual ancestry of Native Americans
>This suggests that populations related to contemporary western Eurasians had a more north-easterly distribution 24,000 years ago than commonly thought
>Furthermore, we estimate that 14 to 38% of Native American ancestry may originate through gene flow from this ancient population
>Acknowledging the low depth of coverage, we determined the most likely phylogenetic affiliation of the MA-1 Y chromosome to a basal lineage of haplogroup R
>The sister lineage to these extant sub-lineages of haplogroup R, haplogroup Q, is the most common haplogroup in Native Americans5 and it was recently shown that, in Eurasia, haplogroup Q lineages closest to Native Americans are found in southern Altai
>However, MA-1, at approximately 24,000 cal. bp, pre-dates time estimates of the Native American–east Asian population divergence event
>This presents little time for the formation of a diverged Native American gene pool that could have contributed ancestry to MA-1, suggesting gene flow from the MA-1 lineage into Native American ancestors
>Consistent with this, D-statistic tests estimated from outgroup-ascertained SNP data20 reveal significant evidence (Z == 3) for Middle Eastern, European, central Asian and south Asian populations being closer to Karitiana than to Han Chinese20 (Fig. 3b and Supplementary Information, section 14.5). Similar signals were also observed when we replaced modern-day Han Chinese with data from chromosome 21 from a 40,000-yearold east Asian individual (Tianyuan Cave, China), which has been found to be ancestral to modern-day Asians and Native Americans
>Thus, if the gene flow direction was from Native Americans into western Eurasians it would have had to spread subsequently to European, Middle Eastern, south Asian and central Asian populations, including MA-1 before 24,000 years ago. Moreover, as Native Americans are closer to Han Chinese than to Papuans (Fig. 3c), Native American-related gene flow into the ancestors of MA-1is expected to result in MA-1 also being closer to Han Chinese than to Papuans. However, our results suggest that this is not the case (D (Papuan, Han; Sardinian, MA-1) = 20.002 ± 0.005 (Z = 20.36)), which is compatible with all or almost all of the gene flow being into Native Americans

The last common ancestor of O and R was K, which according to this chart;

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2336805/table/T2/
>Caveats
>To provide estimates of the age of the nodes, we chose to fix the time to the most recent common ancestor of CT (defined by P9.1, M168, and M294) at 70 thousand years ago (Kya), which is consistent with previous estimates from genetic and archaeological data (Lahr and Foley 1998; Hammer and Zegura 2002; Macaulay et al. 2005), and is the chronological approximation given in Jobling et al. (2004) (p250) for the first major human out-of-Africa dispersals. We estimated the times for intermediate nodes by using a linear interpolation. The age estimates in years should be viewed with caution because we do not know if the calibration date chosen above is accurate.

dates to 40k-53.9kYBP. However, note the caveat - the 70kYBP calibration is arbitrary. Above I place the origin of Y-haplogroup CT at 320kYBP, thus implying that the sub-clades of F evolved n-Kya after that date. R1 is the youngest at 18,500YBP, but as shown above R* emerged 24,000YBP, so; 70,000 - 24,000 = 46,000 years after 320kYBP, or 274YBP.

If the A allele of SLC24A5 evolved in a branch of humanity that split off 46kYBP, that would entail that it evolved 70 - 46 = 25kYBP after 320kYBP, or roughly 295kYBP: This is younger than A000 (1250kYBP,) Denisovans (1000kYBP,) or neanderthals and Y-Adam (765kYBP,) and thus explains it's absence in these populations, except for a particular branch of CT.

Evidence of ancient derived alleles related to pigmentation comes from the presence of OCA2 mutations in archaic hominids;

>http://www.cell.com/current-biology/abstract/S0960-9822(16)31267-2
>they encountered and interbred with archaic hominins, including Neanderthals and Denisovans
>Here, we describe a comprehensive set of analyses that identified 126 high-frequency archaic haplotypes as putative targets of adaptive introgression in geographically diverse populations. These loci are enriched for immune-related genes (such as OAS1/2/3, TLR1/6/10, and TNFAIP3) and also encompass genes (including OCA2 and BNC2) that influence skin pigmentation phenotypes

And of course, if a species of anatomically modern humans existed at Jabel Irhoud circa 315kYBP, is it so much of a stretch that they or their relatives produced light-pigmented descendents in the far north circa 295kYBP? Moreover, this would allow Y-haplogroup R1 to enter the Americas at 274kYBP - exactly when they needed to show up to produce the Hueyatlaco remains.

What this entails is that the alleles associated with light pigmentation arose with the dawn of Y-Adam, because any case of a haplogroup with Y-Adam-derived mutations which now predominantly has the dark pigment causing G allele of SLC24A5 can be explained via introgression from A000. For that matter, Denisovans and neanderthals may have acquired the G allele from A000, and Denisovans could have acquired the dark version of BNC2 at the same time.

Something that has to be kept in mind is that light pigmentation causing alleles require homozygotic conditions to express, and because of that are called recessive. This is because by definition, the light pigment-causing allele is in fact dysfunctional - even a single copy of the dark pigment-causing allele, one from either your mother or father, is enough to pigment the entire organism because both versions are expressed throughout the body.

If you had a pure population of A000 in Africa and a mixed population of A000 derived, P91-8T mutants and pure Y-Adam SLC24A5-A homozygotes in Eurasia, over the long term Y chromosomal signatures such as the P91-8T, if caused by recombination of A000 and Y-Adam sex chromosomes, would be lost in non-A clades since the P91-8T mutation could only be passed on by direct Y descent. Yet, other genes inherited from A000 such as the G allele of SLC24A5 could be passed down to P91-9T descendents.

This could be explained by noting that chimps, gorillas and orangutans all have 48 chromosomes, while all humans have 46. Molecular clock analysis and the 765kYBP origin for neanderthals establishes 765kYBP as the latest date for chromosomal fusion;

>https://www.ncbi.nlm.nih.gov/m/pubmed/27708712/
>The reduction in chromosome number was caused by the head-to-head fusion of two ancestral chromosomes to form human chromosome 2
>Next generation sequencing and molecular clock analyses estimated that this fusion arose prior to our last common ancestor with Neandertal and Denisovan hominins ~ 0.74 - 4.5 million years ago

During this fusion, chromosome Y received a 100,000 basepair transposition from chromosome 1;

>https://www.ncbi.nlm.nih.gov/m/pubmed/11863072/
>During our search for evolutionary breakpoints on the Y chromosome, it transpired that a transposition of an approximately 100-kb DNA fragment from chromosome 1 onto the Y chromosome must have occurred in a common ancestor of human, chimpanzee and bonobo. Only the Y chromosomes of these three species contain the chromosome-1-derived fragment; it could not be detected on the Y chromosomes of gorillas or the other primates examined. Thus, this shared derived (synapomorphic) trait provides clear evidence for a Homo-Pan clade independent of DNA sequence analysis

The common ancestor of bonobos and chimpanzees lived less than one million years ago;

>https://www.ncbi.nlm.nih.gov/m/pubmed/15483319/
>The bonobo and the common chimpanzee are estimated to have diverged approximately 0.86 to 0.89 MYA, and the divergence of the two common chimpanzee subspecies is estimated to have occurred 0.42 MYA

However, chimpanzees and bonobos have interbred since 860kYBP;

>https://www.sciencedaily.com/releases/2016/10/161027142434.htm
>Published in the journal Science, the study from scientists at the Wellcome Trust Sanger Institute and their international collaborators showed that one percent of chimpanzee genomes are derived from bonobos

And the oldest fossil evidence of chimpanzees only dates back to 500kYBP;

>http://www.nature.com/news/2005/050829/full/news050829-10.html
>500,000-year-old teeth shed light on evolutionary split between humans and chimps
>Palaeontologists digging in the dusty wastelands of East Africa have discovered the first known chimpanzee fossil

If it weren't for the evidence of introgression at 1250kYBP in Africa and the 1000kYBP estimate for the formation of the Denisovan gene pool, there would be no reason to believe chimpanzees were older than 860kYBP. However, if A000 was formed by introgression from a 48q-P91-8T hominid, that implies that Y-Adam was descended from a 46q-P91-9T hominid that emerged before 1250kYBP, meaning that the the 48-46 split happened before 1250kYBP. The extreme divergence of human and chimp Y chromosomes suggests an upper limit to the split of 6000kYBP, and this date represents the lower age range of the chimp Y chromosome, which would never recombine or receive information from the Y-DNYA genome - on the other hand, the X would recombine, assuring that it was shared by both chimp and human;

>http://johnhawks.net/weblog/reviews/chimpanzees/genetics/chimpanzee-y-chromosome-2010.html
>Indeed, at 6 million years of separation, the difference in MSY gene content in chimpanzee and human is more comparable to the difference in autosomal gene content in chicken and human, at 310 million years of separation
>An interesting possibility: Maybe the extreme evolution of the Y chromosome in the emerging human and chimpanzee lineages explains the unusual similarity of their X chromosomes

>https://www.nature.com/nature/journal/v463/n7280/full/nature08700.html
>Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content
>By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content, indicating rapid evolution during the past 6 million years. The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor

Comparing this date to the 740k-4500kYBP 2aq-2bq range, 4500kYBP seems to have been the antiquity of the 46q-P91-9T genotype. This entails that the Y-chromosomal Adam of Denisovans, neanderthals and Y-Adam (Y-DNYA) existed for 3250k years before it interbred with the African 48q-P91-8T hominid. However, there may have been as many as 310000kYBP or 310Mya between the divergence of the chimp and human Y.

When the 48q-P91-8T(B) hominid bred with Y-DNYA(A,) the resulting offspring would carry on a full 'B-line' and a full 'A-line' of alleles - except on 2q which would be AB plus unfused 2aq and 2bq, 4q-Xq-13q-18q which have introgression, and Yq which would be AB-1B. What this would entail is that the first generation would have 47 chromosomes - one fused 2aq-2bq chromosome, and a second set of unfused, pure 2aq and 2bq chromosomes which may have introgressed to human 2q, 13q or 18q.

The transposition of information from 1q to Yq would explain the P91-8T mutation, and the fact that 2q would recombine with either 2aq or 2bq would leave only one 2*q to recombine with 4q, 13q or 18q - meaning three seperate, but static and repeatable recombinations would be possible.

If a male 47-P91-8T hybrid was produced with a female 46-P91-9T human and male 48-P91-8T hominid, the result would be a Y chromosome with no Y-DYNA signatures - A000. However, such a hybrid would still have introgressions from 48q-P91-8T on 2q, 4q, Xq, 13q, 18q, and potentially on 19q-22q. The fact that bonobos and chimpanzees have the same 100kb 1q->Yq transposition as humans suggests that the basal Y-DNYA-P91-9T Y chromosome was transfered over to a mostly B-line genome, granting bonobos and chimps the P91-9T allele around 1250kYBP - within the 0.74-4.5Mya estimate of the 2*q fusion. The lack of other human Y signatures can be explained by the general gene loss the chimpanzee Y has experienced - the 1250kYBP-admixture genome seems to have split into a complete A000-46q-P91-8T form, and a truncated Chimp-48q-P91-9T form.

A female 47-P91-8T wouldn't pass on any unusual Yq signatures, but would pass on the introgressions. A000's daughters would also serve this purpose, and this was the vector for the transfer of 2q, 4q, 13q, and 18q introgressions into haplogroup B in Africa, as well as the origin of the mitrochondrial Eve - who only dates back 234kYBP.

Immediately after the initial interbreeding event, you would get a population which was sharply divided in terms of the origin of it's Y, X, and Table C chromosomes. Since the light allele of SLC42A2 would exist only on 5q of the first generation's A-line, there would be a 75% chance of passing it down to a double A-line Y-DNYA homozygote, and a 25% chance to pass it down to another A-line heterozygote - in Africa, the 48q-P91-8T derived B-line for Table C chromosomes would predominate. SLC24A5 would be just as fragile, and in fact all the genes would have a bias towards the B-line in the African admixtured population. On the other hand, the 2q-4q-13q-18q introgressions all have a 25% chance of being passed on with an 46-P91-9T homozygote mate.

Let's examine the implications of this on genes in terms of specific admixture vector;

Table A: Genes on chromosomes showing 48-P91-8T introgression (1250kYBP;)

18q - APCDD1
13q - 5HT2A, FGF9
Xq - 5HT2C - FGF13 - FGF16, GPR143
4q - CLOCK, EDAR, EN1, GAD1, LY87, FGFR3, DRD5, Dentin sialophosphoprotein, HAND2, Melatonin receptor, Osteopontin
2q - 5a-reductase II, 5HT2B, ASXL2, BMP10, FSHR, FAP, GPR35, GPR55, GPR113, GPR155, HOXD1-13, a-MSH, MAP2, PTH1R, PTH2R, PAX3, PAX8, SOX11, Wnt6, UGT1A1, GRB14
1q - 100kb->Y

Table B: Genes on chromosomes inherited from a recombination of A-line and B-line (1250kYBP;)

22q - ZNRF3, A2Ar, MCH, Ku, RTN4R, Somatostatin receptor 1-3
21q
20q - ASIP, ADRA1D, Dynorphin, H3r, Noiciceptin receptor, Oxytocin, Vassopressin
19q
15q - SLC24A5, Aromatase, RHCG, SCZD10, BNC1
14q - BMP4
11q
6q - RSPO3, VEGFA, TFAP2B, RHAG
3q - ADAMTS9, NISCH

Table C: Genes on chromosomes inherited from either A-line OR B-line, not both due to lack of recombination;

17q - A2B, SHBG, SERT, PLD1, PLD2,
16q - MC1R, Norepinephrine transporter,
12q - ITPR2, HOXC13, TMTC2
10q
9q - ABO, BNC2
8q - MSRA
7q - NFE2L3, SDK1
5q - SLC42A2, CPEB4, 5a-reductase I,
1q - TBX15, LYPLAL1, DNM3, RHD

Table A lists chromosomes/genes that require an instance of interbreeding with the 48q-P91-8T hominid to produce the introgression, but thereafter are passed down normally. Table B lists chromosomes/genes that would recombine as normal, and thus be inherited by all descendents of the admixture event. Table C lists chromosomes/genes that would not recombine during an admixture event, and so lists genes that would define two new post-admixture branches. In Africa, humans inherited the B-line, and in the rest of the world the A-line predominated until very recently - African humans, chimps and bonobos would inherit the African B-line of Table C since it contained dark pigment-causing alleles which were adaptive in the south, and Europeans would have been selected to retain the A-line of Table C. Meanwhile, the chromosomes on Tables A and B would recombine, and so their alleles would be expected to show more variance - SLC24A5 is more variable than SLC42A2.

Another example of strict inheritance of TBX15 alleles;

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5430617/
>Archaic Adaptive Introgression in TBX15/WARS2
>The alleles with high PBS values and high frequency in GI are almost absent in Africa, but present across Eurasia
>The high-frequency alleles in GI tend to match the Denisovan and Altai Neanderthal alleles in this region. For example, rs2298080 has an A allele at a frequency of 45.45% in Han Chinese from Beijing (CHB) and at 99.74% frequency in GI. This allele is absent or almost absent (<1% frequency) in all African populations

Table C also contains the ABO and RHD genes, which control bloodtype and Rhesus factor. This suggests that bloodtype is likely to have been sharply divided in inheritance - and indeed, the A allele of TBX15 at rs2298080 reaches it's highest frequency in south America, where type O blood is most common. The fact that neanderthals had type O blood proves that there was a strict inheritance of Table C;

>http://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-8-342
>Our results indicate that the two El Sidrón Neandertal individuals were most likely homozygous for the O01 allele. Nevertheless given a low rate of potential modern human contaminants in an unknown allelic state, we cannot discard the possibility that both Neandertals could have been heterozygous (e.g. OA or OB). The results however suggest the presence of the human O01 allele already in the common ancestor of Neandertals and modern humans and thereby confirming an emergence of the O01 allele more than 1 Mya predating the divergence of the modern human and Neandertal populations

And RHD evolved before neanderthals;

>http://genetics.thetech.org/ask-a-geneticist/rh-did-not-come-neanderthals
>Rh- blood probably arose millions of years ago rather than tens of thousands
>Keep in mind that when I say Rh- here, I mean the form that is common in Europe
>One of the big clues that this form of Rh- has been around for a long time is that it is the most common form in Africa as well as Europe
>What I do mean is that even though being Rh- isn’t very common in Africa, if you have the blood type, then the most common way is the same in both Africa and Europe
>What this all means is that it is extremely unlikely that the common form of Rh- blood originated in Neanderthals and then spread into humans through breeding.  It simply arose too long ago for this to be true
>This also means that even if we see evidence that Neanderthals had this form of being Rh-, that doesn’t mean we got it from them.  A more likely explanation in that case is that we shared common ancestors who had the same form of Rh- blood in their blood
>It is confusing that the Rh- blood type is as common as it is because it can have such profound effects.  If an Rh- mother is pregnant with an Rh+ child, the child is at risk for something called hemolytic disease of the newborn (HDN
>From a biological point of view, if being Rh- had only this effect, then Rh- women should have fewer children.  This means that the DNA that leads to being Rh- should be passed down less often.  Over time, being Rh- should become less and less common and, perhaps, even disappear
>http://genetics.thetech.org/ask/ask381
>HDN makes it look like the mother is rejecting the child. As if the mother and child are from different species

Type O Rh- blood was probably the ancestral form, and Rh+ blood may have been a mutation that would have been strictly inherited on the A-line or B-line of Table C. What this means is that a 46q-P91-9T-Rh- female couldn't carry a hybrid 47q-P91-8T-Rh+ baby - all her viable children would have to inherit the Rh- A-line on Table C. So all introgression into Y-DNYA would have included Y-DNYA Table C genes, and her sons would be Y-47q-P91-8T while her daughters could breed with pure Y-DNYA males and pass on only her autosomal DNA and Xq. On the other hand, a male Y-DNYA could have Rh- children with a 48q-P91-8T-Rh+ mother, and his otherwise human Y would acquire the P91-8T signature via the 1q->Yq transposition.

The children of the Y-DNYA female would be heterozygotes for RHD, with a 1q-Rh+ B-line and 1q-Rh- A-line. A000, Chimpanzees and bonobos inherited two copies of the Rh+ B-line, while non-Africans inherited both - probably because the ratio of B-line to A-line became more biased towards A-line with increasing geographic distance from the epicenter of admixture. Over time, selective pressures promoted the 46q-P91-8T B-line at the equator, and as A-line and B-line recombined fully after the admixture event, the B-line alleles that caused dark pigmentation dominated everywhere but Europe.

Before moving on to Part 5, I'll provide some supplementary charts and data;

Chromosome 4 shows similar evidence of modification during the fusion of 2aq and 2bq;

>https://source.wustl.edu/2005/04/human-chromosomes-2-4-include-gene-deserts-signs-of-chimp-chromosome-merger/

So during this 48q-P91-8T-BT interbreeding, chromosome 1 transposed information to the Y chromosome, ancestral chromosomes 2 and 4 fused, human chromosomes 4, 13, 18 and X, and Y received received information from 48q-P91-8T. Between chimps and humans, chromosomes 3, 6, 11, 13, 14, 15, 18, 19, 20, 21, 22 and X are structually identical, making chromosomes 1, 2, 4, 5, 7, 8, 9, 10, 12, 16 and 17 the 'mutant' chromosomes that define humans;

24/48-Chromosomes;
1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, X, Y,
23/46-Chromosomes;
1, 2, 3,     5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, X, Y.

Thus the only directly heritable chromosomes are;

1, Allelic inheritance during Recombination of 23q A-line and 24q B-line;

1,   2a, 2b, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18,  19, 20, 21, 22,  X
B,    B,  B, B, B, B,B,B, B, B,  B,  B,   B,  B,   B,   B,  B,  B,   B,    B,   B,  B,  B,  B,
 | \     |  /   /\    /    |   |                     |            |     |      |                 |       |     |     |      |    |
A,A, A,  A,   A,    A, A,A, A, A,  A, A,   A,   A,   A,   A,  A,  A,    A,    A,   A,  A,   A,  A,
1, Y, 2,   3,   4,    5, 6,7, 8, 9, 10, 11, 12,  13, 14, 15, 16, 17, 18,  19, 20, 21, 22,  X,

The G allele of SLC24A5 is common among the Han Chinese, and the A allele of BNC2 that causes lighter pigment is absent in modern Asian populations. This would entail that neanderthals were almost as light as modern Europeans, and Denisovans were as light as modern Asians. The list is;

48q-P91-8T - BNC2-G, SLC24A5-G, UGT1A1-3/4T
A000 - BNC2-G, SLC24A5-G, UGT1A1-3/4T
Denisovans - BNC2-G, SLC24A5-G, UGT1A1-6T
Neanderthals - BNC2-A, MC1R-V92M, SLC24A5-G, UGT1A1-6T
Y-Adam - BNC2-A, MCR1R-V92M, SLC24A5-A, UGT1A1-6T