Chromosome 2 Fusion: Evidence for Common Ancestry or Design?

Introduction

Evolutionary scientists have long claimed that apes and humans descended from a common ancestor. One of the strongest arguments for common ancestry comes from human chromosome 2. While apes have 48 chromosomes, humans only have 46 chromosomes. Thus, if these two species are related, evolutionists must explain the difference in chromosomes. Human chromosome 2 is believed to provide the answer.

Human chromosome 2 has many shared features with chimpanzee chromosomes 12 and 13.[1] In fact, the resemblance is so close that chimpanzee chromosomes 12 and 13 are often referred to as 2A and 2B.[2] Thus, it is believed that after humans and chimpanzees diverged from their common ancestor, humans underwent a chromosomal fusion. This fusion resulted in chromosomes 2A and 2B being fused together to form what is now known as human chromosome 2. This would explain why apes have 48 chromosomes while humans only have 46 chromosomes. But what is the evidence that such a fusion event occurred? This paper will examine and critique the evolutionary claim that human chromosome 2 is the result of a fusion event.

Chromosomal Fusions

Are chromosome fusions possible? If so, how likely are they to occur? It is well documented that chromosome fusions do take place. However, these events are rare[3] and often “lead to disease, nonviability, sterility, or sterility of offspring.”[4] Yet, there are cases of chromosomal fusions that do not lead to these issues. One example has been found in yeast. According to research performed by Barbara Poszewiecka and her team, reducing the number of chromosomes in yeast “does not always have to lead to fatal genetic dysfunctions.”[5] While it is true that a reduction of chromosomes does not “always” lead to dysfunction, the likelihood of dysfunction is extremely high. Fazale Rana notes, “When the chromosome number in the sperm doesn’t match that of the egg, fertilization almost always results in either: (1) a nonviable zygote/embryo; (2) a viable offspring that suffers from a diseased state; or (3) a viable but infertile offspring. Again, it is possible, but extremely rare for the resulting offspring to be viable and fertile.”[6] Secondly, Poszewiecka’s study involved yeast, which is much different than a mammal. Therefore, it is difficult to apply this study to the supposed chromosome 2 fusion event in humans.

Another example of a non-deleterious chromosomal fusion comes from an endangered horse breed called Przewalski. This horse has 66 chromosomes, while domestic horses only have 64. It has been proposed that domestic horses had a common ancestor with Przewalski that had 66 chromosomes. After a fusion event, the resultant 64 chromosome horse spread its genetics throughout the population becoming fixed. The Przewalski horse and domestic horses can still interbreed and produce a fertile offspring. However, all other known cases of cross-breeding between the seven different species in the Equidae family, which all have different chromosome numbers, do not produce fertile offspring. Thus, the Przewalski horse is the exception and not the rule. Furthermore, the Equidae family shows that different numbers of chromosomes are more likely to lead to no offspring or non-fertile offspring, than it is to fertile offspring.[7]

Unlike yeast and the Przewalski horse, the fusion event of human chromosome 2 would have been a telomere-to-telomere fusion. According to Jeffrey Tomkins, “documented chromosome fusions in living mammals do not involve telomere-telomere fusions, but instead are composed of a type of sequence called satellite DNA (satDNA) in one of two fusion scenarios: (1) satDNA-satDNA or (2) satDNA-telomere sequence.”[8] In another paper, Tomkins elaborates further on this point:

In all documented extant mammalian chromosome fusions to date, satellite DNA (satDNA) is a key genomic feature comprising the breakage and subsequent fused sequence. In such cases, the junction is either demarcated by telomere-satDNA or satDNA-satDNA, typically involving centromeres or regions proximal to them. Chromosome fusions representing telomere-telomere signatures are not presently documented, except for the hypothetical fusion of human chromosome 2.[9]

Telomere-to-Telomere fusions are highly uncommon because if a telomere is “shortened to a certain point, damaged, or aberrantly fused,” a trigger goes off that results in cell death.[10] Thus, telomeres work to prevent fusions. Moreover, telomere-to-telomere fusion events have been documented in human cancer cells.[11] Thus, not only is a fusion event rare, but it is highly likely to lead to degradation and disease.

A second problem for the chromosome 2 fusion theory is that one must address how such a fusion spread throughout the population. What was the selective advantage of such a fusion, and how did it become fixed in the population? According to evolutionist Daniel Fairbanks, “Genetic drift… predicts that over many generations nearly every mutation or chromosomal rearrangement will eventually suffer one of two fates: it will either spread throughout the species until every member of the species has it, or it will disappear entirely from the species.”[12] Thus, Fairbanks argues that genetic drift explains how the fusion spread amongst the human population. But genetic drift does not explain the selective advantage the fused chromosome provided to our early ancestors over the others in their community. Fairbanks simply asserts that there must have been some advantage in order for it to have spread throughout the population. Genetic drift simply acknowledges that the fused chromosome spread throughout the population, but it does not explain why.

Another attempt to explain how the fusion spread throughout the population comes from BioLogos associate Dennis Venema. Venema proposes that perhaps one fusion event occurred that reduced the 48-chromosome genome down to 47. Later down the line, two relatives, who both had a copy of the fused chromosome, mated and produced an offspring “with two copies of the fused chromosome,” resulting in 46 chromosomes. This new 46 chromosome set spread throughout the population. Venema explains, “Since either a 48-pair set or a 46-pair set is preferable for ease of cell division, this population will either eventually get rid of the [47-pair set], or by chance will switch over completely to the ‘new’ form, with everyone bearing 46 chromosome pairs.”[13] There are several problems with this hypothesis.

First, Venema proposes “chance” as the mechanism that switched the species over to 46 chromosomes. But chance does not explain what selective advantage 46 chromosomes provided to the organism. Second, if the 48-pair set had a selective advantage over the 47-pair set, would not the 47-pair set have been weeded out by natural selection before two relatives could mate to pass on the 46-pair set? Venema states, “A fusion does not precipitate a speciation event, but rather the individual with the fusion remains a part of his or her population, and able to interbreed, even if with reduced fertility.”[14] But if the fusion results in “reduced fertility,” this makes it much more difficult to become fixed in the population. Why would natural selection select a fusion that causes reduced fertility? This is the opposite of what one would expect from natural selection. Thus, natural selection works against Venema’s scenario.[15]

Despite the odds, if we assume that chromosome 2 is the result of a fusion event, what should we expect to find? Evolutionist Ken Miller rightly states that if a fusion event occurred, it “would leave distinct marks in the new chromosome.”[16] These distinct marks consist of telomere tandem repeats found in the middle of chromosome 2 at the fusion site and the presence of a second centromere.

Internal Telomere

The first argument that chromosome 2 is the result of a fusion event comes from the finding of internal telomere sequences at the fusion site. Telomeres are sequences of DNA that are found at the end of chromosomes. Typically, telomeres consist of a six-base sequence TTAGGG that repeats over and over up to 2,500 times.[17] Telomeres serve as “end-caps” on the chromosome to keep the chromosome intact so that it does not unravel (similar to caps on the ends of shoelaces).[18] When one end of a chromosome breaks off, it leaves the telomeres exposed. It would be this exposed end that could fuse together with another chromosome. Thus, if two chromosomes with broken ends existed in a species, it makes sense that these two chromosomes would fuse together. This fusion would result in telomeres in the middle of the new chromosome, where they are not supposed to be. Therefore, if 2A and 2B fused together, scientists should find telomere sequences at the fusion site on human chromosome 2. According to evolutionist Francis Collins, telomere sequences “are found right where evolution would have predicted, in the middle of our fused second chromosome. The fusion that occurred as we evolved from the apes has left its DNA imprint here. It is very difficult to understand this observation without postulating a common ancestor.”[19]

Further evidence of this fusion event is provided when one looks at the DNA sequences before and after the fusion site. The normal TTAGGG telomere sequence is found leading up to the fusion site. However, after the fusion site, the code changes to CCCTAA, which is the inverse of TTAGGG. Moreover, at the fusion site, the sequence is TTAGCTAA. Therefore, it appears that one end of a chromosome broke off at TTAG and the other chromosome broke off at CTAA. These two broken ends then found each other and fused together. Thus, the evolutionists proclaim that the evidence for a telomere-to-telomere (end-to-end) fusion is extremely strong.[20]

Despite such “strong” evidence for an end-to-end fusion, there are two main problems. First, the telomere sequence at the fusion site is highly degraded. Normal human telomeres contain 1,667 to 2,500 six-base tandem repeats (10,000 to 15,000 bases) of TTAGGG.[21] However, the supposed fusion site contains less than 150 tandem repeats (798 bases).[22] What happened to the other tandem repeats? As Tomkins notes, “Even if two very small-size telomeres fused, a region of about 10,000 bases in size should be present.”[23] Scientist Cornelius Hunter adds, “The repetitive telomere sequence is far too short and too dissimilar to indicate a fusion event.”[24]

To account for the large amount of missing repeats, it is proposed that the area surrounding the fusion site is highly degraded. As Fairbanks claims, “This is precisely what we expect if the fusion happened long ago in the remote ancestry of humans. After the fusion event, the repeats no longer functioned as telomeres, so mutations (changes in the DNA sequence) in them had no harmful or beneficial effect.”[25] However, this would require a large amount of degradation in a short amount of time. What evidence is there of such massive degradation? Or is it simply assumed? If the chromosomes fused, the only possible option for the evolutionist is to posit mutations to account for the missing tandem repeats. Yet, such an explanation is ad hoc. The researchers have not found what they expected to find (i.e., 10,000 bases or more of telomeric repeats). Thus, an ad hoc explanation must be substituted for the lack of evidence. If differences are dismissed as mutations while similarities are accepted as evidence of common ancestry, one must ask, ‘How many dissimilarities are required in order to conclude that a fusion did not occur?’

The evolutionists rightly point out that the “fusion site” contains the DNA sequence TTAGCTAA. This appears to show that one chromosome broke off after TTAG and the other at CTAA. These two ends then came together to form chromosome 2. However, the problem that such a code provides evidence of a fusion is that this same DNA sequence is found on multiple chromosomes in humans (chromosomes 1, 6, 9, 10, 15, 16, 18, and 20).[26] The fact that this code is found on other chromosomes, not purported to be fusion sites, causes a problem for the fusion argument. Due to the commonality of this sequence found in the human genome, it does not appear to be the product of a fusion event.

A second problem with the supposed telomere fusion site is that it is located within a functional gene called DDX11L2.[27] DDX11L2 is a noncoding RNA gene that serves multiple functions that will be discussed later in this paper. The fusion site contains a “functional DNA binding domain” and acts “as a second promoter” in the DDX11L2 gene.[28] Moreover, it binds to 12 different transcription factors.[29] The location of the binding sites overlaps “with tracks that are highly significant for transcriptionally active histone modifications.”[30] Furthermore, epigenetic markers, known as histone marks, are found at the fusion site providing further evidence that this region is active and serves a functional purpose.[31]

If the fusion theory is true, one would not expect the “fusion site” to have function. As Fairbanks remarks, “The ancient telomere at the fusion site is now a nonfunctioning relic of evolution embedded in the middle of the chromosome.”[32] Thus, the evolutionist must either deny that the fusion site contains a functional gene or explain how a fusion could result in a functional gene. Either way, the evidence works against the fusion theory.

Cryptic Centromere

Another piece of evidence for a fusion event of chromosome 2 is the existence of a cryptic centromere. “A centromere is a specialized section of DNA located in the center part of a chromosome that serves as an attachment point for the cell machinery that moves the chromosomes around during cell replication (mitosis).”[33] Every chromosome has a centromere. Therefore, if two chromosomes fused together, we should expect to find two centromeres. Evolutionists believe chromosome 2 shows evidence of two centromeres: one active and the other degraded. If a chromosome had two centromeres, it would lead to instability. Therefore, it is proposed that, after the fusion event, one of the centromeres was inactivated. This inactivation left behind “relics of centromeric alphoid DNA.”[34] The inactivation could be the result of epigenetic changes, but it is more likely that the second centromere experienced an excision. In other words, the core DNA sequence of the centromere was removed “resulting in deactivation.”[35]

A deactivation of this sort would leave behind some relics of the centromere DNA sequence. This relic is what is referred to as a cryptic centromere. Evolutionists believe that human chromosome 2 contains a second centromere that has been inactivated and degraded. Evidence for this comes from a couple of studies in which scientists searched the human genome and found alphoid DNA sequences at every centromere.[36] Additionally, these studies “also found alphoid sequences at the site in human chromosome 2 where the remnants of this second centromere should be.”[37] The alphoid sequence is degraded. However, this is to be expected. After the fusion event, the second centromere would have been inactivated in order to gain chromosomal stability. After becoming inactivated, this second centromere would have no function and therefore, mutations to this site would have no impact on the organism. Thus, it is expected that the alphoid sequence show signs of mutations leading to degradation.[38]

Although evolutionists believe they have found remnants of a second centromere on chromosome 2, there are several reasons to doubt such a conclusion. First, a chromosome becomes unstable with two centromeres. Such instability leads to cell death.[39] This means that upon fusion, one of the centromeres had to be deactivated immediately. Rather than a slow, gradual change, the evolutionist must posit a rapid change that deactivated the second centromere. As Fairbanks has pointed out, this is not impossible.[40] However, this makes the fusion event less likely. How so? As already noted, a telomere-to-telomere fusion is extremely unlikely. Additionally, as previously discussed, the chances of an organism with this fusion producing fertile offspring is also unlikely. But now, the evolutionist must posit another aspect to this already unlikely scenario; that is, the immediate deactivation of the second centromere. As each new theory is added to the previous one, the odds of all of them happening increase exponentially. For example, if the odds of a telomere-to-telomere fusion are 1 in 10, and the odds of a centromere deactivation are 1 in 4, then the odds that both of these occur together are 1 in 40! Thus, each new theory decreases the likelihood that the event occurred.

Second, the alphoid sequence found at the cryptic centromere site is found elsewhere in the human genome outside of centromeres.[41] According to Jeffrey Tomkins, “thirteen other human chromosomes contain regions of alphoid repeats outside the centromere.”[42] Thus, the alphoid sequence found on chromosome 2 is not necessarily evidence of a degraded centromere.

Third, the alphoid sequence found at the cryptic centromere site is extremely short for a centromere. A normal human centromere consists of a DNA sequence that is 250,000 to 5,000,000 bases in length.[43] The cryptic site only has a base length of 41,608.[44] However, this includes two insertions. Once the insertions are removed, the base length is diminished to only 33,080 bases.[45] The evolutionists must therefore explain what happened to all the missing bases.[46] Perhaps an excision event occurred which removed some of the DNA after the fusion. This excision event, along with other mutations, would explain the missing sequence. However, such an explanation seems to be ad hoc. Moreover, by multiplying explanations, one is going against Ockham’s razor. Since we find similar short alphoid sequences throughout the genome that are outside of centromeres, there seems to be no need to propose a fusion. The fusion explanation is further downgraded when one considers that this cryptic site serves a function.

The cryptic centromere “is located inside a functionally active protein coding gene called ANKRD30BL.”[47] Ankyrin is a protein that is involved with the plasma membrane and cytoskeleton.[48] Due to its location within an active gene, it is highly unlikely that the “cryptic centromere” is a leftover centromere from a fusion event. The evolutionist must explain how a deactivated centromere has been co-opted for a functional gene. While not impossible, the evolutionist is required to posit an additional theory, making the odds increasingly unfavorable to the overall hypothesis of a fusion event.

Creationist Views

In response to the chromosome 2 fusion theory, Creationists fall into two main groups. One group agrees that chromosome 2 is the result of a fusion. However, they disagree that it provides evidence for common ancestry with apes. Casey Luskin explains, “At most what this evidence requires is that we derive from a 48-chromosome ancestor. Whether that ancestor traces back to a common ancestor we share with apes is a separate question that is not addressed by the fusion issue.”[49] The fusion of chromosome 2 is an apomorphy. An apomorphy is a “trait that is unique to a particular species and all its descendants.”[50] This trait, the fused chromosome, is only found in the human species. Thus, it “cannot provide useful information about phylogenetic relationships.”[51] Furthermore, evolutionists agree that the fused chromosome likely arose “in a small ‘bottleneck’ polygamous clan.”[52] According to the Bible, such a bottleneck did occur at the time of Noah. If Noah carried this fused chromosome, it is possible that he passed it on to his children, who subsequently passed it on to future generations becoming fixed in the population. Thus, even if chromosome 2 is the result of a fusion, it would not disprove Creationism.

The other group of Creationists deny that chromosome 2 is the result of a fusion. Rather, they argue that chromosome 2 is the result of design. As previously mentioned, the fusion site contains a gene called the DDX11L2 gene. This gene produces RNA transcripts and functions as a second promoter.[53] The transcript variants encoded by this gene have been found to be “expressed in at least 255 different cell and/or tissue types.”[54] Furthermore, many of the microRNA binding sites of DDX11L2 are also found on the protein coding gene DDX11.[55] Both DDX11 and DDX11L2 are co-expressed in some of the same tissues.[56] Among other functions, it appears that the DDX11L2 gene regulates and coordinates with its protein coding counterpart, DDX11.[57] While further research is needed to understand all of its functions, the DDX11L2 gene shows “high levels of co-expression to three specific genes involved in blood cell development and chromatin remodeling.”[58] If chromosome 2 were the result of a fusion, one would not expect the fusion site to have function. Yet, the “fusion site” does have function. Such function requires specific design that is known only to be produced by intelligence. Therefore, the evidence of a functional gene is better explained by design than a chance fusion.

One last Creationist view to mention comes from biochemist Fazale Rana. Rana takes a hybrid approach between the two camps. That is, he believes chromosome 2 is the result of a fusion event. However, he believes that such a fusion was intelligently designed. Perhaps God used “a preexisting template” when he formed man.[59] It was out of this template that God took two chromosomes and fused them together. Rana states, “I concur that the evidence strongly suggests that human chromosome 2 appears to be a fusion product. But upon careful reflection, I do not see support for the notion of common descent, but rather for the handiwork of a Creator.”[60] The high unlikelihood of a telomere-to-telomere fusion taking place, producing fertile offspring, and becoming fixed in the population causes Rana to conclude that the fusion event is better explained by design.[61]

Conclusion

While Creationists disagree on whether chromosome 2 is the result of a fusion, evolution requires that such an event did occur. As evolutionist Ken Miller states, “If we don’t find [the fusion site], evolution is wrong. We don’t share a common ancestry” with apes.[62] Thus, evolutionists have a high motive for chromosome 2 to be the result of a fusion. But with the amount of evidence against the fusion hypothesis, and the number of ad hoc hypotheses proposed by evolutionists, it seems this issue is more philosophical than scientific. That is, many scientists require a naturalistic explanation while excluding design. But such philosophical bias impedes research. As Tomkins notes, “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.”[63] Thus, design not only provides a better explanation of chromosome 2, but also promotes further research into the functions of such regions.

Citations 

[1] Kenneth A. Miller, Only a Theory: Evolution and the Battle for America’s Soul (New York, NY: Penguin Group, 2008), 107.

[2] Ibid.

[3] Daniel J. Fairbanks, Relics of Eden: The Powerful Evidence of Evolution in Human DNA (Amherst, NY: Prometheus Books, 2010), 26.

[4] Casey Luskin, “Chromosomal Fusion and Correcting Mistakes: A Retrospective on an Old Debate,” Evolution News, January 24, 2022, https://evolutionnews.org/2022/01/chromosomal-fusion-and-correcting-mistakes-a-retrospective-on-an-old-debate/.

[5] Barbara Poszewiecka, Krzysztof Gogolewski, Pawel Stankiewicz, and Anna Gambin. “Revised Time Estimation of the Ancestral Human Chromosome 2 Fusion,” BMC Genomics (Suppl 6), 616 (2022): 2, https://doi.org/10.1186/s12864-022-08828-7.

[6] Fazale Rana, “Chromosome 2: The Best Evidence for Evolution?” Reasons to Believe, June 1, 2010, https://reasons.org/explore/publications/nrtb-e-zine/chromosome-2-the-best-evidence-for-evolution.

[7] Luskin, “Chromosomal Fusion and Correcting Mistakes.”

[8] Morris III, Henry, John D. Morris, Jason Lisle, James J. S. Johnson, Nathaniel Jeanson, Randy Guliuzza, Jeffrey Tomkins, Jake Hebert, Frank Sherwin, and Brian Thomas, Creation Basics & Beyond: An In-Depth Look at Science, Origins, and Evolution (Dallas, TX: Institute for Creation Research, 2013), 180.

[9] Jeffrey P. Tomkins, “Alleged Human Chromosome 2 ‘Fusion Site’ Encodes an Active DNA Binding Domain Inside a Complex and Highly Expressed Gene – Negating Fusion,” Answers Research Journal 6 (2013): 367, www.answersingenesis.org/contents/379/arj/v6/human_chromosome_fusion.pdf.

[10] Jerry Bergman and Jeffrey P. Tomkins, “The Chromosome 2 Fusion Model of Human Evaluation – Part 1: Re-evaluating the Evidence,” Journal of Creation 25, no. 2 (2011): 108, https://creation.com/chromosome-2-fusion-1.

[11] Jeffrey P. Tomkins, “Debunking the Debunkers: A Response to Criticism and Obfuscation Regarding Refutation of the Human Chromosome 2 Fusion,” Answers Research Journal 10 (2017): 45, www.answersingenesis.org/arj/v10/human_chromosome_2_fusion.pdf.

[12] Fairbanks, Relics of Eden, 226.

[13] Dennis Venema, “Denisovans, Humans and the Chromosome 2 Fusion,” BioLogos, September 6, 2012, https://biologos.org/articles/denisovans-humans-and-the-chromosome-2-fusion.

[14] Ibid.

[15] Ibid.

[16] Miller, Only a Theory, 106.

[17] Tomkins, et. al., Creation Basics, 180.

[18] Ibid.

[19] Francis Collins, The Language of God: A Scientist Presents Evidence for Belief (New York, NY: Free Press, 2006), 138.

[20] Fairbanks, Relics of Eden, 22-27.

[21] Bergman and Tomkins, “The Chromosome 2 Fusion Model – Part 1,” 107.

[22] Ibid.

[23] Tomkins, et. al., Creation Basics, 181.

[24] Cornelius Hunter, “Human Chromosome Two: An Open Letter to BioLogos on the Genetic Evidence, Cont.,” Evolution News, May 31, 2016, https://evolutionnews.org/2016/05/human_chromosome/.

[25] Fairbanks, Relics of Eden, 27.

[26] Donny Budinsky, “Refuting Gutsick Gibbon’s Video Titled ‘Donny Botches Human Chromosome 2 Again,’” Standing for Truth Ministries, 4, https://drive.google.com/file/d/1dJghXsEkARBD-Gr2dvsnuqeujNb1Tjhi/view?usp=sharing.

[27] Tomkins, et. al., Creation Basics, 179.

[28] Tomkins, “Debunking the Debunkers,” 45, 48.

[29] Ibid., 45.

[30] Ibid., 48.

[31] Tomkins, “Alleged Human Chromosome 2 Fusion Site,” 369.

[32] Fairbanks, Relics of Eden, 27.

[33] Tomkins, et. al., Creation Basics, 182.

[34] Giorgia Chiatante, Giuliana Giannuzzi, Francesco Maria Calabrese, Evan E. Eichler, and Mario Ventura, “Centromere Destiny in Dicentric Chromosomes: New Insights from the Evolution of Human Chromosome 2 Ancestral Centromeric Region,” Molecular Biology and Evolution 34, no. 7 (2017): 1670, https://doi.org/10.1093/molbev/msx108.

[35] Ibid., 1677.

[36] Fairbanks, Relics of Eden, 28.

[37] Ibid.

[38] Ibid., 28-29.

[39] Tomkins, et. al., Creation Basics, 182.

[40] Fairbanks, Relics of Eden, 28-29.

[41] Tomkins, “Debunking the Debunkers,” 51.

[42] Ibid.

[43] Ibid.

[44] Ibid.

[45] Ibid.

[46] Ibid.

[47] Ibid.

[48] Ibid.

[49] Luskin, “Chromosomal Fusion and Correcting Mistakes.”

[50] Ibid.

[51] Ibid.

[52] Pawel Stankiewicz, “One Pedigree We All May Have Come From – Did Adam and Eve Have the Chromosome 2 Fusion?” Molecular Cytogenetics 72 (2016): 2, https://doi.org/10.1186/s13039-016-0283-3.

[53] Tomkins, “Debunking the Debunkers,” 45-46.

[54] Ibid., 46.

[55] Ibid.

[56] Ibid.

[57] Tomkins, “Alleged Human Chromosome 2 Fusion Site,” 370.

[58] Ibid., 373.

[59] Rana, “Chromosome 2.”

[60] Ibid.

[61] Ibid.

[62] Playd76, “Ken Miller – 2nd Chromosomal Fusion,” September 24, 2008, video, 2:02, https://www.youtube.com/watch?v=oweUN-GaN3M.

[63] Bergman and Tomkins, “The Chromosome 2 Fusion Model – Part 1,” 108.