Researchers “very shocked” by recent new genes that form distinctly human brain

_{Denyse O'Leary

October 19, 2011

Human evolution, News}

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File:Gray726-Brodman-prefrontal.svg — from Gray's Anatomy, the prefrontal cortex

In “New Genes, New Brain” (The Scientist , October 19, 2011), Cristina Luiggi reports,

The evolution of the human brain may have been driven by a group of novel genes that arose fairly recently in primate evolution.

A bevy of genes known to be active during human fetal and infant development first appeared at the same time that the prefrontal cortex—the area of the brain associated with human intelligence and personality—took shape in primates, a new study published yesterday (October 18) in PLoS Biology found. The timing suggests that the new genes may have been intimately tied to the evolution of the human brain.

Previous research focused on older genes conserved across the animal kingdom, looking at new genes is hoped to provide insight. Like:

“We were very shocked that there were that many new genes that were upregulated in this part of the brain,” said Long, who added that he was also taken aback by synchronicity of the origin of the genes and the development of novel brain structures. It seems that around the same time that the neocortex and the prefrontal cortex arose, and then expanded in humans, a large collection of genes also popped up.

That’s something the old genes were never going to tell researchers.

It feels like a rollout of some kind, no?

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Comments

PaV: "What is the likelihood of this happening by chance? 1 in 10^500,000? Any reasonable person would say that it could not have happened by chance mechanisms." When in doubt, invent some big, big numbers.DrREC_{October 21, 2011
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I agree! Pav's claim has me a bit confused on how s/he arrived at this conclusion. So how about a citation, Pav?Acipenser_{October 21, 2011
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"Is this really an intellectually honest reply?" Yes. PaV, you're making some sort of argument that because cytochrome c is required for animal life, that what exactly? It isn't required for all life. There isn't any meat on this one. PaV: “So, really, just ONE de novo gene is beyond Darwinian explanations.” DrREC: There are several examples of de novo genes with tractable origins. PaV: Lists another example of a de novo gene with tractable origins. Are you familiar with the term 'own-goal' PaV? Contrast: "Cross-species analysis revealed interesting evolutionary paths of how this gene had originated from noncoding DNA sequences: insertion of repeat elements especially Alu contributed to the formation of the first coding exon and six standard splice junctions on the branch leading to humans and chimpanzees, and two subsequent substitutions in the human lineage escaped two stop codons and created an open reading frame of 194 amino acids." With: PaV: “So, really, just ONE de novo gene is beyond Darwinian explanations.” Creation of new fCSI. Thanks for the example. And no, I'm not behind the times. I listed several mechanisms for de novo gene creation, including ones where no coding ORF existed. But thanks for the additional example!DrREC_{October 21, 2011
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The fact that a Darwinist claims that it takes 31.6 million years to fix two amino acid substitutions in a population I really want to read this paper, will be fun to see how you've misconstrued this one :)wd400_{October 20, 2011
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Elizabeth:
What makes you think that the new genes all arrived at once? The tree they give makes it fairly clear how new genes accumulate between branches.
What makes me think that the new genes all arrived at once? The fact that a Darwinist claims that it takes 31.6 million years to fix two amino acid substitutions in a population, coupled to the fact that between the chimp and human lineages we're looking at what, 15-20 million years. Would you like to propose a "gradualistic" mechanism explaining all of this? And, yes, the tree does give us a nice view of how new genes accumulate. But this exactly fits my point: They ALL look the same. That is, the proportion of "new genes" being upregulated as compared to the "old genes" is quite symmetrical; which dovetails with the point I was making above: i.e., what we see in the human/simian differentiation also likely took place at all other major evolutionary tree divergences. Liz Liddle:
but it’s hard for me to imagine how anyone could read it and not find confirmatory evidence of common descent and the effects of natural selection! It even gives the genetic phylogeny!
Confirmatory evidence of common descent? I don't know about you, but it sure looks to me like there are discontinuities there. You can still run MS-DOS on many computers. Should we say that high-powered PCs are the "descendants" of the first, rather primitive ones? Be careful, Lizzie! :)
There is no “mechanism” posited here, and you are not in fact positing one. For some reason you seem to have interpreted the finding as evidence for a single “macroevolutionary speciation event”. What, in the paper, leads you to think such an event occurred, and what “mechanism” for such an event do you see evidence for?
Common sense tells me that if 10^20 replications are necessary to get a two amino acid substitution fixed in a population, then there is no way in hell that Darwinian mechanisms can account for 54 de novo genes---absolutely no way! So, something had to happen. And intelligent agency makes the most sense. And, if an intelligent agent intervenes once, why not take care of all 54 genes? Why intervene 54 times; or a hundred and fifty-four times? Now theistic evolutionists would say that God is nudging the process along. Well, there's simply not enough time for that to happen. An intervention was needed. Again; common sense!
We do not know why the chimp and human lineages originally diverged. It could simply originally have been some kind of physical separation of populations into non-interbreeding groups. At which point, the gradual accumulation of new genes would follow different paths in the two lineages, just as it seems to have done between orangs and champs, and between rhesus monkeys and orangs, and between marmosets and rhesus monkeys.
As to your first two sentences, there is a study out today that challenges your stated view. How timely! :) As to your third sentence: when did this "physical separation" occur? 200 billion years ago? And even that amount of time is insufficient to account for Darwinian mechanisms arriving at the what is finally seen.
However it does look as the there has been steady selection for genes that are beneficially expressed in PFC during development, and for regulatory genes that lead to such expression, not surprisingly, as it looks as though the associated PFC effects lead to greater intelligence, which is likely to have a reproductive advantage.
What you've just stated is filled with Darwinian presuppositions. You talk about "selection". Well, what does that mean? Nothing. Here's how things really stand: genes for PFC are preferentially expressed during development. That's all we KNOW. The rest is but fitting known facts into a Darwinian interpretation. IOW, a "just-so" story. No more. No less.
So we see a steady accumulation along the homind lineage, from marmosets onwards, of genes that are expressed in the PFC, with various populations (rhesus, orang, chimp) getting of the bus a bit early.
I don't think you have any way of knowing whether what you just wrote is true or not. Yes, we see a "steady accumulation". But is it "gradual"; or is it sudden? How do yo propose to distinguish these two, real possibilities?PaV_{October 20, 2011
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ThoughtSpark: Sometimes I don't know who people are here. You haven't blogged before. I presumed you were a Darwinist; but I reread your post from the vantage point of ID/Darwinian skepticism, and I think I realize your point now. Sorry (I was in a terrible hurry this morning)PaV_{October 20, 2011
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But it isn’t essential for all life-certainly not archaea, bacteria, and some fungi. The further you go from animals, the more divergent the sequence.
Is this really an intellectually honest reply? You know full well that you're venturing out into different kingdoms, the existence of which presents problems for Darwinism, as it exhibits a "bush-like" character, and not a "tree-like" character. Further, would you like to posit the way in which cytchrome C came about? Did it come from the archea, e.g.? But that would mean that one "kingdom" gave rise to another "kingdom", thus making them part of only ONE "kingdom". This is the kind of intellectual dishonesty that a predisposition to Darwinism brings about. This is pure rhetoric, and not worthy of scientific inquiry. PaV: “So, really, just ONE de novo gene is beyond Darwinian explanations.” DrREC:
Why? There are several examples of de novo genes with tractable origins. A recombination of two genes, retrotransposition of an exon into a pseudogene, mutations at a transcribed, but non-translatable region, yielding a new ORF.
"Examination of the gene structure and homology further revealed that these genes were generated by DNA-mediated duplication, RNA-mediated duplication (retroposition), and de novo origination (which created a protein without a parental locus) (Figure 3)." From: A Human-Specific De Novo Protein-Coding Gene Associated with Human Brain Functions, Chuan-Yun Li, Yong Zhang, Zhanbo Wang, Yan Zhang, Chunmei Cao, Ping-Wu Zhang, Shu-Juan Lu, Xiao-Mo Li, Quan Yu, Xiaofeng Zheng, Quan Du, George R. Uhl, Qing-Rong Liu*, Liping Wei*, 2009:
For decades, gene duplication, retrotranspositions and gene fusions were believed to be major ways to increase gene number. All involve “mother” genes as the “building blocks” for new genes. However, several recently identified “motherless” genes challenged the idea in that some proteins might have emerged de novo from ancestral non-coding DNAs.
You seem to be a little bit behind the times, DrREC.PaV_{October 20, 2011
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It would appear that the de novo genes are found throughout the clusters; not in just one or two clusters. So the de novo origins are spread throughout the genome, marking many independent de novo origins. What is the likelihood of this happening by chance? 1 in 10^500,000? Any reasonable person would say that it could not have happened by chance mechanisms.PaV_{October 20, 2011
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Of interest to this 'regulatory network' quote at post 6 by PaV:
Our data reveal that evolutionary change in the development of the human brain happened at the protein level by gene origination and also via evolution of regulatory networks,
When they claim evolution of regulatory networks, they are in fact claiming the origination of a novel regulatory codes, which is very similar to someone claiming the proof for the origination of the genetic code itself. i.e. It is a very, very, fantastic claim which is backed up by ZERO empirical evidence other than their Darwinian belief that is must have happened by Darwinian processes since, by golly, there the novel regulatory code sits: notes:
Researchers Crack ‘Splicing Code,’ Solve a Mystery Underlying Biological Complexity Excerpt: “For example, three neurexin genes can generate over 3,000 genetic messages that help control the wiring of the brain,” says Frey. “Previously, researchers couldn’t predict how the genetic messages would be rearranged, or spliced, within a living cell,” Frey said. “The splicing code that we discovered has been successfully used to predict how thousands of genetic messages are rearranged differently in many different tissues. http://www.sciencedaily.com/releases/2010/05/100505133252.htm Nature Reports Discovery of “Second Genetic Code” But Misses Intelligent Design Implications - May 2010 Excerpt: Rebutting those who claim that much of our genome is useless, the article reports that "95% of the human genome is alternatively spliced, and that changes in this process accompany many diseases." ,,,, the complexity of this "splicing code" is mind-boggling:,,, A summary of this article also titled “Breaking the Second Genetic Code” in the print edition of Nature summarized this research thusly: “At face value, it all sounds simple: DNA makes RNA, which then makes protein. But the reality is much more complex.,,, So what we’re finding in biology are: # “beautiful” genetic codes that use a biochemical language; # Deeper layers of codes within codes showing an “expanding realm of complexity”; # Information processing systems that are far more complex than previously thought (and we already knew they were complex), including “the appearance of features deeper into introns than previously appreciated” http://www.evolutionnews.org/2010/05/nature_reports_discovery_of_se.html Canadian Team Develops Alternative Splicing Code from Mouse Tissue Data Excerpt: “Our method takes as an input a collection of exons and surrounding intron sequences and data profiling how those exons are spliced in different tissues,” Frey and his co-authors wrote. “The method assembles a code that can predict how a transcript will be spliced in different tissues.” http://www.genomeweb.com/informatics/canadian-team-develops-alternative-splicing-code-mouse-tissue-data
further note:
Venter vs. Dawkins on the Tree of Life - and Another Dawkins Whopper - March 2011 Excerpt:,,, But first, let's look at the reason Dawkins gives for why the code must be universal: "The reason is interesting. Any mutation in the genetic code itself (as opposed to mutations in the genes that it encodes) would have an instantly catastrophic effect, not just in one place but throughout the whole organism. If any word in the 64-word dictionary changed its meaning, so that it came to specify a different amino acid, just about every protein in the body would instantaneously change, probably in many places along its length. Unlike an ordinary mutation...this would spell disaster." (2009, p. 409-10) OK. Keep Dawkins' claim of universality in mind, along with his argument for why the code must be universal, and then go here (linked site listing 23 variants of the genetic code). Simple counting question: does "one or two" equal 23? That's the number of known variant genetic codes compiled by the National Center for Biotechnology Information. By any measure, Dawkins is off by an order of magnitude, times a factor of two. http://www.evolutionnews.org/2011/03/venter_vs_dawkins_on_the_tree_044681.html Shannon Information - Channel Capacity - Perry Marshall - video http://www.metacafe.com/watch/5457552/ “Because of Shannon channel capacity that previous (first) codon alphabet had to be at least as complex as the current codon alphabet (DNA code), otherwise transferring the information from the simpler alphabet into the current alphabet would have been mathematically impossible” Donald E. Johnson – Bioinformatics: The Information in Life
Further note:
"In the last ten years, at least 20 different natural information codes were discovered in life, each operating to arbitrary conventions (not determined by law or physicality). Examples include protein address codes [Ber08B], acetylation codes [Kni06], RNA codes [Fai07], metabolic codes [Bru07], cytoskeleton codes [Gim08], histone codes [Jen01], and alternative splicing codes [Bar10]. Donald E. Johnson – Programming of Life – pg.51 - 2010 Ends and Means: More on Meyer and Nelson in BIO-Complexity - September 2011 Excerpt: According to Garrett and Grisham's Biochemistry, the aminoacyl tRNA snythetase is a "second genetic code" because it must discriminate among each of the twenty amino acids and then call out the proper tRNA for that amino acid: "Although the primary genetic code is key to understanding the central dogma of molecular biology on how DNA encodes proteins, the second genetic code is just as crucial to the fidelity of information transfer." http://www.evolutionnews.org/2011/09/ends_and_means050391.html
bornagain77_{October 20, 2011
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DrREC, you atheistic/materialistic faith literally bleeds through in every post you write!!! and If you have the sheer audacity to claim Theism as your belief, it will certainly be in name only and completely devoid of any real substance, as for even your very posts witness against you in this matter!!!,,, Tell you what DrREC, there is a null hypothesis that you atheistic/materialistic neo-Darwinists need to falsify to even be considered scientifically legitimate in the first place. If You guys falsify this null hypothesis, I will at least concede that you guys have a plausible foundation within science in which to make your, thus far, completely unsubstantiated pseudo-scientific conjectures with, for the ability of purely ‘random’ material processes to generate transcendent information!!!
Three subsets of sequence complexity and their relevance to biopolymeric information – Abel, Trevors Excerpt: Shannon information theory measures the relative degrees of RSC and OSC. Shannon information theory cannot measure FSC (Functional Sequence Complexity). FSC is invariably associated with all forms of complex biofunction, including biochemical pathways, cycles, positive and negative feedback regulation, and homeostatic metabolism. The algorithmic programming of FSC, not merely its aperiodicity, accounts for biological organization. No empirical evidence exists of either RSC of OSC ever having produced a single instance of sophisticated biological organization. Organization invariably manifests FSC rather than successive random events (RSC) or low-informational self-ordering phenomena (OSC).,,, Testable hypotheses about FSC What testable empirical hypotheses can we make about FSC that might allow us to identify when FSC exists? In any of the following null hypotheses [137], demonstrating a single exception would allow falsification. We invite assistance in the falsification of any of the following null hypotheses: Null hypothesis #1 Stochastic ensembles of physical units cannot program algorithmic/cybernetic function. Null hypothesis #2 Dynamically-ordered sequences of individual physical units (physicality patterned by natural law causation) cannot program algorithmic/cybernetic function. Null hypothesis #3 Statistically weighted means (e.g., increased availability of certain units in the polymerization environment) giving rise to patterned (compressible) sequences of units cannot program algorithmic/cybernetic function. Null hypothesis #4 Computationally successful configurable switches cannot be set by chance, necessity, or any combination of the two, even over large periods of time. We repeat that a single incident of nontrivial algorithmic programming success achieved without selection for fitness at the decision-node programming level would falsify any of these null hypotheses. This renders each of these hypotheses scientifically testable. We offer the prediction that none of these four hypotheses will be falsified. http://www.tbiomed.com/content/2/1/29 “A code system is always the result of a mental process (it requires an intelligent origin or inventor). It should be emphasized that matter as such is unable to generate any code. All experiences indicate that a thinking being voluntarily exercising his own free will, cognition, and creativity, is required. ,,,there is no known law of nature and no known sequence of events which can cause information to originate by itself in matter. Werner Gitt 1997 In The Beginning Was Information pp. 64-67, 79, 107.” (The retired Dr Gitt was a director and professor at the German Federal Institute of Physics and Technology (Physikalisch-Technische Bundesanstalt, Braunschweig), the Head of the Department of Information Technology.) Meyer and Nelson on a Failed Explanation for the Origin of the Genetic Code Jonathan M. – August 2011 Excerpt: ‘codes and digital information are categories of effects uniformly associated with intelligent causes. Indeed, to the extent that Yarus and others have succeeded in establishing affinities between codons and amino acids, they did so only as a direct consequence of their own intelligent manipulation and intervention.’ The Law of Physicodynamic Insufficiency – Dr David L. Abel – November 2010 Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.” The Capabilities of Chaos and Complexity – David L. Abel – 2009 Excerpt: “A monstrous ravine runs through presumed objective reality. It is the great divide between physicality and formalism. On the one side of this Grand Canyon lies everything that can be explained by the chance and necessity of physicodynamics. On the other side lies those phenomena than can only be explained by formal choice contingency and decision theory—the ability to choose with intent what aspects of ontological being will be preferred, pursued, selected, rearranged, integrated, organized, preserved, and used. Physical dynamics includes spontaneous non linear phenomena, but not our formal applied-science called “non linear dynamics”(i.e. language,information). http://www.mdpi.com/1422-0067/10/1/247/pdf Stephen C. Meyer – Signature In The Cell: “DNA functions like a software program,” “We know from experience that software comes from programmers. Information–whether inscribed in hieroglyphics, written in a book or encoded in a radio signal–always arises from an intelligent source. So the discovery of digital code in DNA provides evidence that the information in DNA also had an intelligent source.” Three subsets of sequence complexity and their relevance to biopolymeric information – David L Abel and Jack T Trevors: Excerpt: Genetic algorithms instruct sophisticated biological organization. Three qualitative kinds of sequence complexity exist: random (RSC), ordered (OSC), and functional (FSC). FSC alone provides algorithmic instruction…No empirical evidence exists of either RSC of OSC ever having produced a single instance of sophisticated biological organization…It is only in researching the pre-RNA world that the problem of single-stranded metabolically functional sequencing of ribonucleotides (or their analogs) becomes acute. Biological Information: The Puzzle of Life that Darwinism Hasn’t Solved – Stephen C. Meyer Thus, as my book Signature in the Cell shows, Joyce’s experiments not only demonstrate that self-replication itself depends upon information-rich molecules, but they also confirm that intelligent design is the only known means by which information arises. The Origin of Life: An RNA World? – Jonathan M. – August 22, 2011 (Refutation of Nick Matzke) Excerpt Summary & Conclusion We have explored just a small handful of the confounding difficulties confronting the chemical origin of life. This is not a god-of-the-gaps argument, as Matzke claims, but rather a positive argument, based on our uniform and repeated experience of cause-and-effect. It is not based on what we don’t know, but on what we do know: that intelligence is a necessary and sufficient condition for the production of novel complex and functionally specified information. The design inference is based on sound and conventional scientific methodology. It utilizes the historical or abductive method and infers to the best explanation from multiple competing hypotheses. There remains one and only one type of cause that has shown itself able to create functional information like we find in cells, books and software programs — intelligent design. We know this from our uniform experience and from the design filter — a mathematically rigorous method of detecting design. Both yield the same answer. (William Dembski and Jonathan Witt, Intelligent Design Uncensored: An Easy-to-Understand Guide to the Controversy, p. 90 (InterVarsity Press, 2010). “Premise One: Despite a thorough search, no material causes have been discovered that demonstrate the power to produce large amounts of specified information. “Premise Two: Intelligent causes have demonstrated the power to produce large amounts of specified information. “Conclusion: Intelligent design constitutes the best, most causally adequate, explanation for the information in the cell.” Stephen C. Meyer – The Scientific Basis For the Intelligent Design Inference – video http://www.metacafe.com/watch/4104651 The Capabilities of Chaos and Complexity: David L. Abel – Null Hypothesis For Information Generation – 2009 To focus the scientific community’s attention on its own tendencies toward overzealous metaphysical imagination bordering on “wish-fulfillment,” we propose the following readily falsifiable null hypothesis, and invite rigorous experimental attempts to falsify it: “Physicodynamics cannot spontaneously traverse The Cybernetic Cut: physicodynamics alone cannot organize itself into formally functional systems requiring algorithmic optimization, computational halting, and circuit integration.” A single exception of non trivial, unaided spontaneous optimization of formal function by truly natural process would falsify this null hypothesis. http://www.mdpi.com/1422-0067/10/1/247/pdf Can We Falsify Any Of The Following Null Hypothesis (For Information Generation) 1) Mathematical Logic 2) Algorithmic Optimization 3) Cybernetic Programming 4) Computational Halting 5) Integrated Circuits 6) Organization (e.g. homeostatic optimization far from equilibrium) 7) Material Symbol Systems (e.g. genetics) 8 ) Any Goal Oriented bona fide system 9) Language 10) Formal function of any kind 11) Utilitarian work http://mdpi.com/1422-0067/10/1/247/ag
bornagain77_{October 20, 2011
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DrREC, you atheistic/materialistic faith literally bleeds through in every post you write!!! and If you have the sheer audacity to claim theism as your belief, it will certainly be in name only and completely devoid of any real substance, as for even your very posts witness against you!!!,,, Tell you what DrREC, there is a null hypothesis that you atheistic/materialistic neo-Darwinists need to falsify to even be considered scientifically legitimate in the first place. If You guys falsify this null hypothesis and I will at least concede that you guys have a plausible foundation within science in which to make your, thus far, completely unsubstantiated pseudo-scientific conjectures, for the ability of purely 'random' material processes to generate transcendent information!!!
Three subsets of sequence complexity and their relevance to biopolymeric information – Abel, Trevors Excerpt: Shannon information theory measures the relative degrees of RSC and OSC. Shannon information theory cannot measure FSC (Functional Sequence Complexity). FSC is invariably associated with all forms of complex biofunction, including biochemical pathways, cycles, positive and negative feedback regulation, and homeostatic metabolism. The algorithmic programming of FSC, not merely its aperiodicity, accounts for biological organization. No empirical evidence exists of either RSC of OSC ever having produced a single instance of sophisticated biological organization. Organization invariably manifests FSC rather than successive random events (RSC) or low-informational self-ordering phenomena (OSC).,,, Testable hypotheses about FSC What testable empirical hypotheses can we make about FSC that might allow us to identify when FSC exists? In any of the following null hypotheses [137], demonstrating a single exception would allow falsification. We invite assistance in the falsification of any of the following null hypotheses: Null hypothesis #1 Stochastic ensembles of physical units cannot program algorithmic/cybernetic function. Null hypothesis #2 Dynamically-ordered sequences of individual physical units (physicality patterned by natural law causation) cannot program algorithmic/cybernetic function. Null hypothesis #3 Statistically weighted means (e.g., increased availability of certain units in the polymerization environment) giving rise to patterned (compressible) sequences of units cannot program algorithmic/cybernetic function. Null hypothesis #4 Computationally successful configurable switches cannot be set by chance, necessity, or any combination of the two, even over large periods of time. We repeat that a single incident of nontrivial algorithmic programming success achieved without selection for fitness at the decision-node programming level would falsify any of these null hypotheses. This renders each of these hypotheses scientifically testable. We offer the prediction that none of these four hypotheses will be falsified. http://www.tbiomed.com/content/2/1/29 The following describes how quantum entanglement is related to functional information: Quantum Entanglement and Information Excerpt: A pair of quantum systems in an entangled state can be used as a quantum information channel to perform computational and cryptographic tasks that are impossible for classical systems. http://plato.stanford.edu/entries/qt-entangle/ further notes: "A code system is always the result of a mental process (it requires an intelligent origin or inventor). It should be emphasized that matter as such is unable to generate any code. All experiences indicate that a thinking being voluntarily exercising his own free will, cognition, and creativity, is required. ,,,there is no known law of nature and no known sequence of events which can cause information to originate by itself in matter. Werner Gitt 1997 In The Beginning Was Information pp. 64-67, 79, 107." (The retired Dr Gitt was a director and professor at the German Federal Institute of Physics and Technology (Physikalisch-Technische Bundesanstalt, Braunschweig), the Head of the Department of Information Technology.) Meyer and Nelson on a Failed Explanation for the Origin of the Genetic Code Jonathan M. - August 2011 Excerpt: 'codes and digital information are categories of effects uniformly associated with intelligent causes. Indeed, to the extent that Yarus and others have succeeded in establishing affinities between codons and amino acids, they did so only as a direct consequence of their own intelligent manipulation and intervention.' http://www.evolutionnews.org/2011/08/direct_rna_templating_a_failed050121.html The Law of Physicodynamic Insufficiency – Dr David L. Abel – November 2010 Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.” http://www-qa.scitopics.com/The_Law_of_Physicodynamic_Insufficiency.html The Capabilities of Chaos and Complexity – David L. Abel – 2009 Excerpt: “A monstrous ravine runs through presumed objective reality. It is the great divide between physicality and formalism. On the one side of this Grand Canyon lies everything that can be explained by the chance and necessity of physicodynamics. On the other side lies those phenomena than can only be explained by formal choice contingency and decision theory—the ability to choose with intent what aspects of ontological being will be preferred, pursued, selected, rearranged, integrated, organized, preserved, and used. Physical dynamics includes spontaneous non linear phenomena, but not our formal applied-science called “non linear dynamics”(i.e. language,information). http://www.mdpi.com/1422-0067/10/1/247/pdf Stephen C. Meyer – Signature In The Cell: “DNA functions like a software program,” “We know from experience that software comes from programmers. Information–whether inscribed in hieroglyphics, written in a book or encoded in a radio signal–always arises from an intelligent source. So the discovery of digital code in DNA provides evidence that the information in DNA also had an intelligent source.” http://www.evolutionnews.org/2009/07/leading_advocate_of_intelligen.html Three subsets of sequence complexity and their relevance to biopolymeric information – David L Abel and Jack T Trevors: Excerpt: Genetic algorithms instruct sophisticated biological organization. Three qualitative kinds of sequence complexity exist: random (RSC), ordered (OSC), and functional (FSC). FSC alone provides algorithmic instruction…No empirical evidence exists of either RSC of OSC ever having produced a single instance of sophisticated biological organization…It is only in researching the pre-RNA world that the problem of single-stranded metabolically functional sequencing of ribonucleotides (or their analogs) becomes acute. http://www.biomedcentral.com/content/pdf/1742-4682-2-29.pdf Biological Information: The Puzzle of Life that Darwinism Hasn’t Solved – Stephen C. Meyer Thus, as my book Signature in the Cell shows, Joyce’s experiments not only demonstrate that self-replication itself depends upon information-rich molecules, but they also confirm that intelligent design is the only known means by which information arises. http://www.evolutionnews.org//2009/06/biological_information_the_puz.html The Origin of Life: An RNA World? – Jonathan M. – August 22, 2011 (Refutation of Nick Matzke) Excerpt Summary & Conclusion We have explored just a small handful of the confounding difficulties confronting the chemical origin of life. This is not a god-of-the-gaps argument, as Matzke claims, but rather a positive argument, based on our uniform and repeated experience of cause-and-effect. It is not based on what we don’t know, but on what we do know: that intelligence is a necessary and sufficient condition for the production of novel complex and functionally specified information. The design inference is based on sound and conventional scientific methodology. It utilizes the historical or abductive method and infers to the best explanation from multiple competing hypotheses. http://www.evolutionnews.org/2011/08/the_rna_world_a_response_to_ni049871.html There remains one and only one type of cause that has shown itself able to create functional information like we find in cells, books and software programs — intelligent design. We know this from our uniform experience and from the design filter — a mathematically rigorous method of detecting design. Both yield the same answer. (William Dembski and Jonathan Witt, Intelligent Design Uncensored: An Easy-to-Understand Guide to the Controversy, p. 90 (InterVarsity Press, 2010). “Premise One: Despite a thorough search, no material causes have been discovered that demonstrate the power to produce large amounts of specified information. “Premise Two: Intelligent causes have demonstrated the power to produce large amounts of specified information. “Conclusion: Intelligent design constitutes the best, most causally adequate, explanation for the information in the cell.” Stephen C. Meyer – The Scientific Basis For the Intelligent Design Inference – video http://www.metacafe.com/watch/4104651 The Capabilities of Chaos and Complexity: David L. Abel - Null Hypothesis For Information Generation - 2009 To focus the scientific community’s attention on its own tendencies toward overzealous metaphysical imagination bordering on “wish-fulfillment,” we propose the following readily falsifiable null hypothesis, and invite rigorous experimental attempts to falsify it: "Physicodynamics cannot spontaneously traverse The Cybernetic Cut: physicodynamics alone cannot organize itself into formally functional systems requiring algorithmic optimization, computational halting, and circuit integration." A single exception of non trivial, unaided spontaneous optimization of formal function by truly natural process would falsify this null hypothesis. http://www.mdpi.com/1422-0067/10/1/247/pdf Can We Falsify Any Of The Following Null Hypothesis (For Information Generation) 1) Mathematical Logic 2) Algorithmic Optimization 3) Cybernetic Programming 4) Computational Halting 5) Integrated Circuits 6) Organization (e.g. homeostatic optimization far from equilibrium) 7) Material Symbol Systems (e.g. genetics) 8) Any Goal Oriented bona fide system 9) Language 10) Formal function of any kind 11) Utilitarian work http://mdpi.com/1422-0067/10/1/247/ag
bornagain77_{October 20, 2011
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bornagain77, "Unfortunately for DrREC hopeless nihilistic atheism (which he apparently places so much hope in)" I've never discussed my faith here. "he has ZERO evidence of completely random neo-Darwinian mechanisms generating a single novel gene or protein in life" I listed examples, and the mechanisms that created them. Those mechanistically appear random with respect to need, and also cause deleterious effects/disease. I think what you really mean is that I can't demonstrate they were unguided. Of course I can't. That isn't falsifiable, it isn't science, it is theism attached to evolution--fine as a personal belief. Not science, not support for ID. "indeed the changes we do witness in the genome, some of which DrREC listed, point to higher levels of ‘epigenetic’ programming information in the ‘information hierarchy’ of the cell which is directly orchestrating the ‘base level of information’ of DNA sequences to be in prescribed patterns dictated by that epigenetic information. i.e. ' You could have created this paragraph using a mad-lib for all the meaning it has. Epigenetic literally means on top of the genome. Epigenetic marks serve to regulate the transcription of genes. They aren't a creator of new genes. They aren't even thought to be permanent enough to contribute to evolution in the long run. So you're really stretching to attribute genome changes to them,DrREC_{October 20, 2011
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There is no "complete break with the prior lineage", PaV! What makes you think that the new genes all arrived at once? The tree they give makes it fairly clear how new genes accumulate between branches. Really, you seem to be reading into this something that simply is not there. It's a very interesting paper, but it's hard for me to imagine how anyone could read it and not find confirmatory evidence of common descent and the effects of natural selection! It even gives the genetic phylogeny! There is no "mechanism" posited here, and you are not in fact positing one. For some reason you seem to have interpreted the finding as evidence for a single "macroevolutionary speciation event". What, in the paper, leads you to think such an event occurred, and what "mechanism" for such an event do you see evidence for? We do not know why the chimp and human lineages originally diverged. It could simply originally have been some kind of physical separation of populations into non-interbreeding groups. At which point, the gradual accumulation of new genes would follow different paths in the two lineages, just as it seems to have done between orangs and champs, and between rhesus monkeys and orangs, and between marmosets and rhesus monkeys. However it does look as the there has been steady selection for genes that are beneficially expressed in PFC during development, and for regulatory genes that lead to such expression, not surprisingly, as it looks as though the associated PFC effects lead to greater intelligence, which is likely to have a reproductive advantage. So we see a steady accumulation along the homind lineage, from marmosets onwards, of genes that are expressed in the PFC, with various populations (rhesus, orang, chimp) getting of the bus a bit early. There is no evidence for sudden explosions of genes at each branch point at all. At least not given in that paper.Elizabeth Liddle_{October 20, 2011
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Expression data covering numerous subregions of the developing brain further demonstrate that these young genes are mainly upregulated in the neocortex. They originated in the evolutionary period during which the neocortex was expanding, suggesting the functional association of new genes with this newly evolving brain structure.

Examination of the gene structure and homology further revealed that these genes were generated by DNA-mediated duplication, RNA-mediated duplication (retroposition), and de novo origination (which created a protein without a parental locus) (Figure 3). In other words, young genes created by all major gene origination mechanisms tend to be upregulated in fetal brain. Such generality suggests that a systematic force instead of a mutational bias associated with a specific origination mechanism contributed to the excess of young genes in the fetal brain.
DrREC: the details. How do you interpret them?PaV_{October 20, 2011
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DrREC states:
There are several examples of de novo genes with tractable origins. A recombination of two genes, retrotransposition of an exon into a pseudogene, mutations at a transcribed, but non-translatable region, yielding a new ORF.
Unfortunately for DrREC hopeless nihilistic atheism (which he apparently places so much hope in), he has ZERO evidence of completely random neo-Darwinian mechanisms generating a single novel gene or protein in life, and indeed the changes we do witness in the genome, some of which DrREC listed, point to higher levels of 'epigenetic' programming information in the 'information hierarchy' of the cell which is directly orchestrating the 'base level of information' of DNA sequences to be in prescribed patterns dictated by that epigenetic information. i.e. This 'information hierarchy', though DrREC will never admit it (and indeed he will keep repeating something that is falsified over and over), is devastating to the genetic reductionism model of neo-Darwinism!!! notes:
Revisiting the Central Dogma in the 21st Century - James A. Shapiro - 2009 Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112). http://shapiro.bsd.uchicago.edu/Shapiro2009.AnnNYAcadSciMS.RevisitingCentral%20Dogma.pdf ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ - Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009) Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 A few comments on ‘non-local’ epigenetic information: https://docs.google.com/document/pub?id=1iNy78O6ZpU8wpFIgkILi85TvhC9mSqzUSE_jzbksoHY Falsification Of Neo-Darwinism by Quantum Entanglement/Information https://docs.google.com/document/d/1p8AQgqFqiRQwyaF8t1_CKTPQ9duN8FHU9-pV4oBDOVs/edit?hl=en_US Does Quantum Biology Support A Quantum Soul? – Stuart Hameroff - video (notes in description) http://vimeo.com/29895068
bornagain77_{October 20, 2011
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Why would de novo (human only) and young (primate) genes be clustered, if they formed in independent events? They are found throughout the genome.DrREC_{October 20, 2011
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They're talking about "clusters". Obviously, de novo genes would be "clustered" with the "young" genes. Hence, the independence stems from these de novo genes being spread out amongst the clusters, and not just in one or two.PaV_{October 20, 2011
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"The fact that cytochrome C is essential to cell division and replication, and that it is found, relatively unchanged, in all animal forms" But it isn't essential for all life-certainly not archaea, bacteria, and some fungi. The further you go from animals, the more divergent the sequence "So, really, just ONE de novo gene is beyond Darwinian explanations." Why? There are several examples of de novo genes with tractable origins. A recombination of two genes, retrotransposition of an exon into a pseudogene, mutations at a transcribed, but non-translatable region, yielding a new ORF.DrREC_{October 20, 2011
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What is, IMO, extremely enlightening about all of this is: We are perhaps looking at what a "true", macroevolutionary speciation event looks like; i.e., the introduction of a host of new genes, in locations all throughout the genome, with the added addition of new regulatory regimes, leading to a complete break with the prior lineage. IOW, we may not have been around for the Cambrian Explosion, but it is not entirely off the mark to retroject this finding to exactly what happened back then. This, then, could be posited as the "mechanism" for macroevolution; and, for the time being, as studies further confirm or disconfirm, it could be called a "design intervention."PaV_{October 20, 2011
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What's your point?PaV_{October 20, 2011
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Gil: You wrote:
The notion that this discontinuity is the result of randomly produced gene disparity is irrational and superbly unsupported by any concrete evidence, only Alice-in-Wonderland fantastic speculation. Something else is going on — something powerful, creative, and with purpose.
You can't load Windows Vista operating system on a machine with very little data storage capacity. You have to upgrade to a larger system. The hardware is not the same as the software; but they need to be compatible. We're only dealing, metaphorically, with hardware issues right now.PaV_{October 20, 2011
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DrREC: The fact that cytochrome C is essential to cell division and replication, and that it is found, relatively unchanged, in all animal forms, even from the very earliest living descendants, convinced Sir Fred Hoyle, the renowned astrophysicist, that the Darwinist solution to evolution was impossible. Cytochrome C is a fairly short protein as proteins go. So, really, just ONE de novo gene is beyond Darwinian explanations. So, now what are you going to do if TWO of the genes prove to be de novo.?PaV_{October 20, 2011
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55-65 million. Details..... "Does that solve this problem at all." What problem?DrREC_{October 20, 2011
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Even if the point is conceded, does that give us an extra five million years? Does that solve this problem at all.PaV_{October 20, 2011
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Elizabeth: Darwinism refutes Darwinism. It is an incoherent theory. Isn't it obvious why I highlighted the words in the post you're responding to? Not only do de novo genes need to be accounted for, but also the rise of an integrated system---that is, "new" regulatory networks. This only confounds the task of Darwinism. It is like trying to haul away the Himilayans with a Tonka truck.
I’m seeing a beautiful family tree of new genes along the hominid lineage, with a substantial proportion expressed in PFC.
You see what you want to see. Don't you see that Darwinism has absolutely no way of explaining how all these new genes arose in an evolutionary 'blink of an eye'? But, of course, you don't see----because you refuse to see. Or to answer. Or to explain. Just vague generalities.PaV_{October 20, 2011
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Elizabeth: I think you are the one indulging in "babelfish". If I have improperly interpreted the Darwinian code words, then please tell me where. But, if not, then it should be apparent that a huge part of the problem with biology is that Darwinian presumptions have crept into the language that is used.PaV_{October 20, 2011
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Dear Elizabeth: Since you seem to claim to have read the paper, then perhaps you can point out where they explain just exactly 'where' and 'how' these new genes came about. Could you do that for us? :)
They also show that the number of new genes separating our nearest relations are roughly similar – 318 between Rhesus monkey and orangutan, 72 expressed in PFC; 372 between orangutan and chimp, 72 expressed in PFC; and 280 between chimp and human, 54 expressed in PFC.
How is this in any way relevant to the problems facing Darwinism indicated by these results? And just so you can't just say, "What problems?", let's remember this:
We were very shocked that there were that many new genes that were upregulated in this part of the brain,” said Long, who added that he was also taken aback by synchronicity of the origin of the genes and the development of novel brain structures.
Why were they "shocked"? Why? Because they knew this was completely contrary to Darwinian expectations. That's why. IOW, they knew this was a huge problem for Darwinism. Let's not pretend here.PaV_{October 20, 2011
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As well, besides these 54 novel human ORFan genes that were found in this study, (which is devastating to neo-Darwinian gradualism despite what the 'true believers' may say) I would like to point out this following study, in this following study the authors tried to remove over 1000 unique ORFan genes from the human gene count simply because it was 'not expected' by the neo-Darwinian mindset: notes: This following article, which has a direct bearing on the 98.8% genetic similarity myth, shows that over 1000 'ORFan' genes, that are completely unique to humans and not found in any other species, and that very well may directly code for proteins, were stripped from the 20,500 gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more biased and unfair example of practicing science!
Human Gene Count Tumbles Again - 2008 Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes. Although this was strong evidence that the sequences were not true protein-coding genes, it was not quite convincing enough to justify their removal from the human gene catalogs. Two other scenarios could, in fact, explain their absence from other mammalian genomes. For instance, the genes could be unique among primates, new inventions that appeared after the divergence of mouse and dog ancestors from primate ancestors. Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes. http://www.sciencedaily.com/releases/2008/01/080113161406.htm
The sheer, and blatant, shoddiness of the science of the preceding study should give everyone who reads it severe pause whenever, in the future, someone tells them that genetic studies have proven evolution to be true. If the authors of the preceding study were to have actually tried to see if the over 1000 unique ORFan genes of humans may actually encode for proteins, instead of just written them off because they were not found in other supposedly related species, they would have found that there is ample reason to believe that they may very well encode for biologically important proteins:
A survey of orphan enzyme activities Abstract: We demonstrate that for ~80% of sampled orphans, the absence of sequence data is bona fide. Our analyses further substantiate the notion that many of these (orfan) enzyme activities play biologically important roles. http://www.biomedcentral.com/1471-2105/8/244 Dr. Howard Ochman - Dept. of Biochemistry at the University of Arizona Excerpt of Proposal: The aims of this proposal are to investigate this enigmatic class of genes by elucidating the source and functions of “ORFans”, i.e., sequences within a genome that encode proteins having no homology (and often no structural similarity) to proteins in any other genome. Moreover, the uniqueness of ORFan genes prohibits use of any of homology-based methods that have traditionally been employed to establish gene function.,,, Although it has been hypothesized that ORFans might represent non-coding regions rather than actual genes, we have recently established that the vast majority that ORFans present in the E. coli genome are under selective constraints and encode functional proteins. https://uncommondescent.com/intelligent-design/proteins-fold-as-darwin-crumbles/comment-page-5/#comment-358868
In fact it turns out that the authors of the 'kick the ORFans out in the street' paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias: https://uncommondescent.com/intelligent-design/proteins-fold-as-darwin-crumbles/comment-page-6/#comment-358547 This following study found much more dramatic differences for unique ORFan genes:
Study Reports a Whopping "23% of Our Genome" Contradicts Standard Human-Ape Evolutionary Phylogeny - Casey Luskin - June 2011 Excerpt: For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee. This encompasses genes and exons to the same extent as intergenic regions. We conclude that about 1/3 of our genes started to evolve as human-specific lineages before the differentiation of human, chimps, and gorillas took place. (of note; 1/3 of our genes is equal to about 7000 genes that we do not share with chimpanzees) http://www.evolutionnews.org/2011/06/study_reports_a_whopping_23_of047041.html
bornagain77_{October 20, 2011
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Why, PaV? Seriously, I am not seeing the point you are making. The paper gives a data-supported account of primate and human brain evolution. And you are reading it as some kind of falsification of Darwinism? I see you quote parts, but I'm simply not seeing your argument. What is it, specifically, that you think refutes Darwinism in that paper? I'm seeing a beautiful family tree of new genes along the hominid lineage, with a substantial proportion expressed in PFC. What on earth refutes Darwinian evolution of the human PFC in that account? And why do you think the authors aren't seeing it, and make the quite contrary point?Elizabeth Liddle_{October 20, 2011
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Oh, golly, PaV, you have read the paper! I think you should stop "translating" it and just read what it says! I think your babelfish is on the blink.Elizabeth Liddle_{October 20, 2011
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