Problem 10: Neo-Darwinism's Long History of Inaccurate Predictions about Junk Organs and Junk DNA
Editor's note: This is Part 10 of a 10-part series based upon Casey Luskin's chapter, "The Top Ten Scientific Problems with Biological and Chemical Evolution," in the volume More than Myth, edited by Paul Brown and Robert Stackpole (Chartwell Press, 2014). The full chapter can be found online here. Other individual installments can be found here: Problem 1, Problem 2, Problem 3, Problem 4, Problem 5, Problem 6, Problem 7, Problem 8, Problem 9.
For decades, evolutionists have claimed that our bodies and genomes are full of useless parts and genetic material -- "vestigial" organs -- showing life is the result of eons of unguided evolution. During the Scopes trial in 1925, evolutionary biologist Horatio Hackett Newman contended that there are over 180 vestigial organs and structures in the human body, "sufficient to make of a man a veritable walking museum of antiquities."157
Over time, however, these predictions of vestigial body parts and useless DNA have not held true. As scientists have learned more and more about the workings of biology, important functions and purpose have been discovered for these so-called vestigial structures. Indeed, in 2008 the journal New Scientist reported that, since the days of Professor Newman, the list of vestigial organs "grew, then shrank again" to the point that today "biologists are extremely wary of talking about vestigial organs at all."158 Structures that were previously -- and incorrectly -- considered to be vestigial include:
- The tonsils: At one time, they were routinely removed. Now it's known they serve a purpose in the lymph system to help fight infection.159
- The coccyx (tailbone): Many evolutionists still claim this is a hold-over from the tails of our supposed primate ancestors,160 but it's actually a vital part of our skeleton, used for attaching muscles, tendons, and ligaments that support the bones in our pelvis.
- The thyroid: This gland in the neck was once believed to have no purpose, and was ignored or even destroyed by medical doctors operating under false Darwinian assumptions. Now scientists know that it is vital for regulating metabolism.
- The appendix: Darwinian scientists have claimed the appendix is a "vestige of our herbivorous ancestry,"161 and over eons of evolution its function in humans has been diminished, or lost. But it's now known that the appendix performs important functions, such as providing a storehouse for beneficial bacteria, producing white blood cells, and playing important roles during fetal development.162 In light of this evidence, Duke University immunologist William Parker observed that "Many biology texts today still refer to the appendix as a 'vestigial organ'" but "it's time to correct the textbooks."163
- Brown University evolutionary biologist Kenneth Miller argues that "the human genome is littered with pseudogenes, gene fragments, 'orphaned' genes, 'junk' DNA, and so many repeated copies of pointless DNA sequences that it cannot be attributed to anything that resembles intelligent design."164
- Richard Dawkins likewise writes that "creationists might spend some earnest time speculating on why the Creator should bother to litter genomes with untranslated pseudogenes and junk tandem repeat DNA."165
- In his 2006 book The Language of God, Francis Collins claimed that some "45 percent of the human genome" is made up of "genetic flotsam and jetsam."166 (Flotsam and jetsam, of course, is useless trash floating in the ocean.) Sounding much like Dawkins, he makes the implications clear: "Unless one is willing to take the position that God has placed [shared functionless repetitive DNA] in these precise positions to confuse and mislead us, the conclusion of a common ancestor for humans and mice is virtually inescapable."167
Biologist Richard Sternberg surveyed the literature and found extensive evidence of function for repetitive DNA. Writing in the Annals of the New York Academy of Sciences, he found that functions for repeats include forming higher-order nuclear structures, centromeres, telomeres, and nucleation centers for DNA methylation. Repetitive DNA was found to be involved in cell proliferation, cellular stress responses; gene translation, and DNA repair.168 Sternberg concluded that "the selfish [junk] DNA narrative and allied frameworks must join the other 'icons' of neo-Darwinian evolutionary theory that, despite their variance with empirical evidence, nevertheless persist in the literature."169
Other research has continued to uncover functions for various types of repetitive DNA, including SINE,170 LINE,171 and Alu elements.172 One paper even suggested that repetitive Alu sequences might be involved in "the development of higher brain function" in humans.173 Numerous other functions have been discovered for various types of non-protein-coding DNA, including:
- repairing DNA174
- assisting in DNA replication175
- regulating DNA transcription176
- aiding in folding and maintenance of chromosomes177
- controlling RNA editing and splicing178
- helping to fight disease179
- regulating embryological development180
The day foreseen by Sternberg and Shapiro may have come sooner than they expected. In September, 2012, the journal Nature reported the results of a years-long research project, involving over 400 international scientists studying the functions of non-coding DNA in humans. Called the ENCODE Project, its set of 30 groundbreaking papers reported that the "vast majority" of the genome has function. The lead paper reporting ENCODEs' results stated:
These data enabled us to assign biochemical functions for 80% of the genome, in particular outside of the well-studied protein-coding regions.182
Ewan Birney, ENCODE's lead analysis coordinator commented in Discover Magazine that since ENCODE looked at only 147 types of cells, and the human body has a few thousand, "It's likely that 80 percent will go to 100 percent."183 The same article quoted Tom Gingeras, a senior scientist with ENCODE, noting that, "Almost every nucleotide is associated with a function of some sort or another, and we now know where they are, what binds to them, what their associations are, and more."184 Another Nature commentary noted that "80% of the genome contains elements linked to biochemical functions, dispatching the widely held view that the human genome is mostly 'junk DNA'."185 Discover Magazine put it this way: "The key point is: It's not 'junk'."186
While there's still much we don't know about the genome, the trendline of the research is clearly pointing in one direction: the more we study the genome, the more we detect function for non-coding DNA. Yet the now-dubious "junk-DNA" paradigm was born and bred inside the evolutionary paradigm based upon the idea that our genome was built through random mutations. Yes, a few rogue biologists dared to seek function for non-coding DNA, but the Darwinian "junk DNA" view of genetics has generally hindered the progress of science, as was admitted by a 2003 article in Science:
Although catchy, the term 'junk DNA' for many years repelled mainstream researchers from studying noncoding DNA. Who, except a small number of genomic clochards, would like to dig through genomic garbage? However, in science as in normal life, there are some clochards who, at the risk of being ridiculed, explore unpopular territories. Because of them, the view of junk DNA, especially repetitive elements, began to change in the early 1990s. Now, more and more biologists regard repetitive elements as a genomic treasure.187
Despite widespread Darwinian assumptions to the contrary, the paper concluded that "repetitive elements are not useless junk DNA but rather are important, integral components"188 of animal genomes. Studies suggest that these long stretches of non-coding DNA between genes "constitute an important layer of genome regulation across a wide spectrum of species."189
Like repetitive elements, another kind of "junk" DNA for which function is being discovered is pseudogenes. Pseudogenes are thought to be copies of once-functional genes that have been inactivated through mutations. One paper in Science Signaling observes that "pseudogenes have long been dismissed as junk DNA,"190 but notes:
Recent advances have established that the DNA of a pseudogene, the RNA transcribed from a pseudogene, or the protein translated from a pseudogene can have multiple, diverse functions and that these functions can affect not only their parental genes but also unrelated genes. Therefore, pseudogenes have emerged as a previously unappreciated class of sophisticated modulators of gene expression, with a multifaceted involvement in the pathogenesis of human cancer.191
Indeed, functions for many pseudogenes have already been discovered;192 the ENCODE project alone found over 850 pseudogenes that are "transcribed and associated with active chromatin."193 But what exactly are these pseudogenes doing? A 2011 paper in the journal RNA again argues they can regulate the expression of genes:
Pseudogenes have long been labeled as 'junk' DNA, failed copies of genes that arise during the evolution of genomes. However, recent results are challenging this moniker; indeed, some pseudogenes appear to harbor the potential to regulate their protein-coding cousins.194
Likewise, a 2012 paper in the journal RNA Biology similarly stated that "Pseudogenes were long considered as junk genomic DNA" but "pseudogene regulation is widespread"195 in complex multicellular organisms. The paper proposed that "[t]he high abundance and conservation of the pseudogenes in a variety of species indicate that selective pressures preserve these genetic elements, and suggest they may indeed perform important biological functions."196
Pseudogenes serve as another good example of how Darwinian biologists have assumed that a type of non-coding DNA they didn't understand was functionless genetic junk, and thus ignored their functions. Indeed, the aforementioned paper in RNA Biology explains that one reason why evolutionists have been so slow to abandon the assumption that pseudogenes are junk is because their functions are difficult to detect. The authors observe that "almost all pseudogenes that exhibit significant biological activity are expressed in specific tissue or cell lines," meaning only specific tissues or cell lines may use a given pseudogene for some function. Additionally, it's difficult to detect function for pseudogenes because we have lacked the research tools to understand how they influence gene expression. The paper predicts that "more and more functional pseudogenes will be discovered as novel biological technologies are developed in the future," and concludes "The study of functional pseudogenes is just at the beginning."197 Indeed, two leading biologists writing in Annual Review of Genetics reported that "pseudogenes that haev been suitably investigated often exibit functional roles."198
Many evolutionary biologists are wedded to the view that our genomes are full of junk, and resist the interpretation that virtually all DNA has function. Indeed, a 2012 evolution textbook teaches that "Over half of the genome is composed of neither genes, nor vestiges of human genes, nor regulatory regions. Instead, it is made up of parasite-like segments of DNA..."199 Meanwhile, the evidence continues to point in the opposite direction. While much remains to be learned about the workings of our genome, the research trendline is unambiguous: the more we study non-coding DNA, the more we find evidence of widespread function.
Bonus Problem: Humans Display Many Behavioral and Cognitive Abilities that Offer No Apparent Survival Advantage
In recent years, evolutionary biologists have tried to explain the origin of human moral, intellectual, and religious abilities in terms of Darwinian evolution. Harvard University evolutionary psychologist Marc Hauser has promoted the increasingly common hypothesis that "people are born with a moral grammar wired into their neural circuits by evolution."200
Humans do appear hard-wired for morality, but were we programmed by unguided evolutionary processes? Natural selection cannot explain extreme acts of human kindness. Regardless of background or beliefs, upon finding strangers trapped inside a burning vehicle, people will risk their own lives to help them escape -- with no evolutionary benefit to themselves. For example, evolutionary biologist Jeffrey Schloss explains that Holocaust rescuers took great risks which offered no personal benefits:
The rescuer's family, extended family and friends were all in jeopardy, and they were recognized to be in jeopardy by the rescuer. Moreover, even if the family escaped death, they often experienced deprivation of food, space and social commerce; extreme emotional distress; and forfeiture of the rescuer's attention.201
Francis Collins gives the example of Oskar Schindler, the German businessman who risked his life "to save more than a thousand Jews from the gas chambers."202 As Collins points out, "That's the opposite of saving his genes."203 Schloss adds other examples of "radically sacrificial" behavior that "reduces reproductive success" and offers no evolutionary benefit, such as voluntary poverty, celibacy, and martyrdom.204
In spite of the claims of evolutionary psychologists, many of humanity's most impressive charitable, artistic, and intellectual abilities outstrip the basic requirements of natural selection. If life is simply about survival and reproduction, why do humans compose symphonies, investigate quantum mechanics, and build cathedrals?
Natural Academy of Sciences member Philip Skell explained why evolutionary psychology does not adequately predict human behavior:
Darwinian explanations for such things are often too supple: Natural selection makes humans self-centered and aggressive -- except when it makes them altruistic and peaceable. Or natural selection produces virile men who eagerly spread their seed -- except when it prefers men who are faithful protectors and providers. When an explanation is so supple that it can explain any behavior, it is difficult to test it experimentally, much less use it as a catalyst for scientific discovery.205
Contrary to Darwinism, the evidence indicates that human life isn't about mere survival and reproduction. But in addition to our moral uniqueness, humans are also distinguished by their use of complex language. As MIT professor and linguist Noam Chomsky observes:
Human language appears to be a unique phenomenon, without significant analogue in the animal world. If this is so, it is quite senseless to raise the problem of explaining the evolution of human language from more primitive systems of communication that appear at lower levels of intellectual capacity. ... There is no reason to suppose that the "gaps" are bridgeable.206
Finally, humans are also the only species that seeks to investigate the natural world through science. In fact, the next time someone tries to break down the differences between humans and apes, remind them that it's humans who write scientific papers studying apes, not the other way around.
Science vs. Religion?
This chapter has cited dozens of papers from the technical scientific literature and by credible scientists which, taken together, pose strong scientific challenges to modern evolutionary theory. Yet defenders of neo-Darwinism commonly assert that legitimate scientific objections to their viewpoint do not exist, and that the only criticisms which remain are based upon religion. Clearly, this is not true. In fact, the attempt to re-label criticisms of neo-Darwinian evolution as religion is typically a ploy to dismiss scientific criticisms without addressing them.
The balance of this book, of course, raises both religious and scientific arguments supporting the progressive creation view that God created life on earth over the course of millions of years. This viewpoint has both religious and scientific dimensions, and for that reason is different from the strictly scientific approach taken in this chapter.
The fact that some arguments in this book may be based upon religion, in no way changes the fact that there are strong scientific challenges to neo-Darwinian theory. Likewise, the fact that there are important religious dimensions to this debate does not mean that materialists can ignore the scientific weaknesses in their own arguments. Until those scientific problems are addressed, scientists will continue to grow skeptical of evolutionary theory.
[157.] Horatio Hackett Newman, quoted in The World's Most Famous Court Trial: Tennessee Evolution Case, 2nd ed. (Dayton, TN: Bryan College, 1990), 268. See also Robert Wiedersheim, The Structure of Man: An Index to His Past History (London: MacMillan and Co, 1895; reprinted by Kessinger, 2007).
[158.] Laura Spinney, "Vestigial organs: Remnants of evolution," New Scientist, 2656 (May 14, 2008), at http://www.newscientist.com/article/mg19826562.100-vestigial-organs-remnants-of-evolution.html
[159.] Sylvia S. Mader, Inquiry into Life, 10th ed. (McGraw Hill, 2003), 293.
[160.] Laura Spinney, "The Five things humans no longer need," New Scientist (May 19, 2008), at http://www.newscientist.com/article/dn13927-five-things-humans-no-longer-need.html
[161.] Douglas Theobald, "29+ Evidences for Macroevolution," TalkOrigins.org, at http://www.talkorigins.org/faqs/comdesc/section2.html
[162.] See Loren G. Martin, "What is the function of the human appendix? Did it once have a purpose that has since been lost?," Scientific American (October, 21, 1999), at http://www.scientificamerican.com/article.cfm?id=what-is-the-function-of-t
[163.] William Parker quoted in Charles Q. Choi, "The Appendix: Useful and in Fact Promising," LiveScience (August 24, 2009).
[164.] Miller, "Life's Grand Design," 24-32. Miller cites "orphaned genes" but these are not normally understood to be functionless genes. Rather, orphan genes are functional genes that have no known homology to any other gene. Such orphan genes provide evidence for intelligent design because there is no plausible source for their information.
[165.] Richard Dawkins, "The Information Challenge," The Skeptic, 18 (December, 1998).
[166.] Francis Collins, The Language of God: A Scientist Presents Evidence for Belief (New York: Free Press, 2006), 136-37.
[167.] Ibid., pp. 134-137.
[168.] 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.
[171.] Tammy A. Morrish, Nicolas Gilbert, Jeremy S. Myers, Bethaney J. Vincent, Thomas D. Stamato, Guillermo E. Taccioli, Mark A. Batzer, and John V. Mora "DNA repair mediated by endonuclease-independent LINE-1 retrotransposition," Nature Genetics, 31 (June, 2002): 159-65.
[172.] 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.
[173.] 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.
[174.] Morrish et al., "DNA repair mediated by endonuclease-independent LINE-1 retrotransposition," 159-65; Annie Tremblay, Maria Jasin, and Pierre Chartrand, "A Double-Strand Break in a Chromosomal LINE Element Can Be Repaired by Gene Conversion with Various Endogenous LINE Elements in Mouse Cells," Molecualr and Cellular Biology, 20 (January, 2000): 54-60; Ulf Grawunder, Matthias Wilm, Xiantuo Wu, Peter Kulesza, Thomas E. Wilson, Matthias Mann, and Michael R. Lieber, "Activity of DNA ligase IV stimulated by complex formation with XRCC4 protein in mammalian cells," Nature, 388 (July 31, 1997): 492-95; Thomas E. Wilson, Ulf Grawunder, and Michael R. Lieber, "Yeast DNA ligase IV mediates non-homologous DNA end joining," Nature, 388 (July 31, 1997): 495-98.
[175.] Richard Sternberg and James A. Shapiro, "How repeated retroelements format genome function," Cytogenetic and Genome Research, 110 (2005): 108-16.
[176.] Jeffrey S. Han, Suzanne T. Szak, and Jef D. Boeke, "Transcriptional disruption by the L1 retrotransposon and implications for mammalian transcriptomes," Nature, 429 (May 20, 2004): 268-74; Bethany A. Janowski, Kenneth E. Huffman, Jacob C. Schwartz, Rosalyn Ram, Daniel Hardy, David S. Shames, John D. Minna, and David R. Corey, "Inhibiting gene expression at transcription start sites in chromosomal DNA with antigene RNAs," Nature Chemical Biology, 1 (September, 2005): 216-22; J. A. Goodrich, and J. F. Kugel, "Non-coding-RNA regulators of RNA polymerase II transcription," Nature Reviews Molecular and Cell Biology, 7 (August, 2006): 612-16; L.C. Li, S. T. Okino, H. Zhao, H., D. Pookot, R. F. Place, S. Urakami, H. Enokida, and R. Dahiya, "Small dsRNAs induce transcriptional activation in human cells," Proceedings of the National Academy of Sciences USA, 103 (November 14, 2006): 17337-42; A. Pagano, M. Castelnuovo, F. Tortelli, R. Ferrari, G. Dieci, and R. Cancedda, "New small nuclear RNA gene-like transcriptional units as sources of regulatory transcripts," PLoS Genetics, 3 (February, 2007): e1; L. N. van de Lagemaat, J. R. Landry, and D. L. Mager, P. Medstrand, "Transposable elements in mammals promote regulatory variation and diversification of genes with specialized functions," Trends in Genetics, 19 (October, 2003): 530-36; S. R. Donnelly, T. E. Hawkins, and S. E. Moss, "A Conserved nuclear element with a role in mammalian gene regulation," Human Molecular Genetics, 8 (1999): 1723-28; C. A. Dunn, P. Medstrand, and D. L. Mager, "An endogenous retroviral long terminal repeat is the dominant promoter for human B1,3- galactosyltransferase 5 in the colon," Proceedings of the National Academy of Sciences USA, 100 (October 28, 2003):12841-46; B. Burgess-Beusse, C. Farrell, M. Gaszner, M. Litt, V. Mutskov, F. Recillas-Targa, M. Simpson, A. West, and G. Felsenfeld, "The insulation of genes from external enhancers and silencing chromatin," Proceedings of the National Academy of Sciences USA, 99 (December 10, 2002): 16433-37; P. Medstrand, Josette-Ren�e Landry, and D. L. Mager, "Long Terminal Repeats Are Used as Alternative Promoters for the Endothelin B Receptor and Apolipoprotein C-I Genes in Humans," Journal of Biological Chemistry, 276 (January 19, 2001): 1896-1903; L. Mari�o-Ram�reza, K.C. Lewisb, D. Landsmana, and I.K. Jordan, "Transposable elements donate lineage-specific regulatory sequences to host genomes," Cytogenetic and Genome Research, 110 (2005):333-41.
[177.] S. Henikoff, K. Ahmad, H. and S. Malik "The Centromere Paradox: Stable Inheritance with Rapidly Evolving DNA," Science, 293 (August 10, 2001): 1098-1102; C. Bell, A. G. West, and G. Felsenfeld, "Insulators and Boundaries: Versatile Regulatory Elements in the Eukaryotic Genome," Science, 291 (January 19, 2001): 447-50; M.-L. Pardue and P.G. DeBaryshe, "Drosophila telomeres: two transposable elements with important roles in chromosomes," Genetica, 107 (1999): 189-96; S. Henikoff, "Heterochromatin function in complex genomes," Biochimica et Biophysica Acta, 1470 (February, 2000): O1-O8; L. M.Figueiredo, L. H. Freitas-Junior, E. Bottius, Jean-Christophe Olivo-Marin, and A. Scherf, "A central role for Plasmodium falciparum subtelomeric regions in spatial positioning and telomere length regulation," The EMBO Journal, 21 (2002): 815-24; Mary G. Schueler, Anne W. Higgins, M. Katharine Rudd, Karen Gustashaw, and Huntington F. Willard, "Genomic and Genetic Definition of a Functional Human Centromere," Science, 294 (October 5, 2001): 109-15.
[178.] Ling-Ling Chen, Joshua N. DeCerbo, and Gordon G. Carmichael, "Alu element-mediated gene silencing," The EMBO Journal 27 (2008): 1694-1705; Jerzy Jurka, "Evolutionary impact of human Alu repetitive elements," Current Opinion in Genetics & Development, 14 (2004): 603-8; G. Lev-Maor et al. "The birth of an alternatively spliced exon: 3' splice-site selection in Alu exons," 1288-91; E. Kondo-Iida, K. Kobayashi, M. Watanabe, J. Sasaki, T. Kumagai, H. Koide, K. Saito, M. Osawa, Y. Nakamura, and T. Toda, "Novel mutations and genotype-phenotype relationships in 107 families with Fukuyama-type congenital muscular dystrophy (FCMD)," Human Molecular Genetics, 8 (1999): 2303-09; John S. Mattick and Igor V. Makunin, "Non-coding RNA," Human Molecular Genetics, 15 (2006): R17-R29.
[179.] M. Mura, P. Murcia, M. Caporale, T. E. Spencer, K. Nagashima, A. Rein, and M. Palmarini, "Late viral interference induced by transdominant Gag of an endogenous retrovirus," Proceedings of the National Academy of Sciences USA, 101 (July 27, 2004): 11117-22; M. Kandouz, A. Bier, G. D Carystinos, M. A Alaoui-Jamali, and G. Batist, "Connexin43 pseudogene is expressed in tumor cells and inhibits growth," Oncogene, 23 (2004):4763-70.
[180.] K. A. Dunlap, M. Palmarini, M. Varela, R. C. 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.
[181.] Richard Sternberg and James A. Shapiro, "How repeated retroelements format genome function," Cytogenetic and Genome Research, 110 (2005): 108-16.
[182.] The ENCODE Project Consortium, "An integrated encyclopedia of DNA elements in the human genome," Nature, 489:57-74 (September 6, 2012).
[183.] Ewan Birney, quoted in Ed Yong, "ENCODE: the rough guide to the human genome," Discover Magazine (September 5, 2012), at http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the-rough-guide-to-the-human-genome/
[184.] Tom Gingeras, quoted in Ed Yong, "ENCODE: the rough guide to the human genome," Discover Magazine (September 5, 2012), at http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the-rough-guide-to-the-human-genome/
[185.] Joseph R. Ecker, "Serving up a genome feast," Nature, 489:52-55 (September 6, 2012).
[186.] Ed Yong, "ENCODE: the rough guide to the human genome," Discover Magazine (September 5, 2012), at http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the-rough-guide-to-the-human-genome/
[187.] Makalowski, "Not Junk After All," 1246-47.
[189.] David R. Kelley and John L. Rinn, "Transposable elements reveal a stem cell specific class of long noncoding RNAs," Genome Biology, 13:R107 (2012).
[190.] Laura Poliseno, "Pseudogenes: Newly Discovered Players in Human Cancer," Science Signaling, 5 (242) (September 18, 2012).
[192.] 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.
[193.] The ENCODE Project Consortium, "An integrated encyclopedia of DNA elements in the human genome," Nature, 489:57-74 (September 6, 2012).
[194.] 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.
[195.] Yan-Zi Wen, Ling-Ling Zheng, Liang-Hu Qu, Francisco J. Ayala and Zhao-Rong Lun, "Pseudogenes are not pseudo any more," RNA Biology, 9(1):27-32 (January, 2012).
[198.] Evgeniy S. Balakirev and Francisco J. Ayala, "Pseudogenes, Are They 'Junk' or Functional DNA?," Annual Review of Genetics, 37 (2003): 123-51.
[199.] Carl Zimmer and Douglas Emlen, Evolution: Making Sense of Life, p. 132 (Roberts and Company, 2012).
[200.] Nicholas Wade, "An Evolutionary Theory of Right and Wrong," The New York Times (October 31, 2006), accessed April 28, 2012, http://www.nytimes.com/2006/10/31/health/psychology/31book.html
[201.] Jeffrey P. Schloss, "Evolutionary Accounts of Altruism & the Problem of Goodness by Design," in Mere Creation; Science, Faith & Intelligent Design, ed. William A. Dembski (Downers Grove, IL, Intervarsity Press, 1998), 251.
[202.] Francis Collins quoted in Dan Cray, "God vs. Science," Time Magazine (November 5, 2006), accessed April 28, 2012, http://www.time.com/time/printout/0,8816,1555132,00.html
[204.] Jeffrey P. Schloss, "Emerging Accounts of Altruism: 'Love Creation's Final Law'?," in Altruism and Altruistic Love: Science, Philosophy, & Religion in Dialogue, eds. Stephen G. Post, Lynn G. Underwood, Jeffrey P. Schloss, and William B. Hurlbut (Oxford: Oxford University Press, 2002), 221.
[205.] Philip S. Skell, "Why do we invoke Darwin?," The Scientist, 19 (August 29, 2005): 10.
[206.] Noam Chomsky, Language and Mind, 3rd ed. (Cambridge: Cambridge University Press, 2006), 59.
Image: � lulu / Dollar Photo Club.