It says it's hereditary.

It says that heredity... *Note: This article is from Doubt Darwin: The Sudden Rise of the Life of Beings and the Argument for Intelligent Design. Once I heard of Douglas X's success in reaching a very accurate estimate of protein rarity, I immediately wondered about the reaction of proponents of neo-Darwinism. What would they say after this mathematically and experimentally accurate work, published in the Journal of Molecular Biology in 2004, in which he concluded that there is little likelihood of mutations or selection in an innovative gene or functional protein? X's research confirmed other analyses and experiments, and it was able to go beyond peer-reviewed scrutiny, so none of these possibilities made sense, but the defenders of the adequacy of the new Darwinian mechanisms were far from declaring their surrender, as I will show below. In the same year, I published a scientific and authoritative article on the Cambrian explosion and the problem of the origin of biological information required for its interpretation1, citing Axe's findings and explaining why the scarcity of functional proteins in sequence space poses a major challenge to the adequacy of new Darwinian mechanisms. The paper was published in the journal Interest in Biology, Proceedings of the Biological Society of Washington. Museum scientists and evolutionary biologists across the country were angry at the magazine and its editor-in-chief, Richard Sternberg, for allowing this article to be peer-judged and then published. Countercharges followed, as museum officials confiscated Sternberg's keys, his office and his access to scientific samples, and he was transferred from a friend's supervisor to an enemy's supervisor. D. One in evolutionary biology and the other in systems biology, (2) "He is a priest, not a scientist" when in fact he is a scientist, not a clergyman, (3) "He is an active member of the Republican Party, and works for the George W. Bush campaign" when in fact he is busy with scientific research and does not have enough time to engage in political campaigns, whether Republican or otherwise, (4) "He took a bribe to publish this article" and this is untrue, to the contrary accusations. News headlines about the controversy have appeared in journals such as Science, Nature, The Scientist, and Chronicle of Higher Education; other articles have appeared in the general press, such as The Washington Post and The Wall Street Journal; a central theme has been broadcast on National Public Radio; and Sternberg himself appeared on The O'Reilly Factor. Despite the clamor, there was no official scientific response to the article itself, either in the Journal of Lecturers or in any other scientific journal, and the members of the Biological Society Council in Washington, who supervised the publication of the magazine, insisted that they did not want to answer the article, lest they legitimize it. In the end, two scientists advocating science education policies and belonging to the National Center for Science Education, a lobbying group that seeks to teach evolution in public schools, took the lead, and the three authors – geologist Alan Gishlick, education policy lawyer Nicholas Matzke, and wildlife biologist Wesley R. Elsberry – wrote in response to my article on www.TalkReason.org, a leading atheist website, which is not an attacker. The paper was a scientific review, The Origin of New Genes: Profiles from the Past and Present, which appeared in genetic reviews in Nature Reviews Genetics (2003). The paper, authored by University of Chicago molecular biologist Manyuan Long in partnership with several colleagues, is "a comprehensive representative of the original scientific literature documented." Other biologists have echoed the claims of Geschlich, Matzke, and Elsberry in building up the new gene pool in the context of other public controversies. "At the 2005 Kitzmiller F. Dover Court of Appeals for the Miserable Attempt to Get Teachers in Pennsylvania Schools to Read a Statement on Intelligent Design, the biographer Kenneth Miller cited this paper from Long's testimony, saying that it shows how new genetic information evolved, and Judge John E. Jones further cited Miller's testimony." They argue that “specialists know how new genetic information came into being.”10 But do evolutionary biologists really know this? Let’s take a closer look at the article that claimed to show “the way new genetic information arises.”11 It is said that a genetic... Long's article, which is often cited, refers to several scenarios aimed at explaining the evolution of multiple genes. These studies usually sequence a gene and then look for other similar genes or homologs, and then look for the history of small change between the two genes often corresponding to the gene (or genes) in the presumed common ancestor. To do this, the study also looks at the basis of the genetic sequences; to access similar sequences in organisms of different taxonomic groups. Mutations – occurrences of replication, mixing of exons, retropositions, lateral transfer of genes and point-consent mutations – as well as the effectiveness of natural selection. Evolutionary biologists based on these studies hypothesize that modern genes emerge as a result of these multiple mutations, which they see as forming genes over a long evolutionary history. Given the difference in information in modern genes from the information carried by presumed ancestral genes, these studies consider the mechanisms of mutations – presumably responsible for these differences – to explain the origin of genetic information. But on closer examination, none of these published papers show how genes and natural selection have created entirely new genes or proteins from sequence space in the first place, and they do not show that it is acceptable, or logically probable, for these mechanisms to do so in the time available to them, and these published papers assume that there is a significant amount of prior genetic information – in fact, they assume many complete and unique genes – and then suggest various mechanisms that may have made some gradual change. This type of scenario setting can point to highly productive research methods, but we would often make a clear mistake if we considered hypothetical scenarios to be a proof of fact or a complete adequate explanation. None of the scenarios, cited in Long’s paper, prove the mathematical or experimental probability of the mutation mechanism they claim to explain the origin of the genes, nor do they directly account for many of the supposed mutation processes, which are based on evolution. However, the ability of these scenarios to adequately explain the origin of genetic information depends on the evidence for the entities they hint at – the ancestral genes – and the plausibility of the mutation mechanisms they acknowledge. Take a closer look at both sides of these scenarios. Common ancestral genes? All of the scenarios presented in the papers cited by Long begin with reference to the gene of the common ancestor branching out, from which two or more modern genera develop, these scenarios examine the similarity of sequence (information) in two or more genera, as unambiguous evidence for the common ancestor gene (Figure 11.2). As I mentioned in chapters V and VI, the typical methods for reconstructing evolutionary history presuppose Rather than proving that this biological similarity is caused by common ancestral genes, however, as we have seen in Chapter 6, sequence similarity alone does not always definitively indicate shared ancestry, as similarities sometimes appear between species that cannot be explained by genetics from a common ancestor, such as the similar frontal limbs of moles and insects. Mole cricket – There are certainly other possible explanations for this similarity. First, homologous genes may have evolved independently in two parallel lineages starting with two different genes, and this is confirmed by the hypothesis of convergent evolution. There are many examples of homologous evolution of genes in evolutionary and molecular biology publications13 For example, molecular biologists have discovered that both whales and bats have similar systems of positioning through the resonance of sound, involving both genes and proteins13. Moreover, similar genes are likely to be designed separately in each organism to satisfy their functional needs in different living entities. Given the case in this way, the similarity of sequences does not necessarily reflect the evolution of a common ancestor, but rather design conforming to other functional considerations, determinants, or goals. I know for sure that I have not yet provided any independent reasons for considering the design hypothesis, as a hypothesis explaining the similarity of sequences. Genes with an Open Reading Framework Certainly, some genes and the sequences they contain cannot be explained in the light of those scenarios that Long mentioned in his article; all of these scenarios attempt to explain the origin of two genes that are similar by reference to evolution and transmutation of genes of a common ancestor, but recent genomic studies in many diverse organisms show hundreds or even thousands of genes that do not show any substantial similarity in the sequence with any other known gene. ORFans genes appear in every major group of organisms, including plants and animals as well as single-celled, eukaryotic or prokaryotes, and in some organisms amount to nearly half of the genome.16 Thus, even if it can be assumed that similar gene sequences always refer to a common ancestor gene, these ORFans cannot be explained using scenarios like the ones Long mentioned in his article, and because each ORFans sequence lacks similarity to any other known gene (i.e., none of them are homologs, even in non-evolved species), it is impossible to know which common ancestor gene (ORFans) may be the origin of its own evolution. Some might argue that biologists are mapping more genomes day by day, adding more gene sequences to the protein database, and eventually the mystery associated with ORFans will disappear. However, to this day, things are going in the opposite direction. As scientists explore and map more genomes, they discover more and more ORFans but no corresponding gene numbers. Reasonability of mutation-based processes Even if biologists can prove the existence of common ancestor genes from which the imagined scenarios begin, this does not mean that they have demonstrated the reasonableness of producing Darwinian new mechanisms of genetic information from that ancestor. Also, the word "reasonableness" in this context has an important and scientifically and methodologically specific meaning, as studies in the philosophy of science show that a successful explanation in historical science such as evolutionary biology requires the production of "causal sufficient" explanations. In this principle, Darwin subordinates the scientific reasoning used by one of the leading geographers (Charles Lille) to events in the deep past, with Lille insisting that a good explanation of the origin of geological features must state "the reasons now at work," i.e., reasons known from contemporary experience for their ability to produce studied effects.18 Natural selection, mutations, and other patterns of random change are clearly “working causes right now,” and no one thinks about it. But have these processes proved capable of producing the desired effects, i.e., the genetic information necessary for structural innovations in the history of life? Confiscation is required First, most mutation-dependent processes that evolutionary biologists beg for in the scenarios cited by Long's article postulate the pre-existence of significant amounts of genetic information in genes or model segments of DNA or RNA, and Long's article sheds light on the seven mechanisms of mutations, which serve to form the new DNA: (1) Mixing of exons. (2) Double the gene. (3) Retroposition retropositioning for transcription of messenger RNA. (4) Lateral transfer of genes. (5) Transfer of moving units or genetic elements. (6) The fusion or fusion of genes. 7 Emergence of de novo. Each of these mechanisms, with the exception of non-emergence, begins with pre-existing genes or pre-existing sequences. This functionally defined, pre-existing information is sometimes sufficient to encode the construction of a complete protein or distinct protein fold. These scenarios also assume not only pre-existing and unexplained sources of biological information, but also an explanation of, or even an attempt to explain, the origin of any of these mechanisms that they conceive of as a consensus space. Proponents of mixing exons argue that typical sections of the genome are randomly arranged, and re-arrange themselves – randomly as well – to generate new genes, not far from re-arranging the paragraphs within a new article to generate a new article. The term exon refers to protein-encrypted regions of the genome (in genomes that contain encoded regions of proteins distributed in non-encrypted regions, and protein-encrypted regions are intersected by other non-enable segments that are often known as entrons. Although most proteins are encoded in many exons, a single exon may encode an intrinsic unit of protein structure, such as a functional protein fold. In fact, proponents of gene mixing claim that it supports them, as they explain the emergence of new proteins. They assume that exons undergo blind random mixing to form new genes, but this mechanism is not capable of producing new protein folds. Evolutionary scenarios that rely on other mutation mechanisms presuppose the existence of important sources of pre-existing genetic information. Gene duplication, as the name suggests, involves the production of a duplicate version of a pre-existing gene that is rich in functionally determined information. Retropositioning of a messenger RNA to recombine the recombinant DNA into the genome sequence of another genome involves the replication of the encoded part of a pre-existing gene, as well as the translocation of an existing gene. The transfer of animate genetic elements similarly occurs when a pre-existing gene falls into the strand of DNA known as plasmid, which enters the other organism to be incorporated into the new genome. This process occurs mainly in single-celled organisms, a similar process can occur in eukaryotes; where animate genetic elements known as transposons that occur in each other – sometimes known as jumping genes – jump to another location. The six mutation mechanisms assume the pre-existence of genetic units containing specific genetic information, and some of these mechanisms also rely on the pre-existence of complex molecular machines such as reverse transcriptase used in the retropositioning mechanism or other complex cellular machines involved in DNA replication. In general, what evolutionary biologists think, is like trying to produce a new book by copying the pages of a previous book – gene duplication, gene lateral transfer, moving elemental gene transfer –, rearranging the text sections on each page – mixing exons and repositioning regression and gene fusion –, and introducing random word errors at the character level of each part of the text – the point mutations – and then random reordering the new pages. In any case, all these scenarios are forfeited, as there is a big difference between confusing or gradually changing pre-existing functional sequence models – and containing specific information – and explaining how these models appear to have information-rich sequences in the first place. Has it evolved out of nowhere? For example, one of the papers that Long included in his article looked to explain the origin of a gene’s promotor region – a part of the gene that helps initiate gene transcription to RNA – and concluded that “this unusual regulatory niche didn’t evolve literally.” For example, Long cites a study that seeks to explain the origin of the antifreeze protein in Antarctic fish, cutting out a phrase that said: "Inflate a short sequence of DNA to produce a new protein with a new function."22 Long also cited an article in Science to explain the origin of two genes. Two humans involved in neural development in the fetus, this article attributed their origin to "the emergence of their building blocks from nowhere, which are single genes or pieces of genes that encode the domains of protein", where Exxon "automatically originated from a unique unencrypted sequence", and other research papers resort to similar provisions, as mentioned in a 2009 scientific publication. "Emerging out of nowhere for at least three human genes encoded for proteins since humans separated from chimpanzees," as neither had protein-encoded corresponding sequences in other regions of the genome. A more recent scientific publication in the journal PLoS Genetics announced that: "60 genes encoded for new proteins have arisen out of nowhere in the human lineage since humans separated from chimpanzees."25 This is a far higher estimate than previous modest and conservative estimates admittedly. Another 2009 paper in the journal Genome Research, entitled Appropriately (Darwinian Alchemy: The Evolution of Human Genes from Uncoding RNA), investigated the emergence of genes from nowhere, stating: "The emergence of complete functional genes - producing functional proteins with their own promotors and an ORF for each - from the DNA of scrap appears to be highly unlikely, close to the probability of lead turning into gold." The existence of unique gene sequences has forced researchers to call the idea of gene development out of nowhere more than they would like, after a study on fruit flies stated that "nearly 12% of new genes may have appeared in the black-bellied fruit fly groups Drosophila melanogaster by arising out of nothing; from unencrypted DNA sequences p goes further to admit that the recall of this mechanism has no hard-to-consider origin". Because it only determines time and space in unencrypted DNA before it plays a role, it doesn’t explain how these genes first appeared. There aren’t any details explaining how the “pre-adapted” genes came into being with a future function. Indeed, evolutionary biologists use the term genesis from nothing to describe the unexplained increase in genetic information, and they don’t refer to any known process of mutations. Here we sum up: Many of the mutation-dependent processes that Long mentioned in his article are either: (1) Forfeiture of the request as to the origin of the specific information contained in the genes or parts of genes. (2) It calls for leaps out of nothingness which are not explained at all; it is essentially an evolutionary creation out of nothingness. So, in the end, the scenarios mentioned in Long's article do not explain the origin of the specific information in the genes or their parts, but may require a reason that can solve the problem of harmonic inflation mentioned in the previous chapters. But none of the scenarios discussed in Long's article mentioned this problem, let alone show the mathematical plausibility of the mechanisms mentioned, yet Gishlik, Matzke, and Esprey have cited the originality of Long's article. Professor Miller testified at the famous Dover Court, and convinced the federal judge of the ruling that Long had succeeded in showing how genetic information arose, a famous judicial ruling, but it is clear that no one can solve a dilemma or refute an argument by simply failing to define it.31 Protein folds: plausible but irrelevant scenarios Another problem is closely related to the scenarios mentioned by Long in his article, as these scenarios do not attempt to explain the origin of new protein folds, and few of them analyze genes that differ so much from each other that their protein products may be representative of different folds, as these scenarios usually try to explain the origin of homologous genes, which are genes that produce proteins with similar structural folds and perform the same function, or are very close to each other. For example, Long cites a study comparing the genes RNASE1 and RNASE1B, which encode two homologous digestive enzymes.32 The two proteins do roughly the same job: breaking down RNA molecules in the digestive tract in leaf-eating colobine monkeys, but there is a measurable difference in the optimal pH at which they each function, and more importantly, the amino acid sequences for both are predicted to be the same. Long also referred to a reference study on a protein that encodes natural histone Cid protein, in two species that are closely related to fruit flies (Drosophila melanogaster) and their proximals (Drosophila simulans). The study does not attempt to explain the origin of the gene, it just compared the genes in both species and listed some secondary differences between them, then wondered how these differences appeared. 92.5% at all, and even the natural sequences known to have this high degree of conformation have the same folds. Long also mentioned two other studies on the FOXP2 gene, which regulates gene expression in humans, chimpanzees, other primates, and mammals. This gene plays a role in brain development in humans and other mammals34, however one study says that the protein encoded by this gene in humans has undergone two amino acid changes in the human strain35 during its entire evolutionary life from the common ancestor of chimpanzees and humans. Long’s review cited a large number of similar scenarios – scenarios that seek to explain the evolution of novel gene variants and their homologous proteins – rather than the emergence of new protein folds. This is an important difference because, as we saw in chapter 10, new protein folds represent the smallest selective unit of structural innovations, and are relied upon by the largest structural innovations in the history of life. So, even where these scenarios are plausible, they are irrelevant to the cause of the genetic information necessary to produce this type of structural innovation that occurs in the Cambrian explosion – or many other events in the history of life. Protein Folds: Case-Related, but Unreasonable Scenarios In a few cases, the evolutionary scenarios described in Long’s article appear to be attempts to explain genes that differ somewhat, and that they are reasonably capable of encoding proteins that have different folds. Long, for example, discusses multiple papers, which equate mixing of exons with mixing of protein domains. Remember that a protein field is a tertiary vacuum protein structure (or fold) made of several smaller secondary structures such as alpha sizzles or beta sheets (Figure 10.2). Many proteins have many fields, each with a unique tertiary or folding structure. One form of the exons mixing hypothesis assumes that each exon encodes a specific protein field, and argues that random splicing (excising, mixing, and recombination) of the exons from the genome will cause the sequences of genetic information to be rearranged. As Long hypothesizes, "Exons, also known as field mixing, recombine sequences that encode many protein fields to produce mosaic proteins."36 The mechanism of mixing exons, and the similar idea of genetic fusion, may provide one of the most plausible ways to generate new proteins (composite).37 However, the ability of exons to explain the origin of genetic information necessary to produce new protein folds, or complex whole proteins, is problematic for several reasons. First, the hypothesis of mixing exons seems to assume that each exon involved in the process encodes a protein field that involves a distinct tertiary spatial structure. Proteinists argue that a protein field is equivalent to a protein fold, although distinct protein structures folds may consist of several fields or folds that are smaller. However, some proponents of mixing exons may use the term "protein field" more ambiguously, as they may equate fields with smaller structural units such as folds made from multiple units of secondary structures such as alpha helices or beta strands. But most of the time, if you cut the amino acid chains forming the field into a ridge, they won't come back together as they were, but why? Take a piece of protein or make that protein, you will produce a flexible amino chain – that is, it has lost its original shape or its ability to form a fixed structure – so this form of the hypothesis (mixing of exons) does not have credibility; Because it wrongly assumes that the missing protein buffer is able to blend properly, like building blocks to form new and stable functional vacuum folds. Moreover, even if this physical confusion is reasonable, this form of hypothesis will face another problem, as it still presupposes the existence of unexplained genetic information, specifically the necessary information, which describes not only the small strands, but also those required to arrange these small units into fixed folds, down to functional proteins in the end. Second, the oxygen mixing hypothesis considers the exons to correspond to the boundaries of the domains or protein folds, because it assumes that each exon undergoes a process (mixing) that encodes a specific protein field. In existing genes, the boundaries of the exons do not correspond to the boundaries of the domains involved in large proteins.38 If the mixing of the exons explains how the known proteins did not come into existence, then the boundaries of the exon within the genes must also correspond to the large domains of the proteins. Third, there's another reason to think it's mentally unacceptable to rely on mixing exons to graft protein kinases into new protein kinases from smaller protein kinases, and to know what that reason is, we need to test what the side chain is. The 20 amino acids that make up the proteins have a common backbone of nitrogen, carbon, and oxygen, but each of them has a different chemical group known as the side chain that makes up that backbone. 39 Although many different sequences are generated for secondary structures – alpha filaments and beta filaments – the formation of fixed folds is much more difficult, and requires a lot of specificity in the arrangement of amino acids and their lateral chains. Specifically, elements in small secondary structural units in a protein are surrounded by lateral chains, so they cannot be combined into new ones unless these elements also have complementary subunits40. The need for high-quality amino acid sequence sequences, discussed in the previous chapter, means that the vast majority of amino acid sequence mergers, at the secondary structure level, will not reach fixed folds. As discussed in chapter 10, the extreme scarcity of functional proteins (fixed folds) in the sequence space ensures that the probability of finding a correct sequence is very small, making the fold almost constant. This has been explained by molecular biologist Anne Gouger: "Therefore, -slices and -sheets are structural elements that depend on their sequence within protein folds, so they cannot be repositioned as Lego game pieces."44 It is also difficult to find different amino acid sequences in secondary structural units that stabilize the folds, due to the extreme scarcity of functional and folding sequences within the space of amino acid sequences. Generating specific sequences involving fixed structures, whether in vitro or in the history of life, requires solving the problem of conformational inflation, and even small ordered folds require five or six more secondary structural units of 10 amino acids or close to that. However, many functions that are indispensable for the simplest cell to function require many folds – at least 150 amino acids – to work together in perfect harmony, so the need to produce proteins of this length cannot be avoided at least many times throughout the history of life. Remember that Douglas X values the ratio of the needles (functional sequences) in the straw sticks in the stack (nonfunctional sequences) by 1 to 10 77 of the short sequences -150 amino acids. Of course, in naturally occurring sequences, interactions between the lateral chains in secondary structure units actually keep the folds constant, but these three-dimensional intermolecular proteins rely on extremely rare and well-ordered sequences of amino acids. The question is not whether the problem of (reciprocal research) necessary to produce stable protein folds has been solved, but whether the modern Darwinian mechanisms of random mutations provide a plausible solution. The papers cited by Long in his review give no reason to think that mixing exons – or any other mutation-dependent mechanism – could solve this problem. The hypothesis of mixing exons ignores the need for the quality of the side chains, although the need for such quality has repeatedly thwarted laboratory attempts to manufacture new proteins from secondary structural units in the desired manner. But proponents of mixing exons make no attempt to show how re-arranging protein domains – whether we consider domains to be fragments of folds or whole folds – will solve the cross-problem, face no quantitative experimental Sauer or X estimates of gene scarcity or functional proteins, and face no probability calculations based on these estimates. Advocates of axons mixing eventually insist in a few words, and with apparent confidence, as Long did in his review, that axons mixing often rearranges sequences that encode many protein domains to create mosaic proteins. Salad Long and his colleagues’ emphasis on mixing exons, like many other statements about supposed mutation-dependent mechanisms, blurs the distinction between theory and evidence. Apart from the authoritarian tone of such statements, evolutionary biologists rarely directly observe the mutation-dependent processes they imagine, but they see models of similarity and variation in genes, and thus attribute them to the process they assume. In the absence of such evidence, evolutionary biologists continue to display what one biologist I know calls the “authority of words” – a term that means that they offer vague descriptions of events of the unseen past, some of which may be possible, but none of which have a proven ability to generate the information necessary to produce new forms of life. This kind of evolutionary publication imagines exons as: * Other genes that you "make fun of"46, and/or "donate"47 It comes from “unknown sources.”48 Intensive reconstruction of genes. * Attributes "Serial Continuity Suitable for Sequences"50 to mutations or to "Server Acquisition"51 to the elements of the promoter. Assume that "radical changes in gene structure are due to adaptive rapid development."52 Affirms that "positive selection plays an important role in the evolution of genes", even in cases where the function of the studied gene, and thus the trait it is selected for, is completely unknown.54 Genes imagine coming together from pieces of DNA that have no interconnected functions or none at all.55 * Assume the "creation" of new exons from unique unencrypted genome sequences that evolved by chance.56 * resort to the idea of "chimeric fusion of two genes."57 "Semi-identical"58 proteins in different evolutionary strains are interpreted as "a shocking case of convergent evolution."59 When unable to identify any physical source for the development of a new gene, they insist that "genes appear and evolve rapidly, generating copies that bear little resemblance to their predecessors, because they appear to be hypermutable."60 Ultimately, when all else fails, these scenarios call for “rising out of nowhere” for new genes, as if that phrase differed from anything others have said, as if it were based on scientific evidence of the power of mutation-dependent mechanisms to produce significant amounts of new genetic information.61 These vague accounts are nothing more similar than they are to the games of medieval theological philosophers: Opium didn’t put people to sleep because it contained a sleeping spirit. What causes genes to evolve so quickly? Their high mutation capacity, or perhaps their undergoing rapid adaptive development. How do we explain the origin of two similar genes in two very different separate lineages? What is convergent evolution? It is the presence of two similar genes in two very different separate lineages. How can convergent evolution occur if we know that there is little likelihood of one functional gene in the space of the probabilistic sequences, let alone that the same gene appears twice independently? Do you want to explain the existence of two similar genes in two closely related evolutionary lineages? Try "gene duplication," "chemyr genetic fusion," "regressional repositioning," "intense rearrangement of the genome," or... any other pseudoscientific verbal structures. These ambiguous scenarios raise serious questions about scientists’ ability to take them as conclusive proofs or opposites to anything, not to mention a mathematically rigorous experimental refutation that defies the mutations and natural selection described in the previous chapter. So, despite the official announcement from the Federal Court, and the claims of "extensive documentation in scientific publications of the origin of new genes," evolutionary biologists have not proved how new genetic information emerged, at least not in sufficient quantities to build protein folds, which are the main units of biological innovation. To be fair, modern Darwinists have mathematical models of how their hands work, models that suggest that there can be infinite evolutionary changes in the right conditions. The assumption of accurate representation of these models, based on the equations of population genetics, has given evolutionary biologists confidence in the creative power of various mechanisms based on mutations. (1) Stephen C. Meyer, "The Origin of Biological Information and the Higher Taxonomic Categories." (2) For a detailed discussion of the facts of the Sternberg case, see: "Smithsonian Controversy" www.richardsternberg.com/smithsonian.php; U.S. Office of Special Counsel Letter (2005) at www.discovery.org/f/1488; United States House of Representatives Committee on Government Reform, Subcommittee Staff Report, "Intolerance and the Politicization of Science at the Smithsonian" (December 2006), at www.discovery.org/f/1489; Appendix, United States House of Representatives Committee on Government Reform, Subcommittee Staff Report (December 2006) at www.discovery.org/f/1490. (3) Holden, "Defying Darwin"; Giles, "Peer-Reviewed Paper Defends Theory of Intelligent Design," 114; Agres, "Smithsonian ‘Discriminated ’Against Scientist"; Stokes, " . . . And Smithsonian Has ID Troubles"; Monastersky, "Society Disowns Paper Attacking Darwinism". (4) Powell, "Controversial Editor Backed"; Klinghoffer, "The Branding of a Heretic". (5) Hagerty, "Intelligent Design and Academic Freedom. (6) See www.talkreason.org/AboutUs.cfm. (7) Gishlick, Matzke, and Elsberry, "Meyer’s Hopeless Monster," www.talkreason.org/AboutUs.cfm. (8) Jones, Kitzmiller et al. v. Dover Area School District. (9) Matzke and Gross, "Analyzing Critical Analysis," 42. (10) Matzke and Gross, "Analyzing Critical Analysis," 42. (11) Matzke and Gross, "Analyzing Critical Analysis," 42. 12 See chapter X, p. 15 The four main mechanisms by which a double transcription of DNA occurs. For examples, see: Zhen et al., "Parallel Molecular Evolution in an Herbivore Community"; Liet al., "The Hearing Gene Prestin Unites Echolocating Bats and Whales"; Jones, "Molecular Evolution"; Christin, Weinreich, and Bresnard, "Causes and Evolutionary Significance of Genetic Convergence"; Rokas and Carroll, "Frequent and Widespread Parallel Evolution of Protein Sequences". "In-depth analysis of specific genes, in the context of multi-geneline evolutionary historiography studies, has shown that convergent adaptive evolution, once thought to be very rare, is also a source of conflict between genetic evolutionary trees as is conflict between morphological and molecular lineage trees." ("Understanding Phylogenetic Incongruence," 993). (14) Shen et al., "Parallel Evolution of Auditory Genes for Echolocation in Bats and Toothed Whales"; Li et al., "The Hearing Gene Prestin Unites Echolocating Bats and Whales"; Jones, "Molecular Evolution". (15) Khalturin et al., "More Than Just Orphans"; Merhej and Raoult, "Rhizome of Life, Catastrophes, Sequence Exchanges, Gene Creations, and Giant Viruses"; Beiko, "Telling the Whole Story in a 10,000-Genome World". (16) Suen et al., "The Genome Sequence of the Leaf-Cutter Ant Atta cephalotes Reveals Insights into Its Obligate Symbiotic Lifestyle". (We also found 9,361 unique proteins for A.cephalotes, which account for more than half of their predicted proteome.5 See also Smith et al., "Draft Genome of the Globally Widespread and Invasive Argentina Ant (Linepithema humile)" ("There were a total of 7184 unique genes (45%) in the L. humile of the other three species.") (17) Tautz and Domazet-Lošo, "The Evolutionary Origin of Orphan Genes"; Beiko, "Telling the Whole Story in a 10,000-Genome World"; Merhej and Raoult, "Rhizome of Life, Catastrophes, Sequence Exchanges, Gene Creations, and Giant Viruses." (18) Lyell, Principles of Geology. (19) Pray and Zhaurova, "Barbara McClintock and the Discovery of Jumping Genes (Transposons)." (20) Long et al., "The Origin of New Genes," 867. (21) Nurminsky et al., "Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila," 574. (22) Chen, DeVries, and Cheng, "Evolution of Antifreeze Glycoprotein Gene from a Trypsinogen Gene in Antarctic Notothenioid Fish," 3816. (23) Courseaux and Nahon, "Birth of Two Chimeric Genes in the Hominidae Lineage." (24) Knowles and McLysaght, "Recent de Novo Origin of Human Protein-Coding Genes." (25) Wu, Irwin, and Zhang, "De Novo Origin of Human Protein-Coding Genes." (26) Guerzoni and McLysaght, "De Novo Origins of Human Genes"; see also Wu, Irwin, and Zhang, "De Novo Origin of Human Protein-Coding Genes." (27) Siepel, "Darwinian Alchemy". (28) Siepel, "Darwinian Alchemy". (29) Siepel, "Darwinian Alchemy." (30) As Siepel notes, "The origin of these entirely new genes raises the question of how evolution produces these functional genes, starting with a neutral DNA that is not encoded by natural selection." Although each of these genes is not as complex as an entire organ, such as an eye or even a feather, it still needs a series of non-simple requirements to become functional, such as the presence of an ORF (open-readable frame) gene. 31 Of course, one could argue that mutation processes that are frequently cited to explain the emergence of new genes from pre-existing genetic information cassettes are the same as explaining the origin of the information in those cassettes in the first place. That view suggests that the scenarios cited by Long are not so much confiscated as they generate a reluctance to explain them during the basic development of biological information, i.e. at the point of origin of life. (32) Zhang, Zhang, and Rosenberg, "Adaptive Evolution of a Duplicated Pancreatic Ribonuclease Gene in a Leaf-Eating Monkey". The genes encoding these two proteins differ by 12 nucleotides in their encoded sequences, and these differences produce two time-differing proteins in total negativity. This difference in turn allows RNASE-1B to function at a slightly lower pH than the other RNASE1 protein. 33 In this study ("Adaptive Evolution of Cid, a Centromere-Specific Histone in Drosophila"), Malik and Henikoff conclude that "adaptive evolution has obtained strains of both D. melanogaster and D. melanogaster". Since their separation from the common origin, the simulans have based this conclusion on an analysis of the ratio of "synonymous" mutations in the genome of these two organisms. The study found that many variations/mutations in nucleotide base sequences changed amino acid sequences (hence called "non-tandem" mutations), while the rest did not (called "tandem" mutations). From neutral evolution alone, leading the authors to conclude that adaptive evolution has had offspring of both D. melanogaster and D. simulans since their separation from the common origin." Since some of these differences are found in protein-binding regions on chromosomes, they may have influenced protein binding ability. However, the authors of the paper do not identify any particular functional effect of these amino acid changes, and base their claims on “strong evidence for adaptive evolution in Heston Cid” solely by comparing the relative numbers of a handful of tandem and non-symptom variations between genes. (34) Enard et al., "Molecular Evolution of FOXP2, a Gene Involved in Speech and Language"; Zhang, Webb, and Podlaha, "Accelerated Protein Evolution and Origins of Human-Specific Features." (35) Enard et al., "Molecular Evolution of FOXP2, a Gene Involved in Speech and Language." (36) Long et al., "The Origin of New Genes," 866. (37) Darnell and Doolittle, "Speculations on the Early Course of Evolution"; Hall, Liu, and Shub, "Exon Shuffling by Recombination Between Self-Splicing Introns of Bacteriophage T4"; Rogers, "Split-Gene Evolution"; Gilbert, "The Exon Theory of Genes"; Doolittle et al., "Relationships of Human Protein Sequences to Those of Other Organisms." 38 For example, Arli A. Parikesit and colleagues stated that "although there is a statistically significant relationship between the protein field boundary and the exon boundary, about two-thirds of the protein fields studied have at least one intron in their DNA sequences, and on average, the field contains 3 or 4 introns" ("Quantative Comparison of Genomic-Wide Protein Protein Distributions after 96". (39) Gauger, "Why Proteins Aren’t Easily Recombined." (40) Axe, "The Limits of Complex Adaptation." See also Voigt et al., "Protein Building Blocks Preserved by Recombination." 41 Experimental mixing of genes has proven useful only when the two genes of the parents are substantially the same. See: Friedman, and Bailey-Kellogg, "Algorithms for Optimizing Cross-Overs in DNA Shuffling." 42 In 2012, a research group from the University of Washington announced that it had successfully designed several stable protein folds using a few rules, and a lot of computerized analysis, trial, and error (about 10% of the designed proteins folded as expected). The researchers acknowledged that there is something like a trade-off between stability and functionality in natural proteins. We have yet to investigate whether sequence engineering methods can produce functionally stable folds from nothing, even with the best computing minds and resources to work on this dilemma. Nobuyasu et al., "Principles for Designing Ideal Protein Structures"; Marshall, "Proteins Made to Order." (43) Altamirano et al., "Directed Evolution of New Catalytic Activity Using the Alpha/Beta-Barrel Scaffold." See also Altamirano et al., "Retraction: Directed Evolution of New Catalytic Activity Using the Alpha/Beta-Barrel Scaffold." (44) Gauger, "Why Proteins Aren’t Easily Recombined." (45) Axe, "The Case Against Darwinian Origin of Protein Folds." 46 For example, look at: Long and Langley, "Natural Selection and the Origin of Jingwei, a Chimeric Processed Functional Gene in Drosophila"; Wang et al., "Origin of Sphinx, a Young Chimeric RNA Gene in Drosophila melanogaster"; Begun, "Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila." (47) Long et al., "Exon Shuffling and the Origin of the Mitochondrial Targeting Function in Plant Cytochrome cl Precursor." (48) Long et al., "Exon Shuffling and the Origin of the Mitochondrial Targeting Function in Plant Cytochrome cl Precursor." (49) Nurminsky et al., "Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila." (50) Nurminsky et al., "Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila." (51) Brosius, "The Contribution of RNAs and Retroposition to Evolutionary Novelties." (52) Begun, "Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila." (53) Begun, "Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila." 54 Of the papers cited by Long that employ natural selection although the function of the gene is unknown, as well as the function subject to selection: "Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila"; Long and Langley, "Natural Selection and the Origin of Jingwei, a Chimeric Processed Functional Gene in Drosophila"; Johnson et al., "Positive Selection of a Gene Family During the Emergence of Humans and African Apes." (55) Logsdon and Doolittle, "Origin of Antifreeze Protein Genes." (56) Courseaux and Nahon, "Birth of Two Chimeric Genes in the Hominidae Lineage." (57) Paulding, Ruvolo, and Haber, "The Tre2 (USP6) Oncogene Is a Hominoid-Specific Gene." (58) Chen, DeVries, and Cheng, "Convergent Evolution of Antifreeze Glycoproteins in Antarctic Notothenioid Fish and Arctic Cod." (59) Logsdon and Doolittle, "Origin of Antifreeze Protein Genes." (60) Johnson et al., "Positive Selection of a Gene Family During the Emergence of Humans and African Apes." (61) Nurminsky et al., "Selective Sweep of a Newly Evolved Sperm -Specific Gene in Drosophila"; Chen, DeVries, and Cheng, "Evolution of Antifreeze Glycoprotein Gene from a Trypsinogen Gene in Antarctic Notothenioid Fish"; Courseaux and Nahon, "Birth of Two Chimeric Genes in the Hominidae Lineage"; Knowles and McLysaght, "Recent de Novo Origin of Human Protein-Coding Genes"; Wu, Irwin, and Zhang, "De Novo Origin of Human Protein-Coding Genes"; Siepel, "Darwinian Alchemy". - Dr. Steven Meyer. — Source: Brahin Center website - Published on 2018-10-07 (archived at the Internet Archive) https://braheen.com/articles/evolution-design/يحكى-أن-مورثة