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The chromosome 2 fusion model of human evolution?

One of the most popularized molecular arguments for human-primate evolution is the hypothetical prehistoric head-to-head fusion of two primate chromosomes (corresponding to 2A and 2B in chimpanzee) to form human chromosome number 2. 1,2


Popular reviews on this subject often include a simplified drawing depicting how the putative fusion of two small acrocentric5 ape-like precursor chromosomes could have fused end-to-end to form the larger human chromosome 2, as shown in figure 1. In support of this hypothetical model of chromosome fusion, it is claimed that human chromosome 2 contains two key features that support the model. The first feature purportedly depicts the fusion event and contains genomic sequences representing a head-to-head fusion of telomeres, the highly specific endcap DNA repeat motifs (TTAGGG)n located at the termini of linear mammalian chromosomes.6


The second key site purportedly represents a cryptic, non-functional centromere that was silenced following the fusion event (because a single functional centromere is required for chromosome stability and function). According to these claims, this fusion event accounts for the fact that humans have only 46 (2N) chromosomes and the great apes 48 (2N). Actually, the diploid genomes of gorilla, chimpanzee and orangutan have 48 but some gibbons have 44, and one Malaysian ape has 50.7


Examining the existing genomic evidence for fusion


Of the two genomic features that are claimed to support the fusion model, the primary evidence used is the presence of a reputed fusion site. This site is located in a pericentric region (meaning it is close to the present functional centromere) on the long arm of human chromosome 2.


In his recently published book, the Nature article Miller cites as proof for the fusion states only that “Human chromosome two is unique to the human lineage in being the product of a head-to-head fusion of two intermediate-sized ancestral chromosomes” and provides no evidence for this conclusion. However, Fairbanks offers more detail and claims that there appears to exist a fusion site involving a set of 158 telomere sequences, and, of the 158 repeats, he notes only 44 sets can be manipulated to achieve perfect telomere consensus sequences. Another example of the same claim from a book popularizing human evolution is as follows:

“The DNA sequences in the human chromosome are exactly as expected from this scenario. Telomeres consist of many repeats of the nucleotide sequence TTAGGG, and at the fusion point of the human chromosome, where the two telomeres fused, this sequence is found ‘head to head’. The functional centromere in chromosome 2 lines up with the chimpanzee chromosome 2p13 chromosomal centromere. The remains of the redundant centromere from one of the ancestral ape chromosomes can also be found.”3

As we will document, these popular claims of resounding evidence for a telomere fusion producing human chromosome 2 are, for the most part, unsupported by the scientific literature and actual DNA sequence information (see companion paper). However, we will first briefly clarify the structure and nature of telomeres as to what would be expected if such a fusion event occurred.

Telomeres are typically found at the ends of linear eukaryotic chromosomes and confer stability by preventing fusion via a ‘capping’ function. The telomere region involves a complex and dynamic framework of DNA motif repeats, structural loops, structural and functional RNAs and a wide variety of proteins.6 In a fusion event as described in the human chromosome 2 model, the end result should produce two identifiable telomeres characterized by a specific repeat motif and oriented in a head-to-head configuration. A certain genomic landscape must be present if two chromosomes fused head-to-head as claimed by the current evolutionary model. The consensus 5’ to 3’ telomere motif in humans, chimps, apes, and mammals in general, is (TTAGGG)n and typically occurs in perfect tandem for stretches of DNA from about 10 to 15 kb (10,000 to 15,000 bases) and contains 1,667 to 2,500 telomere repeats at each chromosome end. In a head-to-head fusion of two chromosomes, we would expect at least 5,000 bases of (TTAGGG)n repeats in tandem, albeit in a slightly degenerate state, given a supposed ~1 to 5 million years of evolution since the fusion event occurred. At the point of fusion, we would also expect the orientation of the plus-strand repeat to change to the reverse complement (CCCTAA)n, which should also occur in near-perfect tandem for approximately 5,000 or more bases.

In reality, the putative fusion site is but a vague shadow of what should be present given the model in question. One of the major problems with the fusion model is that, within the 10 to 30 kb window of DNA sequence surrounding the hypothetical fusion site, a glaring paucity of telomeric repeats exist that appear mostly as independent monomers, not tandem repeats. Based on the predicted model, thousands of intact motifs in tandem should exist. For the TTAGGG repeat to the left of the fusion site, less than 35 motifs exist, a normal human telomere would typically have 1667 to 2500.6 For the CCCTAA reverse complement sequence, to the right of the fusion site, less than 150 telomere motifs can be found. Another problem with these two motifs, that we document in our companion research paper, is that their occurrences are found scattered throughout both sides of the fusion site where they would not be expected.

In attempting to correlate rates of evolutionary change with the extreme degeneracy observed in the putative fusion region, they claimed that the “head-to-head arrays of repeats at the fusion site have degenerated significantly from the near perfect arrays of (TTAGGG)n found at telomeres.” They also stated, “if the fusion occurred within the telomeric repeat arrays less than ~6 Ma, why are the arrays at the fusion site so degenerate?”


Because of the ‘degenerate’ nature of the DNA sequence data in this region, a variety of creative and manipulative approaches have been used to make the data look more telomere-like than it actually is. For example, Fairbanks claims that 44 out of 158 repeats match (28%) and that the rest of the sequences are ‘close’.Fairbanks’ data include several additional perfect motifs immediately surrounding the fusion site that do not actually appear in the current GenBank accessions for this region.3Unfortunately, Fairbanks did not cite the accession number(s) for his fusion site sequence printed in his text. When the reading frame is corrected at various motifs near the fusion site, hardly any telomere sequences can be obtained. Fairbanks assumes that major differences between a perfect telomere and the existing sequence are the result of the accumulation of numerous insertions, deletions and other mutations, a post-hoc explanation that lacks strong DNA evidence.

Another problem for the fusion theory is the presence of a wide variety of genes throughout the fusion region. At present, no known protein coding genes have been found in the 10 to 15 kb tandem 6-base (TTAGGG) repeat terminal region of human telomeres.9 In an analysis of a 614 kb area encompassing the postulated chromosome fusion site, Fan et al. found evidence of “at least 24 potentially functional genes and 16 pseudogenes”.10 In the 30-kb region directly encompassing the fusion site, which should definitely be devoid of any genes, there exists two actively transcribed genes, each in a flanking position in regard to the fusion site (one on each side). There are also at least two other genes in the immediate vicinity of the fusion site thought to be inactive due to frame shift mutations. However, research related to the human ENCODE (Encyclopedia of DNA Elements) project has shown that many genes thought to be inactive (pseudogenes) are actually functional.11

If the telomere motifs that populate internal areas of chromosomes serve some important, yet unknown function, the chromosome fusion model actually impedes research aimed at determining possible function in these regions.

Assuming that two telomeres exist in a head-to-head fusion produces another major problem, namely that telomeres are designed to prevent fusion. Broken chromosomes at any location immediately invoke the cell’s double-stranded DNA repair machinery where the aberrant fusion of fragments actually triggers cell fault tolerance mechanisms.6 In the case of an aberrant fusion, a senescence response or programmed cell death (apoptosis) cascade is normally triggered, effectively eliminating the damaged cell from the system.

A cell with telomeres that have progressively shortened over time and reached a threshold length will also activate the double-stranded DNA repair machinery; inducing cell senescence and/or death. When in certain types of germline cells, telomerase adds telomere repeats to shortened telomeres, chromosomes are ‘healed’ and can again become stable. The telomeres cap the ends of linear chromosomes and effectively prevent fusion or trigger cell elimination if the telomere is shortened to a certain point, damaged, or aberrantly fused.6


Examining the evidence for a cryptic centromere


Yet another major problem with the fusion model is the lack of evidence for a cryptic second centromere site. Immediately following the supposed head-to-head telomere fusion, there would have existed two centromeres in the newly-formed chimeric chromosome, one from each of the two fused chromosomes. This type of event had to occur in a cell lineage of the germ-line to be heritable, and one of the centromeres would have had to be immediately eliminated or at least functionally silenced for cell division to progress normally. Evolutionists explain the lack of a clearly distinguishable non-functional secondary centromere by arguing that two centromeres would result in major instability when chromosomes pair up during cell division and consequently would be rapidly selected against. According to the evolutionary model, selection would continue until the second centromere was completely non-functional.

However, the evidence for a second remnant centromere at any stage of sequence degeneracy is negligible. As Fairbanks noted, “Fusion at the telomeres should have left two centromeres in the ancient fused chromosome, but there is only one now.”3 He then evaluated the “evidence that a centromere was once present at a second site”. The supposed evidence includes the finding that “every human and great-ape chromosome centromere contains a highly variable DNA sequence that is repeated over and over, a 171 base-pair sequence called the Alphoid sequence.”3 Fairbanks adds that scientists have “searched for Alphoid sequences in human chromosomes and found them at every centromere, as expected. They also found Alphoid sequences at the site in human chromosome 2 where the remnants of this second centromere should be. These remnants are evidence of a now-defunct centromere.”3

The main problem with Fairbank’s claim is that alpha-satellite DNA or alphoid DNA, although found in centromeric areas, is not unique to centromeres and is also highly variable. Because highly variable alphoid DNA is also commonly found in non-centromeric regions of human chromosomes, their presence does not indicate the remnants of a degenerate centromere.

Based on the reasoning of Fairbanks and others promoting the human chromosome 2 fusion model, one could conclude that human chromosomes contain literally hundreds of degenerate centromeres. As a result, locating a candidate alphoid region to erroneously support the presence of a degenerate centromere on chromosome 2 would not be unexpected or difficult to do, and does not support a cryptic centromere claim. In the companion research paper supporting this review, we show that the alphoid sequence in question does not align closely with known functional centromeric human DNA.

Despite the variation, there is enough sequence similarity for fluorescently labeled alphoid probes to hybridize to most classes of alphoid sequence in stretched chromosomal fibers. Another problem is that, although research has been done on some primates, no systematic study of centromeres exists to determine how common alphoid DNA is in mammals.13 Baldini et al.found that the “highest sequence similarity between human and great ape alphoid sequences is 91%, much lower than the expected similarity for selectively neutral sequences.”13 Alphoid regions, in contrast to many classes of DNA sequences, are not well-conserved among mammalian taxa and even show high levels of diversity between chromosomes in the same genome.14


Cytogenetic anomalies argue against fusion


Other problems with the fusion theory include the fact that standard cytogenetic techniques, such as C-banding, have detected significantly less heterochromatic centromeric DNA on the long arm of human chromosome 2 than predicted by the fusion model. Evolutionists claim this is because the “bulk of the centromeric repetitive DNA has been lost”.13 Conversely, it is more likely that the so-called cryptic centromeric DNA never existed.

Not only does the DNA sequence at the putative cryptic centromere site argue against fusion, but a comparison of the chimp and human chromosomes reveals that the centromere in human chromosome 2 is in a very different location than predicted by a fusion event as shown in part two of this study. This necessitates an implausible series of events, including the loss of both chimp centromeres when chromosomes 2A and 2B fused, and the rapid evolution of a new centromere to provide functionality to human chromosome 2.

Mutations of the magnitude needed to support a fusion event pose serious cytogenetic problems both for the organism during regular somatic cell growth related to mitosis and during the meiotic events occurring in the germ-line tissues. Proper alignment requires the near-identical structure of each pair so that each chromosome aligns only with its sister chromosome. Chromosomal fusion is one major common cause of infertility. If meiosis does occur despite the aberration, the embryo produced from fertilization of these gametes typically self-aborts.15

Do fusions lead to new species?


Evolutionary scientists believe an ape-like ancestor evolved into a new species, called Homo sapiens, along with a major genomic fusion event. While the order of genes and their spatial relationship in the nucleus can affect gene expression, no new information or genes are added by fusing two existing chromosomes, because only the gene packaging is altered. However, the information content of the genome can still be strongly affected. Chromosomal fusion has been identified in a variety of animal taxa, such as ruminants (sheep, goats and cattle) that were phenotypically similar compared to normal animals in their genera although reproductive isolation did occur.16 Evolutionists postulate that such an event may have contributed to a reproductive barrier in early evolving humans who, although they may have had a new karyotype, were still closely related to apes.

Actually, the fusion theory creates problems for Darwinists due to the fact that a complete absence of humans with 48 chromosomes exists. Although very rare, chromosome fusions do occasionally occur in humans but are not easily passed to offspring.


Fusion site DNA sequence analysis

Our DNA sequence analysis confirmed conclusions reached by Fan et al. The putative fusion site is ‘highly degenerate’ and a vague shadow of what should be present given the model proposed.15 One of the major problems with the fusion model is that, within the 20- to 30-kb window of DNA sequence surrounding the hypothetical fusion site, there is a glaring paucity of telomeric repeats, and those that are present are mostly independent monomers, not tandem repeats. In fact, many of the motifs in the 30-kb region surrounding the putative 2qfus site are not only isolated monomers, but are separated by up to several thousand bases of DNA.

Even while completely disregarding a consensus 6-base reading frame when iterating through the repeats, for the left (plus strand) side of the fusion site, there are only 34 intact TTAGGG motifs (table 1). This analysis uses a generous allowance of 92,690 bases to the left of the fusion site where the first TTAGGG repeat is found on BAC RP11-395L14, well beyond the size of any normal human telomere. 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. Recombination, the most likely theoretical source of sequence shuffling leading to the fusion site degeneration would therefore be less of consideration. Also, based on the predicted model, little, if any TTAGGG motifs should exist on the plus strand to the right of the fusion site. However, 18 intact TTAGGG motifs are found on the right of the fusion site; 35% of the total number of TTAGGG motifs located within a generous 156,911 base window surrounding the fusion site.

Table 1. Telomere DNA sequence data for the 177 Kb BAC containing the fusion site.

The reverse complement telomere sequence (CCCTAA) should be present in near-perfect tandem to the right of the fusion site. Like the TTAGGG motif, one would expect approximately 1667 to 2500 CCCTAA motifs if an end-to-end fusion occurred. However, only 136 intact motifs exist to the right of the fusion site, with the last CCCTAA on the BAC clone terminating at 64,221 bases to the right of the fusion (table 1). Again, this very generous stretch of sequence is much longer than a normal human telomere, and contains a paucity of motifs. In similar fashion to the TTAGGG forward motif, the CCCTAA motif was also located on both sides of the fusion site. Our analysis located a total of 18 occurrences of the CCCTAA motif (12% of the total) scattered throughout the opposite side of the fusion site, where it would not be expected to be found. In other words, both the forward and reverse complement of the telomere motif populate both sides of the fusion site. As a side note, the GC content of the 177 kb region encompassing the putative fusion site is significantly higher (45%) than the average (40%) for chromosome 2 (table 2).

Table 2. Telomere DNA sequence data for the for the assembled euchromatic sequence of human chromosome 2.

A complete scan of the 237+ million bases of the assembled euchromatic sequence of chromosome 2 using the Skittle Genome Viewer software package showed that the entire landscape, from end to end, is populated with TTAGGG and CCCTAA motifs. Small, isolated dense clusters of telomere motifs occurred in at least 5 internal locations (data not shown). A complete iteration of the entire plus strand sequence of chromosome 2 (Per script written by Tomkins) indicated a total number of ‘TTAGGG’ and ‘CCCTAA’ occurences at 45,450 and 45,770, respectively (table 2). These numbers are roughly equal, indicating that both the forward and reverse orientation of the telomere motif occurs quite frequently at internal sites across the length of chromosome 2. These numbers indicate that a total of at least 547,320 internal bases on chromosome 2 are composed of widely distributed intact telomere motifs.

An important attribute associated with these internal telomere motifs is that they are largely monomeric. Of the 52 intact TTAGGG motifs on both sides of the fusion site, only three tandem occurrences were found, with the rest existing as independent monomers. Of the 154 intact CCCTAA motifs on both sides of the fusion site, eighteen tandem motifs were found, with the rest appearing as independent monomers. Although the density of motifs and dimeric repeats increases somewhat within the immediate vicinity of the putative fusion region, their positions in the reading frame from one 6-bp telomeric repeat to the next are erratic (not in frame).

Because of the extreme paucity of telomeric repeats, their largely monomeric condition, and their ubiquitous presence on both sides of the supposed fusion site, there exists little data to indicate that they may have once formed 10- to 15-kb stretches of perfect, tandem 6-base repeats. The 2qfus sequence is clearly degenerate beyond the point of indicating that intact telomeres once existed. Given the location in a region of suppressed pericentric recombination, one would expect a considerably higher amount of telomere sequence preservation if the model was tenable.

In attempting to correlate rates of evolutionary change with the extreme degeneracy observed in the putative fusion region, one research group concluded that “the head-to-head repeat arrays at the RP11-395L14 fusion site have significantly degenerated from the near perfect (TTAGGG)n arrays found in telomeres.”15 This caused them to raise the question, “Why are the arrays at the fusion site so degenerate if the fusion occurred within the telomeric repeat arrays less than ~6 Mya?”15


A more valid explanation for the telomere-like features present at the putative fusion site is that they may represent some form of a distinct genomic motif. To test this idea, a 798-bp fragment (figure 2) encompassing the fusion site and the region where the telomeric motifs are more densely populated was used as a query subject in a BLAT17 search on the most recent build of the human genome (v 37.1; with masking disabled. The results revealed a total of 159 significantly placed hits throughout the genome on human chromosomes 1–11, 15, 18–20, X and Y.


. BLASTN results against the most recent builds of the human and chimpanzee genomes using a 798 bp human query sequence representing the core of the chromosome 2 fusion region.


To verify the BLAT results and to identify homologous sites in the chimpanzee genome, the BLASTN algorithm was used (with no masking or gap extension) for comparisons between the 798-bp core 2qfus sequence and the most recent builds of the human (v 37.1) and chimp (v 2.1) genomes maintained at NCBI ( Although the BLASTN query against the human genome was more data intensive than the index-based BLAT search, the results produced a total of 85 significantly placed hits on all human chromosomes except chromosomes 13, 16 and 17 (1–12, 14, 15, 18–22, X and Y). While the number of hits was reduced, compared to BLAT, more chromosomes with homologous sites were identified with the BLASTN search because of the more direct nature of the algorithm (figure 3). Interestingly, human chromosomes 2, 16, 21 and 22 were peppered with the ‘fusion site’ sequence over the length of their entire euchromatic landscape (figure 3).

When the 798-bp core fusion sequence was BLASTN queried against the chimpanzee genome, the significantly placed hit count was reduced to 19, only 22% of the amount observed in the human genome. This is a startling find in light of the wide-spread claims that the human and chimpanzee genomes contain DNA sequence that is supposedly 96 to 98% similar, a claim perhaps related to the fact that the human genome was used as a scaffold to build the chimpanzee genome.8 In addition, the human-chimp hit locations did not show strong synteny, as only 13 of the 19 hits (68%) shared visually similar locations in the genome (on chimpanzee chromosomes 1, 2B, 8, 9, 12, 14, 15, 18, 20 and 22).

There is no real evidence for DNA homology between human and chimpanzee for the 798-bp core fusion sequence. The alignment data also severely calls into question claims of high overall sequence similarity of 96 to 98% between the genomes.


Examining DNA sequence for a cryptic centromere


Following the supposed head-to-head telomere-based fusion of two smaller chromosomes, two centromeres would have had to exist in the newly formed chimeric chromosome, one from each of the two fused chromosomes. According to the evolutionary model, sequence degeneration plus selection would continue until the second centromere was completely non-functional. The DNA evidence in question is based on the fact that human, great-ape, and other mammalian centromeres are composed of a highly variable class of DNA sequence that is repeated over and over called alpha-satellite or alphoid DNA.18Alphoid DNA, although found in centromeric areas, is not unique to centromeres and is even highly variable between homologous regions throughout the same mammalian genome.18


PhyML result with tree rendering by TreeDyn involving the nine Chromosome 2 alphoid sequences (prefix = AF) identified by accession numbers submitted to GenBank by Lonoce et al. (2000; unpublished—see genbank accessions at The 171 bp consensus alphoid is included as a monomer and as repeats (2X, 3X, 4X). Two human alphoid sequences representing functional centromeric fragments identified by accession number are also included (prefix = M).


The basic human alphoid monomer is a 171-base motif represented by a patented synthetic consensus sequence in Genbank (Acc. # CS444613). There also exists two small sequenced clones representing alphoid repeats with proven cellular centromere function.19 Nine different alphoid fragments in the cryptic centromere site associated with the purported chromosome 2 fusion event were also sequenced and submitted to GenBank by an Italian laboratory (see figure 4 for accession numbers). In total, we downloaded and analyzed all 12 of these sequences for similarity to each other and individually for genome-wide homology.

Using the BLAT tool on the most recent version (v 3.7) of the human genome assembly, the nine italian lab alphoid sequences elicited the strongest hits at the chromosome 2 putative cryptic centromere site for all accessions. This confirmed that they were cloned from this region of the genome. The consensus 171-bp alphoid sequence aligned at the cryptic centromere site with 90.6% identity, supporting the conclusion that the site contains alphoid-like sequences.

However, the concern is not if this location contains alphoid sequences that are known to be ubiquitous in the human genome, but how similar these sequences are to each other and to known functional centromeric alphoid repeats. Alphoid sequences located at centromeres form long series of repeat patterns that are very homogeneous in their repetitive structure, producing distinctive higher-order patterns. Alphoid regions that are non-centromeric are more diverse in their monomer content and form higher order patterns with different characteristics compared to centromeres. At present, there are five known supraclasses of human alphoid monomers that combine in various combinations.There is also evidence from research in progress that alphoid monomer classes themselves can be broken down further into specific subfragments that may be present in the genome by themselves or as a sub-fragment in an alphoid repeat region (Tomkins, unpublished data).

In a human alphoid multiple-sequence alignment analysis, we combined the two functional centromeric alphoid sequences with the set of nine Italian alphoid sequences along with the consensus 171-base alphoid sequence in our data set (figure 4). We also created tandem repeats of the consensus 171-base alphoid sequence representing repeats of 2X to 4X in length as individual sequences. Alignments were conducted using the MUSCLE software packagethen refined using the Gblocks program.23

The human alphoid alignments clearly revealed dissimilarity between alphoid sequences and distinct patterns of clustering. Patterns of similarity were computationally evaluated using PhyML24 with tree rendering performed by TreeDyn (figure 4).25 Four major groups were distinguished by the PhyML analysis with the functional centromere sequences clustering by themselves and not with the alphoid sequences located at the purported cryptic centromere site on chromosome 2. The sequences at the cryptic centromere site are clearly a diverse mixture of alphoid monomers, forming three separate groups and not distinctly representative of functional centromeric DNA.

Multiple reports involving both hybridization and sequence-based research of alphoid/centromere similarity between humans and apes have found virtually no apparent evolutionary homology, except for moderate similarity on the X-chromosome centromere.20,27 Baldini et al. found that the “highest sequence similarity between human and great ape alphoid sequences is 91%, much lower than the expected similarity for selectively neutral sequences.”28 Alphoid regions, in contrast to many classes of DNA sequences, are not well-conserved among taxa and even show high levels of diversity between chromosomes in the same genome.18 When the human alphoid sequences in our data set were queried against the chimpanzee genome using both BLAT and BLASTN, we were unable to obtain a single significant hit, verifying the extreme dissimilarity observed in alphoid motifs between taxa. These data corresponded well with several decades of previous research by multiple labs, discussed above.



  1.  Yunis, J.J. and Prakash, O., The origin of man: a chromosomal pictorial legacy, Science 215:1525–1530, 1982. Return to text.
  2.  Ijdo, J.W. et al., Origin of human chromosome 2: an ancestral telomere-telomere fusion, Proc. Natl. Acad. Sci. 88:9051–9055, 1991. Return to text.
  3.  Fairbanks, D.J., Relics of Eden, Quotations and analyses are in reference to Chapter 1, Fusion, Prometheus Books, Amherst, N.Y., pp. 17–30, 2007. Return to text.
  4.  Miller, K.R., Only a Theory: Evolution and the Battle for America’s Soul, Viking, New York, 2008. Return to text.
  5.  Acrocentric chromosome has one arm that is considerably shorter than the other arm. The ‘acro-’ in ‘acrocentric’ refers to the Greek word for ‘peak’. The human genome contains five acrocentric chromosomes: 13, 14, 15, 21 and 22. The naming system of chimpanzee chromosomes ‘2A’ and ‘2B’ was first used by McConkey, E.H., Orthologous numbering of great ape and human chromosomes is essential for comparative genomics, Cytogenet Genome Research105:157–158, 2004. Prior to that, the chimpanzee chromosomes were numbered according to size, as is the system used for all other species. Return to text.
  6.  Tomkins, J. and Bergman, J., Telomeres: implications for aging and evidence for intelligent designJ. Creation 25(1):86–97, 2011. Return to text.
  7.  Jauch, A. et al., Reconstruction of genomic rearrangements in great apes and gibbons by chromosome painting, PNAS 89:8611–8615, 1992. Return to text.
  8.  Fan, Y. 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 12:1651–1662, 2002. Return to text.
  9.  Devanshi, J. and Promisel J.P., Telomeric strategies: means to and end, Annu. Rev. Genet. 44:243–69, 2010. Return to text.
  10.  Fan, Y. et al., Gene content and function of the ancestral chromosome fusion site in human chromosome 2q13-2q14.1 and paralogous regions, Genome Research 12:1663–1672, 2002. Return to text.
  11.  The ENCODE Project Consortium, Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project, Nature447:799–816, 2007. Also see the June 2007 (vol 17) issue of Genome ResearchReturn to text.
  12.  Wells, J., The Myth of Junk DNA, Discovery Institute Press, Seattle, WA, 2011. Return to text.
  13.  Baldini, A. et al., An alphoid DNA sequence conserved in all human and great ape chromosomes: evidence for ancient centromeric sequences at human chromosomal regions 2q21 and 9q13, Human Genetics 90:577–583, 1993. Return to text.
  14.  Alkan, C., et al., Genome-wide characterization of centromeric satellites from multiple mammalian genomes, Genome Research 21:137–145, 2011. Return to text.
  15.  Alberts, B. et al., The cell cycle; in: Molecular Biology of the Cell, 5th ed., Garland Science, New York, pp. 1053–1114, 2008. Return to text.
  16.  Lightner, J.K., Karyotype variability within the cattle monobaramin, Answers Research J. 1:77–88, 2008. Return to text.
  17.  Alexander, D., Creation or Evolution: Do We Have to Choose? Monarch, Oxford, UK, p. 212, 2008. Return to text.
  18.  The Chimpanzee Sequencing and Analysis Consortium, Initial sequence of the chimpanzee genome and comparison with the human genome, Nature 437:69–87, 2005. Return to text.
  19.  Warren, R.L., Physical map assisted whole-genome shotgun assemblies, Genome Res. 16:768–775, 2010. Return to text.
  20.  Hughes, J.F. et al., Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content, Nature 463:536–539, 2010. Return to text.
  21. Return to text.


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