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Responses to Objections

Junk DNA and Chromosomal Fusion: A Critique of Collins’s Arguments for Common Descent Between Humans and Apes

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Junk DNA and Chromosomal Fusion: A Critique of Collins’s Arguments for Common Descent Between Humans and Apes

*Note: The article is from the book Science and the Origin of Man. For more details please review the book. Francis Collins, the pioneer of the proponents of divine evolution, presented two genetic arguments to demonstrate the existence of a common ancestor between man and the great apes: Junk DNA...

Junk DNA and Chromosomal Fusion: A Critique of Collins’s Arguments for Common Descent Between Humans and Apes *Note: The article is from the book (Science and the Origin of Man), for more details please review the book. Francis Collins, the leading proponent of divine evolution, presented two genetic arguments to demonstrate the existence of a common ancestor between humans and great apes: Junk DNA and Chromosomal Fusion. The first, which is scrap DNA, fell because the non-coding DNA has important cellular functions, so it is not a "junk" and the second argument, which is a "junk" is lost. In his 2006 best-selling book, The Language of God, geneticist Francis Collins claims that human DNA "provides strong support for Darwin's theory of evolution, the descent from a common ancestor as a result of natural selection acting on random variations, and more specifically, human DNA proves that humans and great apes share a common ancestor". Collins, who heads the Human Genome Project, was previously known to be a member of the Christian evangelical community. He shared Darwinian evolutionary theory and embryonic stem cell research.[2] In 2008, Collins received a $2 million grant from the John Templeton Foundation, which helped him establish the BioLogos Foundation, which aims to convince Christian leaders and the general public of the theory of evolution. The first argument is that man shares with other mammals unencrypted DNA that supposedly has no function – junk – meaning, according to Collins, “the conclusion that a common ancestor between man and mice is almost inevitable.” The second argument is that human chromosome 2 resulted from a merger of two chromosomes similar to that of monkeys, and Collins sees this as hard evidence to understand without assuming a common ancestor between humans and monkeys. These are the most common arguments of evolutionists for the existence of a common ancestor between humans and apes but, as we will see later in this chapter, Collins relied heavily on outdated science, questionable assumptions, and more specifically: Numerous studies have uncovered extensive evidence of unencrypted DNA functions that turned out to be not just genetic junk in any way. - Chromosome fusion in humans may indicate that the human race witnessed this fusion event, but it tells us nothing about human ancestry and common ancestry with apes, and furthermore, this genetic evidence – chromosomal fusion in humans – is not as strong as Collins and others portray it. In short, DNA-based evidence does not prove Collins' conclusion about human evolution. Unencrypted DNA isn't junk anymore! Collins calculates that he avoided the usual, simple argument that functional genetic similarity between two species requires a common ancestor, acknowledging that functional genetic similarity alone does not, of course, prove the existence of this common ancestor; because the designer is able to use the same successful design rules over and over again,6 and instead put forward a different argument, as he cited a type of DNA called "ancient repetitive elements" as a function.7 Old duplicate elements (AREs) are common in the mammalian genome and are present in us humans as well as in great apes and mice, and are found in the same genomic location as all of these organisms. Collins asserts that these old duplicate elements (AREs) are "neglected, worthless genetic debris, and represent an overwhelming challenge to those who hold the idea that all these species of organisms have found their own, self-contained creation." Also as loud as Collins in this regard is the Darwinist atheist Richard Dawkins, who also wrote: "Perhaps those who believe in creation should spend serious time pondering this question: Why does the Creator bother to put a genome with successive repetitions of junk?" Collins and Dawkins have made a theological argument based on the premise that God does not do it that way, rather than making a scientific claim, and I will leave the test of the validity and durability of their theological outlook to others, but their scientific outlook has been altered by the evidence. With a brief look at the scientific publications, we find the opposite of what Dawkins and Collins claim, and that refined DNA, like other types of unencrypted DNA, is not just useless genetic junk, as scientists who have open minds realized this long before Collins wrote his book; in 2002 biologist Richard Steinberg found statistical records of scientific publications in this area and found extensive evidence of the existence of functions for these ancient repetitive elements (AREs). • The satellite repeats form the upper structure of the nucleus. • Replications of the satellites form the central particle centromeres. • Replications of recombinant and other recombinant elements REs are involved in the chromatin condensation process. • Telomeres and long nuclear elements interspersed LINE. • "Subtelomeric nuclear positioning /chromatin boundary elements". • Non-TE interspersed chromatin base elements. • Short Interspersed Nuclear Elements (SINEs) act as nuclear centers to complete the methylation process. • Short interspersed nuclear elements (SINEs) act as chromatin comma elements. • Interstitial short nuclear elements (SINEs) involved in cellular reproduction. • Interstitial short nuclear elements (SINEs) involved in the response to cellular intensities. • Interspersed short nuclear elements (SINEs) involved in translation (possibly related to cellular intensity response) • Short interstitial nuclear elements (SINEs) involved in the binding of cohesion protein to chromosomes. • LINEs involved in DNA repair (10) Steinberg concluded: "These narratives of the existence of scrap DNA are linked to other icons of neo-Darwinian evolutionary theory, and although they differ from experimental science, some continue to publish them." Further genetic research in this regard continued to uncover the functions of different types of DNA replications including: short nuclear elements interspersed with SINEs(12), long nuclear elements interspersed with LINEs(13) as well as elements of Alu(14) until a paper suggested the role of repeated Alu sequences in the development of higher functions of the human brain(15). Multiple other functions of different types of unencrypted DNA have also been discovered, including: • DNA repair.(16) • Help with DNA transcription (17) • organization of DNA transcription.(18) • Assisting and supporting the process of pigment folding.(19) • Control and encode RNA release processes.(20) • Help fight diseases.(21) • Regulation of fetal growth processes.[22] Steinberg and James Shapiro, a geneticist at the University of Chicago, predicted in 2005 that "the day will come when our idea of what we used to call 'junk' will be dropped, and we will find that it is a key component of cellular control systems that are in fact 'specialized'." In 2007, The Washington Post reported that the massive scientific project known as the ENCODE project had found that “the vast majority of human genetic code, estimated at three billion bases, performs a range of previously unknown functions.” According to an article in Nature about the project: "The new bio-view of the world of unencrypted DNA - which we used to call junk DNA - is attractive and confusing, and the results of researchers in the global collaborative project known as the Encyclopedia of DNA Coding Elements (ENCODE) have shown that between (74%-93%) of the DNA found in a specific part of the genome - which contains a small percentage of encoded protein sequences - may be transcribed." Most unencrypted DNA has a regulatory role, as small RNAs of all types appear to be important in controlling DNA-level gene expression and RNA transcription in ways that are beginning to unfold. In 2007, a scientific paper appeared in Nature Reviews Genetics, titled "Wide transcriptional processes and their involvement in gene regulation processes" that discusses the breadth, complexity, and vitality of these mysterious functions of unencrypted DNA, and states: "The evidence suggests that most of the human genome's energy is cloned, meaning that there is a wide overlap of transcriptional and regulatory functions. Similarly, a 2008 paper in the journal Science reveals that almost all parts of the genome of eukaryotic organisms (which have been well studied) are copied, leading to huge amounts of RNA molecules that are not encoded for proteins and have certain functions: "The last few years have revealed that the genome of the studied eukaryotes is copied almost completely, producing a huge number of RNA molecules that are not encoded for proteins and are called ncRNAs." The paper goes on to detail the important roles of these duplicate elements in cell control, saying, "The abundance of duplicate sequences copied may represent a comprehensive strategy in the genome for controlling chromatin regions, and may be conserved across eukaryotic organisms." In 2003, an article in the journal Science reported that many of the recombinant DNAs known before and now by Collins have discouraged scientists from working to discover the functions of unencrypted duplicate elements: "Although the term "scrap DNA" is attractive, it has held back most researchers who have been studying unencrypted DNA for many years, and who would have inserted themselves into the genome waste, except for the small number of decomposers in their search?" The genome.”29 Although the opposing Darwinian assumptions are widespread, the paper concludes that "replicate elements are not useless; rather, they are important integral components of the eukaryotic genome." In addition to the duplicate elements, there is another type of junk DNA that Collins liked to support the existence of a common ancestor between humans and apes; this type is the pseudogene gene, and Collins wrote in his book (Language of God) that the pseudogene caspase-12 has no function in humans, and then asked: "Why did God create that problem by putting a non-functional gene in that exact location?" Similarly, Kenneth Miller, a biologist at Brown University, cited the false gene as crucial evidence in the case of a common ancestor, because "a common ancestor is the only possible explanation for many similar errors in the same gene." As in the case of older replicators (AREs), many of the functions of these genes have been discovered.34 Important biologists, who are editors of the Annual Review of Genetics, have declared that “false genes examined often have no functional functions.”35 A 2011 paper in the journal RNA, titled False Genes, found that “false genes do not have functional functions.” A study suggested that the pseudogene caspase-12 cited by Collins is capable of producing a protein called CARD-only protein; It is a type of protein that has a functional role in humans,39 and the study indicated that the pseudogene called caspase-12 is involved in some of the pathways of biological processes, prompting scientists to study that pseudogene to understand its function: "It is interesting to study the participation of the pseudogene (caspase-12) in biological pathways similar to those of similar genes structurally, Like the gene called ICEBERG, so is the gene called COP/Pseudo-ICE, which is from CARD-only proteins. Collins made the mistake of simply claiming, despite our extreme ignorance of unencrypted DNA, that the vast majority of duplicate DNA is jobless, that it is “worthless genetic debris,” and that false genes are broken DNA. The revolution in the last 5-10 years in the genomics field has exposed a plethora of functions that our unencrypted DNA elements perform. Despite Collins' apparent decline, the BioLogos Foundation, which Collins co-founded, continues to spread the image of junk DNA among members of the believing community to demonstrate that they must embrace the idea of biological evolution.42 Scrap DNA has become a term of the past in the unencrypted DNA view, inferring a common ancestor between humans and great apes. Chromosomal fusion without a common ancestor The second major argument that Francis Collins needed to demonstrate the existence of a common ancestor between humans and apes is his claim that the structure of human chromosome 2 is similar to the structure of the chromosome we expect to form by merging the ends of two chimp chromosomes with each other; humans have 23 pairs of chromosomes while chimpanzees and apes have 24 chromosomes. Quite the contrary; it is very easy to understand this evidence without acknowledging the existence of a common ancestor, and assuming that human chromosome 2 is the product of a merger, as Collins claims, the chromosomal merger indicates that the merger between two chromosomes occurred one day in our ancestors, and when spoken logically, this does not mean that we are descended from a common ancestor with monkeys or that early humans were somehow similar to monkeys. Even if our ancestors had 24 pairs of chromosomes one day, this does not mean that they are completely different from modern humans. Anthropologist Jonathan Marks of the University of North Carolina notes: “It is not the chromosomal fusion that gave us language or made us walk on two legs instead of four, nor the big brain or make art or chew gum, it is just a meaningless neutral change, and it cannot be said to be good or bad in itself.”44 At best, the evidence for chromosomal fusion in humans implies that one of our ancestors experienced chromosomal fusion, and it became consistent in the human community later on, but this evidence tells us nothing about our shared ancestry with apes. A chromosomal fusion in humans does not provide evidence of a common ancestor between humans and chimpanzees. This fusion can be explained by the presence of a common ancestor (A) or by a common design (B), which does not assume a common ancestor between species. If we look from outside the Darwinian box, the following scenario would be equally likely with the common ancestor: • The human lineage is designed separately from the monkey lineage. • Our lineage witnessed the chromosomal fusion event. • This trait spread in the human community as it crossed the genetic "bottleneck" (the stage at which the human race became small). In this scenario, the fusion event appears without the need for a common ancestor with the apes, as shown in Figure 1.4, and the B model fits the reality just like Model A. In Model B, humans do not share a common ancestor with the apes; if the human race has seen a chromosomal fusion event, this model shows that the chromosomal fusion event is easily explained without assuming a common ancestor with the apes. To further illustrate the idea of non-identification of chromosomal fusion on the common ancestor of humans and apes, let's imagine the hypothetical situation: In 2050, members of a small and isolated human tribe experienced a second chromosomal fusion, while remaining natural and capable of reproduction, and we will call this tribe (humans with multiple chromosomal fusion), and in 2100 the world has seen wars, diseases and famines that destroyed the rest of humanity. So we must have descended from a monkey-like creature with 48 pigments.” For our part, we see that these humans with the second chromosome merger recently are far from inferring the existence of a common ancestor between humans and chimpanzees, and they have provided false logical reasons to prove this ancestor, why should we be convinced that this story differs from our true case of one rather than two chromosome mergers? The Darwinist might reply, "The evidence for chromosomal fusion suggests that our ancestors had 48 chromosomes, as is the case today with chimpanzees and great apes, and furthermore, the human chromosome number 2 resulting from chromosomal fusion is made up of pieces similar to those of chromosomes 2a and 2b in apes. results.” This Darwinian response uses the fact that humans and apes have almost the same genetic structures, but the high degree of functional genetic similarity between humans and chimpanzees does not necessarily prove the existence of a common ancestor; In the first chapter, Anne Gouger explained why functional genetic similarity between humans and chimpanzees does not prove the existence of a common ancestor: functional genetic similarities may result from functional requirements and joint design, and not from being inherited from a common ancestor. Because a designer may use successful design rules over and over again." The chromosomal fusion evidence at best reinforces what we all know: that there is a great genetic similarity between chimpanzees and humans. All of the above is true if we assume that the chromosomal fusion event occurred in human history, but how solid is the real evidence for this controversial claim? In his use of chromosomal fusion as evidence for a common ancestor between humans and chimpanzees, biologist Kenneth Miller claims that: "The evidence for lineage from the missing chromosomal case is not in doubt", but the truth is that the evidence for chromosomal fusion is not as conclusively clear as the evolutionists like Kenneth Miller claim. Telomeric DNA at the end of chromosomes in the normal state contains thousands of iterations of a six-stranded sequence (TTAGGG), but the so-called adhesion point in human chromosome 2 contains far less DNA than would be assumed if two chromosomes were fused, and evolutionary biologist Daniel Fairbanks admits that the site contains only 158 iterations, of which only 44 complete copies (46). In addition, a paper published in Genome Research found that our so-called telomere sequences are "remarkably different from typical telomere iterations." The paper showed surprise at this finding because the supposed fusion event occurred so recently, and this time is too short to show those significant differences in sequence. Finally, the presence of telomere DNA in mammalian chromosomes is not rare, nor does it necessarily indicate an ancient fusion point between a pair of chromosomes. Evolutionary biologist Richard Steinberg points out that interstitial telomeric sequences (ITSs) are common in the mammal genome, but evolutionists select the remains of telomere sequences found in human chromosome 2 to attest to the occurrence of chromosomal fusion: "Of all Known interstitial telomere sequences (ITSs) – much of which are found in the genomes of chimpanzees and humans, as well as in the genomes of mice, rats, and cows – the only interstitial telomere sequences that can be associated with a chromosomal fusion locus or event are ITS sequences at 2q13. The ends of the chromosomes are fused in primates, and in short, highlighting ITS repeats at 2q13 is pure data selection."[48] Most of these are not DNA scars as some would prefer to photograph them. There are at least three reasons why the evidence differs from what the chromosomal fusion story predicts: • The point of alleged fusion in (human chromosome 2) contains a much smaller number than the supposed existence of ITS. • The hypothesized telomere sequences are highly conscious and far from what we would expect if chromosomal fusion had occurred recently. • The discovery of the presence of ITS in mammalian chromosomes is not rare and does not necessarily indicate a chromosomal fusion event. But even if human chromosome 2 is the result of the fusion of a pair of chromosomes, it is not evidence of a common ancestor, at best, that the ancestors of humans today have witnessed the incident of chromosome fusion, but it does not tell us anything about whether our ancestry is due to a common ancestor with the apes. Conclusion In the past few years, several genetic arguments have been put forward to the public as crucial new evidence that humans share a common ancestor with apes and other animals. Francis Collins has been at the forefront of those working to popularize those arguments, especially within the believing community. Regardless of Collins' use of emphatic terms, the genetic evidence he provided does not support his claim. The evidence we have discussed in this chapter confirms what we already know that humans and chimpanzees share similar functional gene sequences. This similarity can be explained by having a common design to the same degree that can be explained by assuming a common ancestor. Nothing. With each passing month, new studies reveal many functions of unencrypted DNA. In particular, biologists have discovered extensive evidence for functions of unencrypted elements, such as the ancient repetitive DNA elements (AREs), as well as the pseudogenes, which Collins and others have claimed to have no functions and are genetic debris and worthless waste. So did Collins’s chromosomal fusion argument, and even if chromosomal fusion did occur, that would tell us nothing about whether we share a common ancestor with apes, and it is not entirely clear whether chromosomal fusion did indeed occur, and ITS does not necessarily indicate chromosomal fusion, and these sequences in human chromosomal 2 are far apart from those we would expect if there were. As a supporter of the idea that intelligent design can explain many aspects of nature in a better way than random undirected processes, I want to point out that intelligent design does not conflict in principle with a common ancestor. In essence, intelligent design is not against the common ancestor, but with the claim that the complexity in life was created by random undirected processes such as random mutations and natural selection, and therefore the model of a common ancestor is compatible with the idea of a common guided design. However, unlike proponents of Darwinian evolution, intelligent design theorists are not bound to accept a common ancestor between humans and apes, and are free to follow the evidence wherever it leads, and the evidence will not lead them to Francis Collins’ conclusions. (1) Francis Collins, The Language of God: A Scientist Presents Evidence for Belief (New York: Free Press, 2006), 127-28. (2) See: David Klinghoffer, “Francis Collins: A Biography.” Wesley J. Smith, “Collins Heads NIH,” To the Point (July 30, 2009). David Klinghoffer, “Francis Collins on Abortion,” BeliefNet (July 8, 2009). (3) For information about the Templeton grant to launch BioLogos, see “The Language of God: BioLogos Website and Workshop,” John Templeton Foundation, accessed March 19, 2012, http://www.templeton.org/what-wefund/grants/the-language-of-god-biologos-website-and-workshop. (4) Collins, Language of God, 136-37. (5) Ibid., 138. (6) Ibid., 134. (7) Ibid., 136-37. (8) Ibid. (9) Richard Dawkins, “The Information Challenge,” The Skeptic, 18 (December,1998). (10) Richard Sternberg, “On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic-Epigenetic System,” Annals of the New York Academy of Sciences, 981 (2002): 154-88. (11) Ibid. (12) Sternberg, “On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic-Epigenetic System,” 154-88. (13) Tammy A. Morrish, Nicolas Gilbert, Jeremy S. Myers, Bethaney J. Vincent, Thomas D. Stamato, Guillermo E. Taccioli, Mark A. Batzer, and John V. Moran, “DNA repair mediated by endonuclease-independent LINE-1 retrotransposition,” Nature Genetics, 31 (June, 2002): 159-65. (14) Galit Lev-Maor, Rotem Sorek, Noam Shomron, and Gil Ast, “The birth of an alternatively spliced exon: 3’ splice-site selection in Alu exons,” Science, 300 (May 23, 2003): 1288-91; Wojciech Makalowski, “Not junk after all,” Science, 300 (May 23, 2003): 1246-47. (15) Nurit Paz-Yaacova, Erez Y. Levanonc, Eviatar Nevod, Yaron Kinare, Alon Harmelinf, Jasmine Jacob-Hirscha, Ninette Amariglioa, Eli Eisenbergg, and Gideon Rechavi, “Adenosine-to-inosine RNA editing shapes transcriptome diversity in primates,” Proceedings of the National Academy of Sciences USA, 107 (July 6, 2010): 12174-79. 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Burghardt, K. Hayashi, J. L. Farmer, and T. E. Spencer, “Endogenous retroviruses regulate periimplantation placental growth and differentiation,” Proceedings of the National Academy of Sciences USA, 103 (September 26, 2006): 14390-95; L. Hyslop, M. Stojkovic, L. Armstrong, T. Walter, P. Stojkovic, S. Przyborski, M. Herbert, A. Murdoch, T. Strachan, and M. Lakoa, “Downregulation of NANOG Induces Differentiation of Human Embryonic Stem Cells to Extraembryonic Lineages,” Stem Cells, 23 (2005): 1035-43; E. Peaston, A. V. Evsikov, J. H. Graber, W. N. de Vries, A. E. Holbrook, D. Solter, and B. B. Knowles, “Retrotransposons Regulate Host Genes in Mouse Oocytes and Preimplantation Embryos,” Developmental Cell, 7 (October, 2004): 597-606. (23) Sternberg Shapiro, “How Repeated Retroelements format genome function,”108-16. (24) Rick Weiss, “Intricate Toiling Found In Nooks of DNA Once Believed to Stand Idle,” Washington Post (June 14, 2007), accessed March 6, 2012, http://www.washingtonpost.com/wp-dyn/content/article/2007/06/13/AR2007061302466_pf.html. (25) Erika Check Hayden, “Human Genome at Ten: Life is Complicated,” Nature,464 (April 1, 2010): 664-67. (26) Philipp Kapranov, Aarron T. Willingham, and Thomas R. Gingeras, “Genome- wide transcription and the implications for genomic organization,” Nature Reviews Genetics, 8 (June, 2007): 413-23. (27) Paulo P. Amaral, Marcel E. Dinger, Tim R. Mercer, and John S. Mattick, “The Eukaryotic Genome as an RNA Machine,” Science, 319 (March 28, 2008): 1787-89. 28. (28) Ibid. (29) Makalowski, “Not Junk After All,” 1246-47. (30) Ibid. (31) Collins, The Language of God, pg. 139. (32) Karl Giberson and Francis Collins, The Language of Science and Faith: Straight Answers to Genuine Questions (Downers Grove, IL: InterVarsity Press, 2011),43. (33) Private correspondence with Dr. Miller. (34) See for example D. Zheng and M. B. Gerstein, “The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?,” Trends in Genetics, 23 (May, 2007): 219-24; S. Hirotsune et al., “An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene,” Nature, 423 (May 1, 2003): 91-96; O. H. Tam et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature, 453 (May 22, 2008): 534-38; D. Pain et al., “Multiple Retropseudogenes from Pluripotent Cell-specific Gene Expression Indicates a Potential Signature for Novel Gene Identification,” The Journal of Biological Chemistry, 280 (February 25, 2005):6265-68; J. Zhang et al., “NANOGP8 is a retrogene expressed in cancers,” FEBS Journal, 273 (2006): 1723-30. (35) Evgeniy S. Balakirev and Francisco J. Ayala, “Pseudogenes, Are They ‘Junk’or Functional DNA?,” Annual Review of Genetics, 37 (2003): 123-51. (36) Ryan Charles Pink, Kate Wicks, Daniel Paul Caley, Emma Kathleen Punch, Laura Jacobs, and David Paul Francisco Carter, “Pseudogenes: Pseudo-functional or key regulators in health and disease?,” RNA, 17 (2011): 792-98. Collins acknowledges that the caspase-12 gene produces an important functional protein in chimpanzees, so it is not the case that humans share the same unencrypted gene sequence as other organisms. This gene is not false in all humans. According to a paper published in The American Journal of Human Genetics, 28% of humans in sub-Saharan Africa have a functional copy of this gene, and it is found in lower proportions in other human populations. See: Yali Xue, Allan Daly, Bryndis Yngvadottir, Mengning Liu, Graham Coop, Yuseob Kim, Pardis Sabeti, Yuan Chen, Jim Stalker, Elizabeth Huckle, John Burton, Steven Leonard, Jane Rogers, and Chris Tyler-Smith, “Spread of an Inactive Form of Caspase-12 in Humans Is Due to Recent Positive Selection,” The American Journal of Human Genetics, 78 (April, 2006): 659-70. (38) M. Lamkanfi, M. Kalai, and P. Vandenabeele, “Caspase-12: an overview,” Cell Death and Differentiation, 11: (2004)365-68. (39) Sug Hyung Lee, Christian Stehlik, and John C. Reed, “COP, a Caspase Recruitment Domain-containing Protein and Inhibitor of Caspase-1 Activation Processing,” The Journal of Biological Chemistry, 276 (September 14, 2001): 34495-500. (40) Lamkanfi, Kalai, and Vandenabeele, “Caspase-12: an overview,” 365-68. (41) Collins, quoted in Catherine Shaffer, “One Scientist’s Junk Is a Creationist’s Treasure,” Wired Magazine Blog (June 13, 2007), accessed March 6, 2012, . (42) See discussion in Jonathan Wells, The Myth of Junk DNA (Seattle: Discovery Institute Press, 2011), 98-100. (43) Collins, The Language of God, 138. (44) Jonathan Marks, What it means to be 98% Chimpanzee: Apes, People, and their Genes (Los Angeles: University of California Press, 2003), 39. (45) Kenneth R. Miller, Only a Theory: Evolution and the Battle for America’s Soul (New York: Viking, 2008), 107. (46) Daniel Fairbanks, Relics of Eden: The Powerful Evidence of Evolution in Human DNA (Amherst, NY: Prometheus, 2007), 27. (47) Yuxin Fan, Elena Linardopoulou, Cynthia Friedman, Eleanor Williams, and Barbara J. Trask, “Genomic Structure and Evolution of the Ancestral Chromosome Fusion Site in 2q13-2q14.1 and Paralogous Regions on Other Human Chromosomes,” Genome Research, 12 (2002): 1651-62. (48) Richard Sternberg, “Guy Walks Into a Bar and Thinks He’s a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity,” Evolution News & Views (May 14, 2009), accessed March 6, 2012. http://www.evolutionnews.org/2009/05/guy_walks_into_a_bar_and_think020401.html (internal citations removed). (49) Collins, The Language of God, 133-34.50. Ibid., 136-37.51. For an in-depth discussion of these studies, see Wells, The Myth of Junk DNA. (50) Ibid., 136-37. - Casey for a knife. — Source: Brahin Center website - Published on 2018-01-11 (archived at the Internet Archive) https://braheen.com/articles/evolution-design/الدنا-الخردة-والاندماج-الصبغي-نقد-حجج-كولينز-في-إثبات-الانحدار-المشترك-للبشر-والقرود

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