Humans and Chimpanzees

Chimpanzee Sequencing and Analysis Consortium.  “Initial sequence of the chimpanzee genome and comparison with the human genome.”  Nature 437:69–87.  Sep 1, 2005.  A draft genome sequence of the common chimpanzee, made from one male chimpanzee and compared with the human genome.  It found about 35 million single-nucleotide changes and about 5 million insertion and deletion events, and it gives the substitution rate as a mean of 1.23 percent.  The article relies on it for the 1.23 percent figure and for the paper's own statement that insertions and deletions dwarf that figure.

1. 1a.

   Page 73, right column, end of "Insertions and deletions":  “On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb.  This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions”. ↩ ↩

2. 1b.

   Table 2, page 75:  “Transposable element activity in human and chimpanzee lineages”.  Chimpanzee-specific against human-specific.  ERV class 1: 234 (>1 Mb)† chimpanzee-specific and 5 (8 kb)‡ human-specific.  ERV class 2: 45 (55 kb)§ chimpanzee-specific and 77 (130 kb)§ human-specific.  The footnotes read † PtERV1 and PtERV2, ‡ HERV9, § Mostly HERV-K.  Table 2 counts the aligned parts of the two genomes only, so it is not a whole-genome census.  The four cells sum to 361, not the 391 that circulates. ↩

3. 1c.

   Page 72:  “Sites containing CpG dinucleotides in either species show a substantially elevated divergence rate of 15.2% per base; they account for 25.2% of all substitutions while constituting only 2.1% of all aligned bases.” ↩

Wood, Todd Charles.  “The chimpanzee genome and the problem of biological similarity.”  Occasional Papers of the Baraminology Study Group 7:1–18.  Feb 20, 2006.  A review by a young-earth creationist biologist, then at Bryan College's Center for Origins Research, of what the 2005 chimpanzee genome means for creationism.  It accepts the measured differences, rejects several popular creationist arguments against them, and concludes that creation biology needs an explanation of the pattern of similarity rather than an appeal to a common designer.  The article uses it as the most careful young-earth treatment of the question.

1. 2a.

   Page 7:  “The question is not how similarity arose but why this particular pattern of similarity arose. To say that God could have created the pattern is merely ad hoc.” ↩ ↩ ↩

Gunz, Philipp et al.  “Australopithecus afarensis endocasts suggest ape-like brain organization and prolonged brain growth.”  Science Advances 6(14):eaaz4729.  2020.  A study that scanned eight fossil Australopithecus afarensis skulls, two of them infants, by conventional and synchrotron CT, measuring brain volume and the imprints of brain folds on the inside of the skull.  It found an ape-like brain organisation and a long period of brain growth.  This page uses only its opening comparison of living human and chimpanzee brains.  Mirror:  PMC

1. 3a.

   Section Abstract:  “Human brains are three times larger, are organized differently, and mature for a longer period of time than those of our closest living relatives, the chimpanzees.” ↩ ↩

Buggs, Richard J. A.  “How much of a human genome is identical to a chimpanzee genome?”  richardbuggs.com.  May 6, 2025.  A personal blog post by Richard Buggs, who co-wrote the FluentDNA paper.  He adds two figures from the 2025 Nature genome paper, gap divergence of 13.3% and single-nucleotide divergence of 1.6%, to get 85.1% of human autosome bases (the non-sex chromosomes) matching the chimpanzee one-to-one.  The article calls this honest arithmetic and counts it as one of several denominators for the human-chimpanzee figure.

1. 4a.

   “When the latest human genome assembly was used as a target, and the latest chimpanzee assembly was aligned to it, the authors report gap divergence of 13.3% and single nucleotide variant divergence of 1.6% (these results can be found in Supplementary Figure III.11 and 12 respectively, for hg0002 vs PanTro3).”  “Adding the average gap divergence and average single nucleotide variant divergence together gives a total difference of 14.9%.  Thus, as I understand it, for the latest assemblies, 85.1 % of the nucleotides in the human genome have one-to-one exact matches in the chimpanzee genome.”  The post misquotes its own 2018 result as 82.34%, which was the panTro4 figure; the panTro6 figure was 84.38%. ↩

Tomkins, Jeffrey P.  “Documented Anomaly in Recent Versions of the BLASTN Algorithm and a Complete Reanalysis of Chimpanzee and Human Genome-Wide DNA Similarity Using Nucmer and LASTZ.”  Answers Research Journal 8:379–390.  Oct 7, 2015.  A journal article in which the author tested six versions of the BLASTN search program on chimpanzee and human DNA and found that every version after 2.2.25+ left out significant numbers of query sequences.  He then reran his 2013 chromosome comparison with the older version, 2.2.25+, and with two other alignment programs, nucmer and LASTZ.  BLASTN and nucmer both gave 88% similarity for the alignable parts of the chimpanzee genome, and LASTZ gave 73%; the reanalysis still set BLASTN to ungapped mode.  The article uses it because the author says the bug may have affected his earlier results, and this paper gives the revised 88% figure, which counts only the alignable parts of the genome.

1. 5a.

   Section Abstract:  “It has come to the attention of this author that recent versions of the BLASTN algorithm employed as a local installation may be omitting significant levels of query sequences in large-scale genomic searches.  This claim potentially affects the results of past research done by this author, particularly in relation to human-chimp DNA similarity.” ↩

Tomkins, Jeffrey P.  “Comparison of 18,000 De Novo Assembled Chimpanzee Contigs to the Human Genome Yields Average BLASTN Alignment Identities of 84%.”  Answers Research Journal 11:205–209.  Sep 5, 2018.  A journal article in which Jeffrey P. Tomkins aligned 18,000 de novo assembled chimpanzee contigs (stretches of DNA built from sequencing reads) against the human genome, using BLASTN, a DNA search program, and against two chimpanzee genome assemblies, panTro4 and panTro5.  Its average identity to human was 84%, which the author set beside Buggs' 84.38%.  The article uses it for that 84% figure and for the panTro4 control row.

1. 6a.

   Section Summary and Conclusion:  “The identities of the alignable DNA in this study and that obtained from LASTZ alignments are both 84% and in perfect agreement.  Furthermore, neither this study nor the LASTZ matched nucleotides account for the unalignable regions of the genome between human and chimpanzee.  From the LASTZ alignment data, Buggs calculated, '4.06% had no alignment to the chimp assembly.'  If this non-alignable sequence data is combined with the known alignment data (Buggs 2018), a reasonably accurate estimate of overall human-chimpanzee genome similarity would be close to 80% assuming that the genome sizes are similar.” ↩

Kronenberg, Zev N. et al.  “High-resolution comparative analysis of great ape genomes.”  Science 360(6393).  Jun 8, 2018.  A research article in which the authors built new chimpanzee and orangutan genome assemblies without using the human genome as a guide, then compared them with new human genomes and a gorilla genome.  They counted structural variants, which are differences of 50 DNA letters or more, and found that the number of these variants grew with evolutionary distance from humans.  The article uses it for the authors' statement that earlier ape assemblies had been "humanized" by human guidance, and for its structural-variant counts, which use two human genomes as controls.

1. 7a.

   Section Introduction:  “the higher quality human genome assemblies have often been used to guide the final stages of nonhuman genome projects, including the order and orientation of sequence contigs and, perhaps more importantly, the annotation of genes.  This bias has effectively "humanized" other ape genome assemblies, minimizing potential structural and transcript differences observed between the species.” ↩

2. 7b.

   Section Results, Structural variation analyses:  “More than 93% of inversions are flanked by large complex segmental duplication (SD) blocks, 38% of which show evidence of other structural and copy number variation at the boundaries of the inversion”.  “Interestingly, ~28% (8/29) of these ape–human inversions are also polymorphic among humans”. ↩

Yoo, DongAhn et al.  “Complete sequencing of ape genomes.”  Nature 641:401–418.  May 8, 2025.  A genome paper in Nature that sequenced six ape species (chimpanzee, bonobo, gorilla, Bornean orangutan, Sumatran orangutan and siamang) and completed 215 chromosomes from telomere to telomere, meaning each one is sequenced end to end with no gaps.  It found that 12.5–27.3% of an ape genome failed to align or did not fit a simple one-to-one alignment, so the apes differ more than earlier estimates had shown.  The article uses its supplementary tables for the human-chimpanzee figures and for a control that compares two human genomes.

1. 8a.

   Table III.20, section Supplementary Information, SI pages 34–36:  The table spans three pages: autosomes on p. 34, X on p. 35, Y on pp. 35–36.  It is the 16-way diploid Progressive Cactus alignment, identical 1:1 column.  Autosomes: GRCh38 87.87%; HG002 88.80%; chimpanzee 83.89%; bonobo 83.79%; gorilla 83.08%; Bornean orangutan 79.79%.  Chromosome X: GRCh38 86.13%; HG002 maternal 85.34%; chimpanzee primary 79.88%.  Chromosome Y: GRCh38 8.87%; HG002 paternal 27.02%; chimpanzee primary 4.32%.  Table III.17, section Supplementary Information, SI page 31:  “Alignment coverage of T2T-CHM13 (hs1) in the African ape pangenome”.  (Minigraph-Cactus) gives the HG002 paternal Y 99.94% in all four columns and the chimpanzee primary Y 12.59% identical 1:1. ↩

2. 8b.

   Figure III.11, section Supplementary Information, SI page 26:  Mean autosomal SNV divergence, read off the figure: hg002 vs PanTro3 0.015979; PanTro3 vs hg002 0.014633; hg002 vs GorGor1 0.019912; hg002 vs PonAbe1 0.036406; within hg002 0.001605; within PanTro3 0.002733; within GorGor1 0.005750; within PonAbe1 0.003539. ↩

3. 8c.

   Section Supplementary Note XII, SI page 101:  “We identified a total of 1,175 inversion variants larger than 10 kbp as well as one large-scale chromosome fusion and one translocation (Supplementary Fig. XII.43) across six species; the breakdown of identified inversions is as follows: 188 in bonobo, 171 in chimpanzee, 199 in gorilla, 180 in Bornean orangutan, 180 in Sumatran orangutan, and 257 in siamang.”  Section Supplementary Note XII, SI page 102:  “Filtering out the false inversion calls of 1,175 inversions larger than 10 kbp, 1,140 inversion calls remain.” ↩

4. 8d.

   Page 406:  “In total, 416 inversions had an annotated gene mapping to at least 1 of the breakpoints, with 724 apparently devoid of protein-coding genes (Supplementary Table XII.67). Of these inversions, 63.5% (724 out of 1,140) had annotated human SDs at one or both ends of the inversion, a result that represents a significant 4.1-fold enrichment (one-sided, simulation empirical P < 0.001). The strongest signal was for inverted SDs mapping to the breakpoints (6.2-fold; one-sided, simulation empirical P < 0.001), which suggested that non-allelic homologous recombination is driving many of these events.”  The same split, 416 and 724, appears for genes and for duplications.  Supplementary Note XII, page 102, gives both counts separately. ↩

5. 8e.

   Page 406:  “We parsimoniously assigned >64% of homozygous inversions to the ape phylogeny (Supplementary Fig. XII.45), with the remaining inversions predicted to be recurrent. The number of inversions assigned to each branch, based on maximum parsimony, correlated with the length of the branch (linear regression, R2 = 0.77), with the greatest number assigned to the siamang lineage (n = 44). However, the human lineage showed fivefold less than the expected number of inversions based on the branch length, and the trend still held when using the Bornean orangutan as a reference instead of human.” ↩

6. 8f.

   Page 403:  “Our analyses dated the human–chimpanzee split between 5.5 and 6.3 million years ago (Ma; minimum to maximum estimate of divergence), the African ape split at 10.6–10.9 Ma and the orangutan split at 18.2–19.6 Ma (Fig. 2a). We inferred ILS for an average of 39.5% of the autosomal genome and 24% of the X chromosome.”  “we estimated that the human–chimpanzee–bonobo ancestral population size (average Ne = 198,000) is larger than that of the human–chimpanzee–gorilla ancestor (Ne = 132,000)”. ↩

Wood, Todd C.  “RTB and the Chimp Genome, part 4.”  Todd's Blog.  Jan 2011.  A blog post by Todd Wood, then at Bryan College's Center for Origins Research, that rejects Rana's reading of the chimpanzee DNA that does not align to the human genome.  The post describes its numbers as preliminary data from a larger project.  The article uses it for Wood's test, in which those unaligned fragments matched human DNA at a median 97.4 percent identity.

1. 9a.

   “The Megablast results indicated that 42,570 of these 48,975 'unalignable' sequences aligned to some region of the human genome.  How similar are those fragments?  The median percent identity is 97.4%.  So they're just as similar as everything else in the chimp and human genomes.  The only difference is that you can't specify which precise region of the human genome the 'unalignable' chimp fragments should align to.” ↩

Marks, Jonathan.  What It Means to Be 98% Chimpanzee: Apes, People, and Their Genes.  University of California Press.  2002.  A book on what the 98 percent figure means, by Jonathan Marks.  The article uses it for the point that the scale of matching starts at 25 percent, because unrelated DNA matches about a quarter of positions by chance.

1. 10a.

   Page 28:  “if you compare the DNA of a human and a daffodil, the 25% mark is actually the zero mark, and since humans and daffodils do share a common ancestry, you would expect them to be generally more similar than 25%.  Say, about 35%.” ↩

Yunis, Jorge J., and Om Prakash.  “The origin of man: a chromosomal pictorial legacy.”  Science 215(4539):1525–1530.  Mar 19, 1982.  A comparison of high-resolution banded chromosomes from orangutan, gorilla, chimpanzee and human.  It proposed that human chromosome 2 is two ape chromosomes joined end to end.  The article uses it as the origin of that prediction, not for any number.

1. 11a.

   Section Abstract:  “A comparative analysis of high-resolution chromosomes from orangutan, gorilla, chimpanzee, and man suggests that 18 or 23 pairs of chromosomes of modern man are virtually identical to those of our 'common hominoid ancestor', with the remaining pairs slightly different.” ↩

IJdo, J. W. et al.  “Origin of human chromosome 2: an ancestral telomere-telomere fusion.”  Proceedings of the National Academy of Sciences USA 88(20):9051–9055.  Oct 1991.  A molecular genetics study, published in October 1991, that screened about 1.4 million colonies of a human genomic cosmid library, then tested the positives with a telomere probe.  Two cosmids that map to band 2q13 on chromosome 2 were sequenced, and the authors used fluorescence in situ hybridisation on chromosomes from six unrelated people.  They call the locus a relic of an ancient telomere-to-telomere fusion of two ancestral ape chromosomes.  The article rests its account of the 2q13 telomere arrays on this paper and quotes its claim that the locus is a relic of the fusion.

1. 12a.

   Page 9054, section Discussion:  “The data we present here demonstrate that a telomere-to-telomere fusion of ancestral chromosomes occurred, leaving a pathognomonic relic at band 2q13.” ↩

Yang, Zikun et al.  “Incomplete lineage sorting of segmental duplications defines the human chromosome 2 fusion site early during African great ape speciation.”  Cell Genomics 6(1):101079.  Jan 2026.  A 2026 genome study, published online in December 2025, by teams at Shanghai Jiao Tong University and the University of Washington, among others.  It characterized the fusion site at single-base resolution, found three segmental duplications (large copied blocks of DNA) that are more than 5 million years old, and used CRISPR-Cas9 to deplete the fusion site in human neural progenitor cells, which altered the expression of some genes.  The article uses it for the telomere-to-telomere size of the junction, the three satellite arrays of the dead centromere, the expression of the genes at the site, the comparison with the archaic genomes, and its age of 5 to 7 million years.

1. 13a.

   Section Centromere retention and degeneration in human chr2:  “A sequence comparison using unique k-mers from this region shows that ∼97.5% (8,246/8,460) and ∼96.7% (8,181/8,460) are also identified in Neanderthal and Denisovan genomes, respectively, confirming that the centromeric degeneration occurred long before the divergence of modern and archaic humans.” ↩

2. 13b.

   Section Discussion:  “suggesting that the fusion event occurred >5 mya.  Thus, the fusion event is not a recent evolutionary event but potentially occurred during African great ape speciation when the effective population size was predicted to be much larger than contemporary ape populations.” ↩

3. 13c.

   Section Highlights:  “The fusion event is driven by ILS and occurred ∼5–7 million years ago”.  Section Discussion:  “we speculate that this fusion event probably did not arise in the genus Homo but rather occurred in ancestral great ape populations.” ↩ ↩

Tomkins, Jeffrey, and Jerry Bergman.  “The chromosome 2 fusion model of human evolution — part 2: re-analysis of the genomic data.”  Journal of Creation 25(2):111–117.  Aug 2011.  A creationist re-analysis of the available genome data at the chromosome 2 fusion site, in Journal of Creation, a creationist journal.  It argues that the site is too ambiguous to show a fusion, and that its core of about 800 bases is a motif found throughout the genome, with no counterpart on chimpanzee chromosome 2A or 2B.  The article uses it as the creationist case it answers.

1. 14a.

   Page 112:  “Based on the predicted model, thousands of intact TTAGGG motifs in tandem should exist.  This is true even if allowing for an extremely high rate of degeneracy, which is an unreasonable expectation because meiotic recombination is suppressed in pericentric DNA due to its close proximity to the centromere.” ↩

Letsolo, Bo T. et al.  “Fusion of short telomeres in human cells is characterized by extensive deletion and microhomology, and can result in complex rearrangements.”  Nucleic Acids Research 38(6):1841–1852.  Apr 2010.  A laboratory study that used single-molecule methods to isolate and sequence telomere fusion events in human cells.  The cells were HEK293 and MRC5 fibroblasts driven into telomere crisis, and 298 fusion junctions were sequenced base by base.  Every fusion deleted at least one telomere, with a mean combined deletion of 2.443 kb.  The article uses it for the measured picture of real human telomere fusions, and as the answer to the claim that a real fusion would leave thousands of intact repeats.

1. 15a.

   Page 1846:  “The TTAGGG telomere repeat content at the fusion junctions was limited, with 38% to 60% of fusions in the HEK293 and MRC5 cells, respectively containing no telomere repeats.  Of the fusions that did contain TTAGGG repeats immediately adjacent to the fusion point, the mean length was 5.8 ± 0.7 (SE) repeats.” ↩

Capper, Rebecca et al.  “The nature of telomere fusion and a definition of the critical telomere length in human cells.”  Genes & Development 21(19):2495–2508.  Oct 1, 2007.  A laboratory study of telomere fusion junctions in human cells, which measured how many TTAGGG repeats a telomere must keep before it can fuse.  It sets the threshold of 13 repeats, and it is the companion measurement to Letsolo 2010 from the same laboratory.  The article uses it to explain why a telomere with thousands of repeats cannot fuse, and why the one known route to long repeats at a fusion needs a deliberate knockout.

1. 16a.

   Page 2504, section Discussion:  “Thus, we conclude that telomeres of <13 pure TTAGGG repeats distal to the TVR region are fusogenic, and that in the absence of telomerase fusogenic telomeres >13, repeats are likely to be rare.  We speculate that telomeres of <13 repeats do not bind sufficient TRF1 and TRF2 to confer telomeric function.” ↩

Fan, Yuxin et al.  “Genomic structure and evolution of the ancestral chromosome fusion site in 2q13–2q14.1 and paralogous regions on other human chromosomes.”  Genome Research 12(11):1651–1662.  Nov 2002.  A genome sequence study of more than 600 kb of DNA around the fusion site, built from a BAC clone and compared with the same sequences elsewhere in the genome.  It found two head-to-head arrays of telomere-like repeats with no other sequence between them, and pieces of the site duplicated on chromosome 9 and matched at the end of chromosome 22.  The article uses it for the measured structure of the site, for the counts of its repeat units, and for the puzzle Fan raised about how degenerate the arrays are.

1. 17a.

   Page 1658:  The answer that follows the question.  “There are three possible explanations: (1) Given the many instances of degenerate telomeric arrays within the subtelomeric regions of human chromosomes (Riethman et al. 2001), the chromosomes joined at interstitial arrays near, but not actually at, their ends.  In this case, material from the very ends of the fusion partners would have been discarded.  (2) The arrays were originally true terminal arrays that degenerated rapidly after the fusion.  This high rate of change is plausible, given the remarkably high allelic variation observed at the fusion site.  The arrays in the BAC and the sequence obtained by Ijdo et al. (1991) differ by 12%, which is high even if some differences are ascribed to experimental error.  (3) Some array degeneracy could be a consequence of sequencing errors.” ↩

Poszewiecka, Barbara et al.  “Revised time estimation of the ancestral human chromosome 2 fusion.”  BMC Genomics 23(Suppl 6):616.  Aug 2022.  A 2022 computer study that counted weak-to-strong DNA substitutions (AT changes to GC) around the fusion site, using a counting method the authors built.  It estimated the fusion at 0.9 million years ago, with a 95% confidence interval of 0.4 to 1.5 million years, and also reconstructed evolutionary distances among the great apes.  The article uses it as one of the mainstream dates it compares, beside the earlier 0.74 million year estimate by Dreszer and colleagues.

1. 18a.

   Section Abstract, page 1 of 15:  “By analyzing the enrichment of these substitutions around the fusion site of HSA2 we estimated its formation time at 0.9 Mya with a 95% confidence interval of 0.4-1.5 Mya.”  Section Page 2 of 15:  Of Dreszer and colleagues:  “As a result, they estimated the fusion time at 0.74 Mya with a 95% confidence interval 0-2.81 Mya.” ↩

Belshaw, Robert et al.  “Long-term reinfection of the human genome by endogenous retroviruses.”  Proceedings of the National Academy of Sciences USA 101(14):4894–4899.  Apr 6, 2004.  A computer study of the human genome that searched for copies of HERV-K(HML2), the youngest human ERV family, and compared their sequences across primates.  It found that every gene in the family, including env, has been kept nearly unchanged by natural selection, so the family spread mainly by reinfection of the germline rather than by copying within it, and an infectious pool persisted for 30 million years.  The article uses its figures for how many human ERV elements there are, the ratio of solo LTRs, and its finding that the family kept adding copies after humans and chimpanzees split.

1. 19a.

   Page 4894:  “HERVs) comprise ~5–8% of the human genome, with 98,000 elements and fragments, but phylogenetic analysis of conserved regions within their pol and env genes indicates that they form only a small number of clades among nonhuman exogenous and endogenous retroviruses.”  The 98,000 figure is Belshaw's citation to the HERVd database, not his own measurement. ↩

Wang, Gary P. et al.  “HIV integration site selection: Analysis by massively parallel pyrosequencing reveals association with epigenetic modifications.”  Genome Research 17(8):1186–1194.  2007.  A research paper that used pyrosequencing, a method that reads DNA sequence in bulk, to map 40,569 unique sites where HIV inserted itself into human DNA.  It found that insertion favors stretches of DNA marked as active and avoids stretches marked for silencing, and that favored sites lie on one face of the DNA wrapped around its protein spools, called nucleosomes.  The article uses it for the 41 cases where two separate insertions landed on the same base pair, and for its point that insertion is not random.

1. 20a.

   Page 1188:  “We found 41 sites that hosted two independent integration events at exactly the same base pair in the human genome.  Sites were only included in the analysis if the proviruses integrated at a single site were in opposite orientations, indicating independent events.”  The abstract gives the denominator:  "Here we used pyrosequencing to map 40,569 unique sites of HIV integration."  This is one virus in one immortalised T-cell line, not a germline-transmitted retrovirus in an ape. ↩

Inai, Yoko et al.  “The Whole Structure of the Human Nonfunctional L-Gulono-γ-Lactone Oxidase Gene — the Gene Responsible for Scurvy — and the Evolution of Repetitive Sequences Thereon.”  Journal of Nutritional Science and Vitaminology 49(5):315–319.  2003.  A DNA sequence study from the Department of Biochemistry at Wakayama Medical University in Japan, which searched a public database for the human copy of the vitamin C gene GULO and mapped what is left of it.  It found that only five of the rat gene's twelve exons (coding segments) remain in the human genome, and that the human and guinea pig remnants share 47 of the 129 substitutions (changes in the DNA letters) seen in the human sequence.  The article uses it because the two separate losses of this gene left the same changes at the same positions far more often than chance.

1. 21a.

   Page 316:  “When the human and guinea pig sequences (647 nucleotides in total) of the regions of exons 4, 7, 9, 10, and 12 were compared, we found 129 and 96 substitutions in humans and guinea pigs, respectively, when compared with the rat sequences.  The same substitutions from rats to both humans and guinea pigs occurred at 47 nucleotide positions among the 129 positions where substitutions occurred in the human sequences.  A high percentage of the same substitutions in the total substitutions (36%) indicates that there were many hot spots for nucleotide substitution throughout the sequences examined.” ↩

Lavialle, Christian et al.  “Paleovirology of 'syncytins', retroviral env genes exapted for a role in placentation.”  Philosophical Transactions of the Royal Society B 368(1626):20120507.  2013.  A review by a French research group on 'syncytins', placenta genes built from the envelope genes of ancient retroviruses.  It describes six such genes captured independently in different mammal groups, and reports that knocking out syncytin genes in mice prevents placenta development and kills the embryo.  The article uses it for the independent captures, which it says are shown by the genes sitting at different places in different species.

1. 22a.

   Page 6:  “Although they share similar features, the primate and muroid syncytins are clearly not orthologous genes — they are not syntenic in the two species clades — indicating that they are the result of independent gene captures that occurred separately in the genome from ancestors of each lineage.” ↩

Liu, Yingguang, and Charles Soper.  “The Natural History of Retroviruses: Exogenization vs. Endogenization.”  Answers Research Journal 2:97–106.  Sep 30, 2009.  A creationist essay that argues from published research on endogenous retroviruses (ERVs, viral remnants built into genomes) and reports no measurements of its own.  It proposes that ERVs were created as part of the host genome and that exogenous retroviruses came from them, which the authors call "exogenization, as opposed to endogenization."  The same lead author's 2018 conference paper with Tam Nguyen adds no quantitative account, so this paper remains the fuller statement, and the article uses it as the best creationist answer on shared ERV positions and as the paper that admits the syncytin-1 loci are a problem for creationists.

1. 23a.

   Section The Problem of ERVs:  “Since humans and primates share similar ERVs, not only in sequence but also in position, it is assumed that exogenous retroviruses infected the common ancestor of both.  The best alternative explanation is that orthologous ERVs were created to occupy similar genomic loci in separate species by a single designer to carry out similar physiological functions.” ↩

Huang, Peng et al.  “Comparative analysis of three-dimensional chromosomal architecture identifies a novel fetal hemoglobin regulatory element.”  Genes & Development 31(16):1704–1713.  2017.  A laboratory study that compared how chromosomes fold in fetal and adult human red blood cell precursors, using two methods that map which distant pieces of DNA touch each other.  It deleted the HBBP1 region, which holds a pseudogene (a broken copy of a gene that no longer makes its protein), in a cultured adult-type cell line, and γ-globin transcription rose strongly; neither side of the creation debate appears to have used it.  The article cites it for the deletion that raised γ-globin and for a second deletion that removed only the HBBP1 transcript and changed nothing.

1. 24a.

   Page 1709:  “We generated two independent clones with biallelic deletions, and in both of them, HBBP1 expression was lost.  However, β-globin and γ-globin transcription remained at control levels, suggesting that the HBBP1 genomic region, but not the HBBP1 transcript per se, is necessary for maintaining γ-globin silencing in adult erythroid cells.”  Ma et al. 2021 reports a function for the transcript in the opposite direction, but by overexpression rather than at the endogenous locus. ⁴⁹. ↩

The synteny article's test of Yoo 2025, Supplementary Table XII.67.  Inversion calls in different apes were merged when they overlap by at least 80 percent each way, Yoo's own rule.  Of 823 merged inversions over 10,000 letters, 220 are shared by two or more apes, and 150 of those, 68 percent, fit the tree of the six apes built from DNA letters.  If the apes sharing each inversion were drawn at random, about 30, or 13.5 percent, would fit.  The test is unrooted and treats a missed call in one ape as a real absence.  Details in Synteny, Gene Order, and the Y Chromosome. ↩

Venema, Dennis R., and Darrel R. Falk.  “Signature in the synteny.”  The BioLogos Forum.  Apr 19, 2010.  A BioLogos essay presenting shared gene order between humans and chimpanzees as evidence of common ancestry, written in reply to intelligent-design writers.  The source of the "no good biological reason" claim that young-earth writers answer.  Mirror:  Archive.org

1. 26a.

   Paragraph What makes shared synteny:  “What makes shared synteny for humans and chimpanzees challenging from an anti-common descent viewpoint is that there is no good biological reason to find the same genes in the same order in unrelated organisms, and every good reason to expect very different gene orders.”  Paragraph In summary:  “In summary, should God have wished to avoid the appearance of common ancestry between humans and chimpanzees, there seem to have been many gene orders and chromosome structures available to Him to use for either species.” ↩

Lazar, Nathan H. et al.  “Epigenetic maintenance of topological domains in the highly rearranged gibbon genome.”  Genome Research 28(7):983–997.  2018.  Maps of three-dimensional chromatin contacts in the gibbon, whose chromosomes are among the most reshuffled of any ape, compared with 67 breaks in gibbon-human gene order.  Most breaks fall on the boundaries of regulatory domains.  The authors weigh fragile boundaries against selection that removes breaks inside domains, and favour both.

1. 27a.

   Section Results, Large new TADs are rarely generated:  “When looking at boundaries of TADs sized 500 kb–1 Mb, we find that 55 of 67 BOS overlap with TAD boundaries in gibbon; for 31 of these BOS, both sides colocalize with TAD boundaries in the human genome, which represents the ancestral state.” ↩

Hughes, Jennifer F. et al.  “Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content.”  Nature 463:536–539.  Jan 28, 2010.  The finished sequence of the chimpanzee male-specific Y region, from one male, compared with the human one.  The Page laboratory found large differences in structure and gene content and proposed four causes.  The source of most numbers quoted on both sides of this topic.

1. 28a.

   Page 537:  “we found that the degree of similarity between orthologous chimpanzee and human MSY sequences (98.3% nucleotide identity) differs only modestly from that reported when comparing the rest of the chimpanzee and human genomes (98.8%). Surprisingly, however, >30% of chimpanzee MSY sequence has no homologous, alignable counterpart in the human MSY, and vice versa”. ↩

Makova, Kateryna D. et al.  “The complete sequence and comparative analysis of ape sex chromosomes.”  Nature 630:401–411.  Jun 13, 2024.  Telomere-to-telomere X and Y chromosomes of five great apes and the siamang, one male each, compared with the complete human X and Y.  It measured alignability, divergence, structural variants per branch, palindromes, satellites and gene copy numbers.  The main source for the Y here, including the within-kind comparisons.

1. 29a.

   Page 402:  “The same pattern was observed for closely related species, with only 60–87% of the Y chromosome, but more than 95% of the X chromosome, aligned between them”.  The paper's two pairs of closely related species are chimpanzee with bonobo and Bornean with Sumatran orangutan. ↩

2. 29b.

   Page 403, figure 1b:  Share of each reference Y covered by alignments to each other ape's Y.  Human Y covered by chimpanzee 26.2 percent;  chimpanzee Y covered by human 45.1 percent;  chimpanzee Y covered by bonobo 65.3 percent;  bonobo Y covered by chimpanzee 59.6 percent;  Bornean orangutan Y covered by chimpanzee 30.8 percent;  chimpanzee Y covered by Bornean orangutan 40.6 percent. ↩

Wood, Todd Charles.  “Baraminological analysis places Homo habilis, Homo rudolfensis, and Australopithecus sediba in the human holobaramin.”  Answers Research Journal 3:71–90.  2010.  A young-earth statistical baraminology study of published skull and tooth measurements of fossil hominins and living apes, proposing which taxa share a created kind with humans.  Cited for its proposed grouping of both chimpanzee species and its conclusion that humans and apes are separate kinds.

1. 30a.

   Page 86, table Summary of proposed holobaramins:  The row "Australopith #2" lists Pan troglodytes, Pan paniscus, Gorilla gorilla, Au. afarensis, Au. garhi and S. tchadensis, with Pongo pygmaeus among possible additional taxa.  “The discontinuity here demonstrated between Homo sensu lato (including “Au.” sediba) and nonhuman primates confirms the creationist prediction that humans and apes are separate created kinds.” ↩

Lightner, Jean K.  “Mammalian Ark kinds.”  Answers Research Journal 5:151–204.  2012.  A survey, published by Answers in Genesis, assigning living mammals to the kinds that would have been on the Ark, usually at the level of the family, with hybrid records as the main evidence.  Cited for its single great ape kind.

1. 31a.

   Page 171:  “Pongidae (Great ape kind) Wilson and Reeder (2005) place the great apes in Hominidae with humans, but given the significant differences between us and apes compared to some of the differences between other families, this seems ludicrous. Therefore, the older designation Pongidae is used here. There are three genera and six species in this family, which includes the gorilla, chimpanzee, and orangutan.” ↩

The synteny article's rough comparison.  Makova and colleagues in 2024 assign about 1,841 structural changes to the chimpanzee and bonobo Y branches over about 16 million aligned letters, about 112 per million.  Hallast and colleagues in 2023 report an average of 88 structural changes per human Y against the reference Y over about 23 million letters, about 3.8 per million.  The ratio is about 21 by count and 29 per million letters.  The two studies used different methods, so the factor could be off by about two either way. ↩

Langergraber, Kevin E. et al.  “Generation times in wild chimpanzees and gorillas suggest earlier divergence times in great ape and human evolution.”  Proceedings of the National Academy of Sciences 109(39):15716–15721.  Sep 25, 2012.  A field and genetics study from the Max Planck Institute for Evolutionary Anthropology, with Svante Pääbo and Linda Vigilant as senior authors.  It measured generation lengths from parentage records of 226 wild chimpanzee and 105 mountain gorilla offspring, combined them with family-measured human mutation rates, and recalculated published ape split dates without fossil calibration, putting the human-chimp split at 7 to 13 million years.  The article uses it for the origin of the old 1 × 10^-9 rate, the generation lengths and the recalculated dates.

1. 33a.

   Page 15716:  “Recently, researchers have commonly used a mutation rate of 1 × 10−9 mutations per site per year (e.g., refs. 4, 6, 8, 15) derived from the observed DNA sequence difference of around 1.3% between the human and chimpanzee genomes (8, 15, 16) and an assumed DNA sequence divergence between these species at 7 Ma, as well as from an observed sequence difference of 6.46% between the human and macaque genomes (17) and an assumption of their DNA sequence divergence at 25 Ma.”  “Although ubiquitous, this approach has an inherent circularity and is subject to possible error because it relies on the accuracy of the ages of fossils.” ↩ ↩

2. 33b.

   Page 15718:  “We estimate the split time between the human and chimpanzee lineages at between 7 and 13 million years, whereas previous estimates range from 4 to 6 million years.” ↩

Kong, Augustine et al.  “Rate of de novo mutations and the importance of father's age to disease risk.”  Nature 488:471–475.  Aug 23, 2012.  A whole-genome sequencing study of 78 Icelandic parent-child trios by deCODE genetics.  It found 4,933 new mutations, a rate of 1.20 × 10^-8 per letter per generation, about two more per year of the father's age, and almost four times as many from fathers as from mothers.  The article uses it for the family rate and for the pattern of new mutations:  their CpG hotspot, their transition share and their paternal bias.

1. 34a.

   Section Abstract:  “Here we show that in our samples, with an average father’s age of 29.7, the average de novo mutation rate is 1.20×10−8 per nucleotide per generation.”  Section Mutations by type and by chromosome:  “From that, 4933 mutations correspond to a germline mutation rate of 1.20×10−8 per”. ↩

Scally, Aylwin et al.  “Insights into hominid evolution from the gorilla genome sequence.”  Nature 483:169–175.  Mar 8, 2012.  The first gorilla genome, from the Wellcome Trust Sanger Institute and partners, compared with the human, chimpanzee and orangutan genomes using a model, CoalHMM, that infers the family tree at each position along the DNA.  It found that 30 % of the genome does not follow the species tree, and it showed how the human-chimp split date depends on which mutation rate is assumed.  The article uses it for incomplete lineage sorting and for the dates.

1. 35a.

   Section Speciation of the great apes:  “CoalHMM’s results would correspond to speciation time estimates THC and THCG of 3.7 and 5.95 Mya respectively (Fig. 1b).”  “indicate that a lower value of 0.5-0.6 × 10−9 bp−1y−1 is plausible (based on average hominine generation times of 20 to 25 y). This would give substantially older estimates of approximately 6 and 10 Mya for THC and THCG, potentially in better agreement with the fossil record.”  The first figure uses the old rate of 10^-9 per year. ↩

Sun, James X. et al.  “Supplementary Note for A direct characterization of human mutation based on microsatellites.”  Nature Genetics 44.  2012.  The 70-page supplement to the same study.  Its chapter 10 reruns the dating with Kong and colleagues' whole-genome family rate in place of the repeat-segment rate and sets the results against the fossil record.  The article uses it for the human-orangutan conflict and for the authors' view of the slowdown hypothesis.

1. 36a.

   Page 66:  “the inferred date of human-chimpanzee speciation is 8.32-11.8 Mya”.  “The inferred human-orangutan genetic divergence date of 34.0-46.2 Mya is so much older than the upper bound from the fossil record of <18 Mya on human-orangutan speciation that the date is implausible”. ↩

Besenbacher, Søren et al.  “Direct estimation of mutations in great apes reconciles phylogenetic dating.”  Nature Ecology & Evolution 3:286–292.  2019.  A family study of great apes from Aarhus University and partners:  ten parent-offspring trios, seven chimpanzee, two gorilla and one orangutan, with 397 new mutations.  Extending the human parental-age model to these apes, it found their yearly rates about 1.5 times the human rate and used them to date the human-chimp split at 6.6 million years.  The article uses its rates and dates, and notes how few families they rest on.

1. 37a.

   Section Abstract:  “The yearly trio-based mutation rate estimate of around 0.43 × 10−9 is markedly lower than previous indirect estimates of about 1 × 10−9 per year from phylogenetic comparisons of the great apes calibrated by fossil evidence.”  “and by a factor of 1.48 ± 0.08 for the three species combined. These estimates suggest an appreciable slowdown in the yearly mutation rate in the human lineage that is likely to be recent as genome comparisons almost adhere to a molecular clock. If the nonhuman rates rather than the human rate are extrapolated over the phylogeny of the great apes, we estimate divergence and speciation times that are much more in line with the fossil record and the biogeography.” ↩

Sanford, John et al.  “The waiting time problem in a model hominin population.”  Theoretical Biology and Medical Modelling 12:18.  2015.  A computer simulation of how long a hominin population needs to establish a short, specific string of DNA letters.  It modified Mendel's Accountant so that a starting string and a target string could be set, simulated a population of at least 10,000 with 20-year generations and very strong selection, and found that a two-letter string takes on average 84 million years and a five-letter string 2 billion years.  Sanford, a former Cornell plant geneticist, is the leading young-earth writer on genetics.  The article uses its results and its own statement of when the waits shorten.

1. 38a.

   Page 1:  “We simulated a classic pre-human hominin population of at least 10,000 individuals, with a generation time of 20 years, and with very strong selection (50 % selective elimination).”  “To establish a string of two nucleotides required on average 84 million years. To establish a string of five nucleotides required on average 2 billion years.”  “Routine establishment of specific beneficial strings of two or more nucleotides becomes very problematic.” ↩

Durrett, Rick, and Deena Schmidt.  “Waiting for two mutations:  with applications to regulatory sequence evolution and the limits of Darwinian evolution.”  Genetics 180(3):1501–1509.  2008.  A mathematical paper from Cornell on how long a population waits for two specific mutations when the first gives no benefit, applied to gene-control sites in fruit flies and humans and set against Michael Behe's arguments.  The article uses its human result as the mainstream counterpart to Sanford's.

1. 39a.

   Page 1501:  “for humans with a much smaller effective population size, this type of change would take >100 million years.”  Page 1507:  “Multiplying by 25 years per generation gives 216 million years.”  “Our previous work has shown that, in humans, a new transcription factor binding site can be created by a single mutation in an average of 60,000 years”. ↩

Carter, Robert W.  “Genealogical vs phylogenetic mutation rates:  answering a challenge.”  Proceedings of the Ninth International Conference on Creationism, 168–180.  2023.  A conference paper by a young-earth geneticist at Creation Ministries International, defending the use of fast family-measured mitochondrial rates for a young human timescale and modelling mutation accumulation with Mendel's Accountant.  In passing it states how a young-earth model reads the great-ape dates.  The article uses that statement.

1. 40a.

   Page 172:  “As far as timing the rise of the great ape lineages, all they are doing is uncovering the differences God built into their initial genomes. One of the basic premises of creation thought is that God designed hierarchically (Cserhati and Carter 2020), so some pairs of created groups are necessarily more similar than others and uncovering those differences does nothing to address the creation-evolution debate.” ↩

The split article's arithmetic.  New mutations per child follow Kong and colleagues' measured rise with the father's age, applied to the fathers' ages of the Masoretic text from Adam to Abraham, which gives about 2,000 new mutations per lineage.  From Abraham to today, 145 to 168 generations at today's rate add about 5,000 to 5,800 more.  The total, about 7,000 to 7,800 per lineage, is 0.040 to 0.045 percent of 35 million differences for both lineages together.  Making them all by mutation would need 2,200 to 2,500 times today's rate.  Details in The Human-Chimp Split and the Mutation Rate. ↩

The split article's arithmetic.  If several different strings, or several different places, would each serve equally well, a usable string appears that many times as often, and the expected wait falls by the same factor.  Within 6 million years, Sanford's 84 million years for a two-letter string needs about 14 equally good targets, and his 2.31 billion years for a five-letter string needs about 385. ↩

Herculano-Houzel, Suzana.  “The remarkable, yet not extraordinary, human brain as a scaled-up primate brain and its associated cost.”  Proceedings of the National Academy of Sciences 109(Suppl 1):10661–10668.  2012.  A review by the neuroscientist whose laboratory created the isotropic fractionator, a way of counting brain cells from a suspension of free nuclei.  It argues from those counts that the human brain, with about 86 billion neurons, follows the same scaling rules as other primate brains, and that the energy cost of neurons may explain why great apes have smaller brains than their bodies would predict.  This page uses it for the size of the difference and for the continuity argument.  Mirror:  PMC

1. 43a.

   Section Human Brain as a Scaled-Up Primate Brain:  “Remarkably, at an average of 86 billion neurons and 85 billion nonneuronal cells ( 25 ), the human brain has just as many neurons as would be expected of a generic primate brain of its size”. ↩

2. 43b.

   Section Cost of Being Human:  “Humans are not the largest living primates: Gorillas overlap with or exceed humans in body size, but their brains amount to about one-third of the size of the human brain”. ↩

Sockol, Michael D. et al.  “Chimpanzee locomotor energetics and the origin of human bipedalism.”  Proceedings of the National Academy of Sciences 104(30):12265–12269.  2007.  A laboratory study that measured oxygen consumption, gait and forces in adult chimpanzees walking on treadmills on two legs and on four, and in humans walking.  It found human walking far cheaper than either chimpanzee gait, and attributed the saving to the more extended human hip and longer hind limb.  This page uses its headline comparison.  Mirror:  PMC

1. 44a.

   Section Abstract:  “Furthermore, human walking is ≈75% less costly than both quadrupedal and bipedal walking in chimpanzees.” ↩

Fitch, W. Tecumseh et al.  “Monkey vocal tracts are speech-ready.”  Science Advances 2(12):e1600723.  2016.  An x-ray video study of the vocal tract of a living macaque during calls, facial displays and feeding, with the measured shapes fed into a computer model of speech.  It found that the monkey tract can make a wide range of vowels, so the limit on primate speech is in the brain, not the throat.  The study is of macaques, not chimpanzees.  Mirror:  PMC

1. 45a.

   Section Introduction:  “Despite repeated attempts, no nonhuman primates have ever been trained to produce speech sounds, not even chimpanzees raised from birth in human homes”. ↩

2. 45b.

   Section Discussion:  “We conclude that if a macaque monkey had a brain capable of vocal learning and combinatoric operations over speech sounds, its vocal tract would be able to produce clearly intelligible speech.” ↩

Whiten, Andrew.  “The scope of culture in chimpanzees, humans and ancestral apes.”  Philosophical Transactions of the Royal Society B 366(1567):997–1007.  2011.  A review by the primatologist who led the 1999 study that pooled records from chimpanzee field sites to identify their traditions.  It compares chimpanzee and human culture under about a dozen headings, from the number and spread of traditions to the fidelity of copying and cumulative change.  It finds real culture in chimpanzees and a large gap in its scope and accumulation.  Mirror:  PMC

1. 46a.

   Section 2(a)(i), Existence of multiple and diverse traditions:  “Human culture differs from this in encompassing countless variations, spanning a huge diversity of behaviour, technology, ideas and much else.  No other species comes close to this.”  “led to an initial count of 39 traditions”. ↩

2. 46b.

   Section 2(a)(iv), Cumulative cultural evolution:  “Others argue for the existence of cumulative culture in animals [ 7 ], but the cases discussed appear rudimentary compared with the achievements of humans”. ↩

Robson, Shannen L., and Bernard Wood.  “Hominin life history: reconstruction and evolution.”  Journal of Anatomy 212(4):394–425.  2008.  A review of the timing of birth, growth, reproduction and death in living great apes and humans, and of what fossils can show about when the human pattern arose.  Its Table 2 compiles values for wild female apes from long-term field studies and for women in foraging societies such as the Ache and !Kung.  Mirror:  PMC

1. 47a.

   Table 2:  Chimpanzee:  maximum life span 53.4 years, age at first birth 13.3, age at weaning 4.5, interbirth interval 5.46.  Modern human foragers:  85, 19.5, 2.8 and 3.69. ↩

Ross, Marcus R. et al.  “Human History from Adam to Abraham:  Integrating Paleoanthropology with a Young-Age Creation Perspective.”  Proceedings of the International Conference on Creationism 9:66–87.  2023.  The fullest recent young-earth treatment of the human fossil record, presented at the movement's main technical conference by three young-earth scientists including Todd Wood of Core Academy of Science.  It sorts fossils into human and non-human by signs of advanced behaviour and places all of them after the Flood.

1. 48a.

   Page 68:  “Specifically, we recognize six distinct categories of evidence that attest to advanced, human cognition and therefore the image of God.”  “3. The crafting of unnecessary objects that attest to artistic creativity or preferences … 5. Intentional burial of the dead”. ↩

Ma, Shu-Ping et al.  “Long noncoding RNA HBBP1 enhances γ-globin expression through the ETS transcription factor ELK1.”  Biochemical and Biophysical Research Communications 552:157–163.  2021.  A cell-culture study in which the authors overexpressed HBBP1 (made far more of its RNA than normal) in cultured HUDEP-2 cells and found that γ-globin rose at both the RNA and protein level.  The authors also report that the transcription factor ELK1 binds the γ-globin promoter directly.  The article cites it to set this result, which adds HBBP1 rather than removing it, against Huang's deletion of the same region.

1. 49a.

   Section Abstract:  “When HBBP1 was overexpressed, γ-globin expression was increased at the transcript and protein levels in HUDEP-2 cells.”  “Surprisingly, ELK1 also directly bound to and activated the γ-globin proximal promoter.”  This is a gain-of-function result (adding more of a molecule rather than removing it) in cultured cells, and the second sentence is the authors' own report that ELK1 acts on γ-globin directly, which breaks the chain the first sentence would need.  It does not test the endogenous locus and does not bear on Huang's deletion, which does. ↩