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Can new genes arise from junk DNA?

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From Quanta Magazine:

Emerging data suggests the seemingly impossible — that mysterious new genes arise from “junk” DNA.

Genes, like people, have families — lineages that stretch back through time, all the way to a founding member. That ancestor multiplied and spread, morphing a bit with each new iteration.

For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.

Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.

The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis. More.

Hmmm. Whenever scientists use terms like “somehow springs into existence,” find your boots, your bicycle lock key, or your car keys.

But this is a good conversation to be having.

Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.

Evolution isn’t what we used to think.

See also: The Myth of Junk DNA

and

Talk to the fossils: Let’s see what they say back.

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Comments
I'm not quite sure what you are trying to ask. Terminators don't have anything to do with stop codons which is what you asked about in the first place. Calculating the probability of hitting a transcription terminator is not straightfoward, partly because transcription is pretty sloppy in big eukaryotes. In reply to your other comments. About 1% of random ORFs will be 100 codons or longer . Of course 100 is arbitrary, you can do the calculation for any length you like (it's 1 - [ Sum 1 to n [(1-3/64)^(n-1) * 3/64 ] ]). So, yes, most randomly generated ORFs will be shorter than 100 codons. But the question for do novo genes is about random ORFs that have a biological function. There might well be more very short random proteins, but if such small proteins are unlikely to have functions they won't stick around or get fixed by selection. I chose 100 as a middle ground, as I say, it's easy to calculate for any number. You'll have to ask the people that are making a big deal of do novo genes whether ENCODE undercuts them -- thought I still can't see how it would.wd400
August 30, 2015
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wd400, Thanks. So just looking at basic probabilities any de novo gene is likely to be very short. I think the words I was looking for were promoter and terminator. https://en.wikipedia.org/wiki/Promoter_%28genetics%29 https://en.wikipedia.org/wiki/Terminator_%28genetics%29 ENCODE may be relevant because it seems to indicate a high probability that the region is already being transcribed. Perhaps the while idea of a de novo gene is absurd. Your choice of a 100 codon sequence seems pretty arbitrary, and obviously there is a much greater probability of shorter de novo sequences, by your own admission. Is there evidence for this?Mung
August 29, 2015
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"There are plenty of ways to test such an idea." Caveat: Just be sure not to ask Darwinists for any real time empirical evidence/tests of unguided material processes ever creating new genes. Because there is ZERO evidence in that regards. Be sure only to ask for historical genetic evidence that assumes the conclusion of evolution into the premise of its analysis of genetic sequences. Then they got plenty of evidence because they've already pulled a shell game on you by assuming the de novo sequences evolved in their analysis of the sequences. Yet they have never actually experimentally established that it is even remotely possible for unguided material processes to create genes in the first place. i.e. it's a shell game! Three Shell Game https://www.youtube.com/watch?v=IFLa_tl4Rk0bornagain77
August 28, 2015
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Evolutionism requires de novo genes- how else did the first life arise if not from de novo genes? That is the whole argument- that materialistic processes couldn't produce those de novo genes.Virgil Cain
August 28, 2015
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JDD, Sure, I don't that was what mung was asking. But if you calcualte the probability of start followed by n non-stop codons it's 1/64 * (1-3/64)^n, which is abut 0.01% for 100 codons.
The problem with this is, it is purely a “just so” story with no actual evidence to support it
Nah. There are plenty of ways to test such and idea. The distribution of the age of genes is an obvious one. I presented another test above: we expect de novo genes to have relatively non-specific roles. Box, I don't think you understood by point. You would end up with tissue-specific expression of transcripts in one go, because the expression of a gene depends on the local conditions re DNA methylation and accessibility. Those conditions already make tissue-specific expression patterns and they would apply to any newly expressed transcript int a given region too. For the rest of your comment you seem to conflate "LUCA" with a lone organism. That's not the case at all, LUCA would have been the result of evolution itself (and quite likely one of many creatures alive at the time). The "L" is for last, after all.wd400
August 28, 2015
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Dr JDD @ 107, that sounds a lot like Dr. Meyer's criticism of Dr. Marshall's attempted peer-reviewed rebuttal of 'Darwin's Doubt':
When Theory Trumps Observation: Responding to Charles Marshall's Review of Darwin's Doubt - Stephen C. Meyer - October 2, 2013 Excerpt: Of course, Marshall thinks that these networks could have had a different, more flexible, character in the past. Yet, given what dGRNs do, namely, that they enable different cell types to organize themselves, and differentiate themselves from each other, in precise ways at precise times during the development of specific animal forms, it is hard to see how dGRNs could have functioned as regulatory networks and also exhibited the kind of flexibility that Marshall envisions. Developmental gene regulatory networks are control systems. A labile dGRN would generate (uncontrolled) variable outputs, precisely the opposite of what a functional control system does. It is telling that although many evolutionary theorists (like Marshall) have speculated about early labile dGRNs, no one has ever described such a network in any functional detail -- and for good reason. No developing animal that biologists have observed exhibits the kind of labile developmental gene regulatory network that the evolution of new body plans requires. Indeed, Eric Davidson, when discussing hypothetical labile dGRNs, acknowledges that we are speculating "where no modern dGRN provides a model" since they "must have differed in fundamental respects from those now being unraveled in our laboratories."8 By ignoring this evidence, Marshall and other defenders of evolutionary theory reverse the epistemological priority of the historical scientific method as pioneered by Charles Lyell, Charles Darwin and others.9 Rather than treating our present experimentally based knowledge as the key to evaluating the plausibility of theories about the past, Marshall uses an evolutionary assumption about what must have happened in the past (transmutation) to justify disregarding experimental observations of what does, and does not, occur in biological systems. The requirements of evolutionary doctrine thus trump our observations about how nature and living organisms actually behave. What we know best from observation takes a back seat to prior beliefs about how life must have arisen. http://www.evolutionnews.org/2013/10/when_theory_tru077391.html
Further notes:
Stephen Meyer Answers Charles Marshall (Peer Reviewed Paper) on Darwin's Doubt - October 2013 (4 part response) http://www.evolutionnews.org/2013/10/stephen_meyer_r077371.html Stephen Meyer vs. hostile reviewer Charles Marshall (audio of debate) - Dec. 1, 2013 https://www.youtube.com/watch?v=wKqzQwT3JXk Response to Critics - Marshall - Part 1 https://www.youtube.com/watch?v=zqYUoRVswRY Response to Critics - Marshall - Part 2 https://www.youtube.com/watch?v=Cg8Mhn2EKvQ Response to Critics - Marshall - Part 3 https://www.youtube.com/watch?v=fR_Agl41TbE
bornagain77
August 28, 2015
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… that creative " Cosmic Substance," with its "nebulous potentiality," and " indefinable latency," to which in the end of his days Professor Huxley transferred the sceptre of creation, rudely snatched from the hand of his water-god Bathybius". --- William Bullen Morris Bathybius haeckelii was a substance that British biologist Thomas Henry Huxley claimed a source of all organic life. In 1868 Huxley studied an old sample of mud from the Atlantic seafloor taken in 1857. When he first examined it, he had found only protozoan cells and placed the sample into a jar of alcohol to preserve it. Now he noticed that the sample contained an albuminous slime that appeared to be criss-crossed with veins. Huxley thought he had discovered a new organic substance and named it Bathybius haeckelii, in honor of German biologist Ernst Haeckel. Haeckel had theorized about Urschleim ("primordial slime"), a protoplasm from which all life had originated. Huxley thought Bathybius could be that protoplasm, a missing link (in modern terms) between inorganic matter and organic life. Huxley published a description of Bathybius and also wrote to Haeckel to tell him about it. Haeckel was impressed and flattered and procured a sample for himself. In the next edition of his textbook The History of Creation Haeckel suggested that the substance was constantly coming into being at the bottom of the sea. Huxley did not agree but speculated that Bathybius formed a continuous mat of living protoplasm that covered the whole ocean floor. In 1872 the Challenger expedition began; it spent three years studying the oceans. The expedition also took soundings at 361 ocean stations. They did not find any sign of Bathybius, regardless of the claim that it was a nearly universal substance. In 1875 ship's chemist John Young Buchanan analyzed a substance that looked like Bathybius from an earlier collected sample. He noticed that it was a precipitate of calcium sulfate from the seawater that had reacted with the preservative liquid (alcohol). Buchanan suspected that all the Bathybius samples had been prepared the same way and notified Thomson, the leader of the expedition. Thomson sent a polite letter to Huxley and told about the discovery. Huxley realized that he had been too eager and made a mistake. He published part of the letter in Nature and recanted his previous views. Later, during the 1879 meeting of the British Association for the Advancement of Science, he stated that he was ultimately responsible for spreading the theory and convincing others. Most biologists accepted this acknowledgement of error. Haeckel, however, did not want to abandon the idea of Bathybius because it was so close to proof of his own theories about Urschleim. He claimed without foundation that Bathybius "had been observed" in the Atlantic. He continued to support this position until 1883. Huxley's rival George Charles Wallich, in turn, claimed that Huxley had committed deliberate fraud and also accused Haeckel of falsifying data; Haeckel did draw a series of pictures of the evolution of his Urschleim, supposedly based on observations.
Silver Asiatic
August 28, 2015
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Box: We know that gene misregulation is a classic hallmark of disease. This is why there is a buzz in industry around epigenetic control of genes, how it works and is aberrant in disease, and how to modify it to treat disease. This is in adults as well. When we consider the regulation of developmental genes we see an even narrower windows for deviation from the tight genetic control - otherwise disaster occurs. The EVO narrative would have us believe that initially these genes didn't need to be so tightly controlled but over time as they play an important role, and as other new genes evolve to be important, the regulation systems evolved and in turn regulation became more important. The problem with this is, it is purely a "just so" story with no actual evidence to support it. The only evidence that can be used is less complex species have less complex regulation. But this is a fallacy as it is circular and also does not demonstrate how you can maintain a viable organism while transitioning from one level of complex regulation to the next. It also misses the point that even simple organisms have quite complex regulation control of their genes. This is not evidence based science - it is who can come up with the best story science.Dr JDD
August 28, 2015
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OT: Of semi related note from crevo:
Fate of a mutation in a fluctuating environment - March 17, 2015 Excerpt: Evolution in variable environments depends crucially on the fates of new mutations in the face of fluctuating selection pressures. In constant environments, the relationship between the selective effect of a mutation and the probability that it will eventually fix or go extinct is well understood. However, our understanding of fixation probabilities in fluctuating environmental conditions is limited. Here, we show that temporal fluctuations in environmental conditions can have dramatic effects on the fate of each new mutation, reducing the efficiency of natural selection and increasing the fixation probability of all mutations, including those that are strongly deleterious on average. This makes it difficult for a population to maintain specialist adaptations, even if their benefits outweigh their costs. Abstract Natural environments are never truly constant,,, http://www.pnas.org/content/early/2015/08/21/1505406112.abstract More Flaws in Darwin’s Mechanism - August 27, 2015 http://crev.info/2015/08/more-flaws-in-darwins-mechanism/
That is certainly not a good finding if you are a neo-Darwinists, to put it very mildly. And that finding is on top of this finding:
Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load: Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space. http://bioinformatics.cau.edu.cn/lecture/chinaproof.pdf Biological Information – Purifying Selection (Mendel’s Accountant) 12-20-2014 by Paul Giem https://www.youtube.com/watch?v=SGJZDsQG4kQ Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory - 2008 Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue. Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person. http://www.icr.org/i/pdf/technical/Using-Numerical-Simulation-to-Test-the-Validity-of-Neo-Darwinian-Theory.pdf
What motivates many neo-Darwinists to persist in promoting such a failed theory? I think money may play a huge part in their lack of scientific integrity.
Lynn Margulis Criticizes Neo-Darwinism in Discover Magazine (Updated) - Casey Luskin April 12, 2011 Excerpt: Population geneticist Richard Lewontin gave a talk here at UMass Amherst about six years ago, and he mathemetized all of it--changes in the population, random mutation, sexual selection, cost and benefit. At the end of his talk he said, "You know, we've tried to test these ideas in the field and the lab, and there are really no measurements that match the quantities I've told you about." This just appalled me. So I said, "Richard Lewontin, you are a great lecturer to have the courage to say it's gotten you nowhere. But then why do you continue to do this work?" And he looked around and said, "It's the only thing I know how to do, and if I don't do it I won't get grant money." - Lynn Margulis - biologist http://www.evolutionnews.org/2011/04/lynn_margulis_criticizes_neo-d045691.html
bornagain77
August 28, 2015
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WD400,
Box: How do we get to a regulatory system given that a novel gene arises from junk-DNA. How do you envision the steps towards a (novel) regulatory system?
WD400: I explained one way — an element with it’s own cis-regulatroy sequences integrates alongside. That way you get expression down stream.
Ok, so the novel gene is expressed by CREs. Let's assume we are talking about a new protein. How do we get to regulation of the proper amount? And how does it reach its proper location? Simply producing a new protein without regulation, as you suggest, must be a threat to the organism.
WD400: Because expression also depends on DNA accessibility and methylation state you end up with tissue-specific expression too.
Sure .... If the new protein is only functional in the context of tissue-specific expression (due to epigenetic modifications such as DNA methylation) — IOW the protein has a very specific function — the problem of "how to get to regulation" increases. How can the new protein be tolerated by the organism, when it takes many generations to "install" regulation? How can the new gene be selected for if without regulation it has no function? And how can a step-by-step coming into existence of regulation be selected for if it is only functional when complete?Box
August 28, 2015
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Wd400 - you must also consider the frame the stop codon is in relative to the probability of a start codon (met) with appropriate transcriptional control sites up and downstream of the met start. This will significantly reduce the 0.8% probability figure.Dr JDD
August 28, 2015
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wd400 claims that evolution predicts that "genes get longer over time" except, or course, for when evolution predicts that genes will stay exactly the same size over time. Like, for instance, when Graur and company supposedly refuted ENCODE's finding of widespread functionality in the genome by appealing to "how much of our genome has avoided accumulating changes over 100 million years"
DNA mostly 'junk?' Only 8.2 percent of human DNA is 'functional', study finds - July 24, 2014 Excerpt: To reach their (8.2%) figure, the Oxford University group took advantage of the ability of evolution to discern which activities matter and which do not. They identified how much of our genome has avoided accumulating changes over 100 million years of mammalian evolution -- a clear indication that this DNA matters, it has some important function that needs to be retained. http://www.sciencedaily.com/releases/2014/07/140724141608.htm
So evolution predicts that genes will both grow longer and that genes will avoid accumulating change over time? How can that be? And exactly where is the mathematical equation, and empirical evidence, that predicts these two different results? Of course there is no mathematical equation, nor empirical evidence, that makes such contradictory predictions. The exact 'prediction' that Darwinists choose to invoke, i.e. staying the same or growing larger, depends entirely upon which data set the evolutionist is trying to avoid falsification by. Of supplemental note: In the following podcast, Dr. Sternberg’s emphasis is on ENCODE research, and how that research overturned the ‘central’ importance of the gene as a unit of inheritance. As well he reflects on how that loss of the term ‘gene’ as an accurate description in biology completely undermines the modern synthesis, (i.e. central dogma), of neo-Darwinism as a rational explanation for biology.
Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 5 http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-5/
Here is the rest of Dr. Sternberg's lecture for those who may be interested in listening to it:
Podcast: Richard Sternberg PhD - " On Human Origins: Is Our Genome Full of Junk DNA? part 1 http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna/ Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 2 (Major Differences in higher level chromosome spatial organization) http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-2/ Podcast: Richard Sternberg PhD - " On Human Origins: Is Our Genome Full of Junk DNA? Part 3 http://intelligentdesign.podomatic.com/entry/2014-11-17T14_14_33-08_00 Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 4 http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-4/
bornagain77
August 28, 2015
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WD400: But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.
Box: I’m not sure I get your point. Starting with LUCA I see an obvious problem: the finding of biological function cannot always have been an exceedingly rare event in the evolutionary narrative. Right?
WD400: (…) your post is the classic retreat to the origin of life tactic.
My “starting with LUCA” isn’t an attempt to bring abiogenesis into the discussion. I did no such thing. I merely pointed out that your story doesn’t hold when we start with LUCA. If new functional sequences from LUCA’s junk DNA and her descendants are “an exceedingly rare event”, then it’s hard to see how this process can "still provide us will all the superfamilies we know about”.
WD400: Without selection lineages would not be able to explore sequence nearly as efficiently (…)
Interesting point. So this adds to the problem: starting with LUCA, in the absence of large selection lineages, exploring sequence space is inefficient.Box
August 27, 2015
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The test is pretty easy: are the functional de novos shorter. If we assume codons are sampled uniformally then the probability of getting a stop is 3/64. It would be different if you wanted to include nucleotide composition,but that differs among species any way. The probability of getting a string n codons long without a stop is (1-3/64)^n. So, there's a 0.8% of a 100 codon run having no stops, should be plenty of those in a 3 billion bp genome. I've no idea what ENCODE has to do with such a scenario.wd400
August 27, 2015
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wd400: The prediction is if de novos really are performing biological functions, then those functions will not be as biochemically-specific as those usually performed by older proteins and they will use shorter a/a sequences to perform them. The claim then is that genes get longer over time and gain in specificity over time. Is this testable? A question about length. So the cell starts reading a stretch of DNA not previously transcribed. How likely is it that a stop codon will be encountered after some number of codons? Is this scenario even realistic any more given the findings of the ENCODE project?Mung
August 27, 2015
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wd400 goes fishing for a just so story to save his blind faith in his Darwinian religion,,, i.e. Evolutionists have never demonstrated the origin of a single gene in the laboratory, and Darwinian evolution certainly never predicted ORFan genes in the first place. In fact, as pointed out previously, ORFans falsify a major prediction of evolution (see Cornelius Hunter post 92), but in case evolution ever did predict ORFans then I guess wd400 is hoping it would have predicted this following pattern,,,
"The prediction is if de novos really are performing biological functions, then those functions will not be as biochemically-specific as those usually performed by older proteins and they will use shorter a/a sequences to perform them."
And yet 'new' ORFan genes are found to be just as essential as 'older' genes:
Genes from nowhere: Orphans with a surprising story - 16 January 2013 - Helen Pilcher Excerpt: When biologists began sequencing genomes they discovered up to a third of genes in each species seemed to have no parents or family of any kind. Nevertheless, some of these "orphan genes" are high achievers (are just as essential as 'old' genes),,, http://ccsb.dfci.harvard.edu/web/export/sites/default/ccsb/publications/papers/2013/All_alone_-_Helen_Pilcher_New_Scientist_Jan_2013.pdf Can new genes arise from junk DNA? - August 2015 Excerpt: Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.,,, “How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.” https://uncommondescent.com/junk-dna/can-new-genes-arise-from-junk-dna/ New genes in Drosophila quickly become essential. – December 2010 Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages. http://www.sciencemag.org/content/330/6011/1682.abstract
Dr. Giem has a lecture video on the subject:
New Genes Are Essential 6-13-2015 by Paul Giem - video https://www.youtube.com/watch?v=6qgGPV1AO1E
As to ORFan length, the following study is relevant: The following researchers removed 1,177 “orphan” DNA sequences, which were long stretches of 300 or more nucleotides, from the human gene catalogs simply because they did not fit the Darwinian story line:
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.,,, 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 In fact it turns out that the authors of the preceding '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
As should be needless to say, 'adjusting evidence' to fit a theory is NOT how science is done!bornagain77
August 27, 2015
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It's certainly clear that one of us doesn't understand what I'm saying... The prediction is if de novos really are performing biological functions, then those functions will not be as biochemically-specific as those usually performed by older proteins and they will use shorter a/a sequences to perform them. Again, I really don't know how that can be explained more simply. You seem to want to read some other meaning into itwd400
August 27, 2015
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wd400 - ok, wow. There's clearly nothing anyone can say at this point. Box and BA77 - you saw exactly what he did right there. I'm very glad about that because nobody would believe it if it was just me. Talk about losing it. Mapou is going to have a melt-down. If de novo genes are more common, then that means there is more function, and evolution predicted that. ???? My head is going to fall off. Ok, you win WD. I mean, nobody can beat that argument. More seriously, it's pretty clear you don't understand what we're saying. It's probably best just for me to leave it at that (I was not trolling previously but I also will not continue that line of discussion).Silver Asiatic
August 27, 2015
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wd400 @ 94, and just what part of the rest of your evidence free 'just so story' do you think helps you with ORFans? You live in a pseudo-scientific fantasy land sir in which no matter how contradictory the finding, evolution morphs into what ever theoretical posture it needs to in order to explain the contradictory evidence away! As I have heard said before, the only evidence for the unlimited plasticity predicted Darwinism is within the theory itself. It can explain anything and be falsified by nothing.bornagain77
August 27, 2015
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EugeneS succinctly lays out the vast difference between agent causality and the chance/necessity causality of atheists. To which wd400 responds with dumb founded surprise that there could be such a sharp dividing point:
"That may be the strangest ID argument I’ve ever seen. Best of luck with it, I guess."
Here are a few references that have been cited several times over the past few years which wd400 apparently has never seen before:
Is Life Unique? David L. Abel - January 2012 Concluding Statement: The scientific method itself cannot be reduced to mass and energy. Neither can language, translation, coding and decoding, mathematics, logic theory, programming, symbol systems, the integration of circuits, computation, categorizations, results tabulation, the drawing and discussion of conclusions. The prevailing Kuhnian paradigm rut of philosophic physicalism is obstructing scientific progress, biology in particular. There is more to life than chemistry. All known life is cybernetic. Control is choice-contingent and formal, not physicodynamic. http://www.mdpi.com/2075-1729/2/1/106/ The Law of Physicodynamic Incompleteness - David L. Abel - 2011 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." If only one exception to this null hypothesis were published, the hypothesis would be falsified. Falsification would require an experiment devoid of behind-the-scenes steering. Any artificial selection hidden in the experimental design would disqualify the experimental falsification. 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." https://www.academia.edu/11759341/Physicodynamic_Incompleteness_-_Scirus_Sci-Topic_Page The Formalism > Physicality (F > P) Principle - * David L. Abel - 2011 ABSTRACT: The F > P Principle states that “Formalism not only describes, but preceded, prescribed, organized, and continues to govern and predict Physicality.” The F > P Principle is an axiom that defines the ontological primacy of formalism in a presumed objective reality that transcends both human epistemology, our sensation of physicality, and physicality itself. The F > P Principle works hand in hand with the Law of Physicodynamic Incompleteness, which states that physicochemical interactions are inadequate to explain the mathematical and formal nature of physical law relationships. Physicodynamics cannot generate formal processes and procedures leading to nontrivial function. Chance, necessity and mere constraints cannot steer, program or optimize algorithmic/computational success to provide desired nontrivial utility. As a major corollary, physicodynamics cannot explain or generate life. Life is invariably cybernetic. The F > P Principle denies the notion of unity of Prescriptive Information (PI) with mass/energy. The F > P Principle distinguishes instantiation of formal choices into physicality from physicality itself. The arbitrary setting of configurable switches and the selection of symbols in any Material Symbol System (MSS) is physicodynamically indeterminate—decoupled from physicochemical determinism. https://www.academia.edu/12952944/The_F_P_Principle_The_Formalism_Physicality_Principle_
bornagain77
August 27, 2015
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The rest of my comment appears just up there Box, anyone can read it.wd400
August 27, 2015
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#92 bull's eye, BA77!
WD400: “the idea that sequence space will have more function than previously thought if de novo genes are common is also a prediction of evolutionary biology.”
Translation:
We now think that there is not much function in sequence space, but we predict that IF de novo genes are found to be common we will adjust our belief accordingly. Yes folks, yet another dashing prediction of evolutionary biology!
Box
August 27, 2015
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wd400:
"the idea that sequence space will have more function than previously thought if de novo genes are common is also a prediction of evolutionary biology."
And there you have it folks. No need for experimentation to establish just how common functionality is in sequence space. (Behe, Axe, Gauger, etc..). If functional ORFans are common then evolution must have predicted it. Save for the fact that, of course, evolution predicted no such thing at all and in fact 'predicted' quite the opposite.
Similar species share similar genes - Cornelius Hunter The only figure in Darwin’s book, The Origin of Species, showed how he envisioned species branching off of one another. Similar species have a relatively recent common ancestor and have had limited time to diverge from each other. This means that their genes should be similar. Entirely new genes, for instance, would not have enough time to evolve. As François Jacob explained in an influential paper from 1977, “The probability that a functional protein would appear de novo by random association of amino acids is practically zero.” (Jacob) Any newly created gene would have to arise from a duplication and modification of a pre-existing gene. (Zhou et. al.; Ohno) But such a new gene would retain significant similarity to its progenitor gene. Indeed, for decades evolutionists have cited minor genetic differences between similar species as a confirmation of this important prediction. (Berra, 20; Futuyma, 50; Johnson and Raven, 287; Jukes, 120; Mayr, 35) But this prediction has been falsified as many unexpected genetic differences have been discovered amongst a wide range of allied species. (Pilcher) As much as a third of the genes in a given species may be unique, and even different variants within the same species have large numbers of genes unique to each variant. Different variants of the Escherichia coli bacteria, for instance, each have hundreds of unique genes. (Daubin and Ochman) Significant genetic differences were also found between different fruit fly species. Thousands of genes showed up missing in many of the species, and some genes showed up in only a single species. (Levine et. al.) As one science writer put it, “an astonishing 12 per cent of recently evolved genes in fruit flies appear to have evolved from scratch.” (Le Page) These novel genes must have evolved over a few million years, a time period previously considered to allow only for minor genetic changes. (Begun et. al.; Chen et. al., 2007) Initially some evolutionists thought these surprising results would be resolved when more genomes were analyzed. They predicted that similar copies of these genes would be found in other species. But instead each new genome has revealed yet more novel genes. (Curtis et. al.; Marsden et. al.; Pilcher) Next evolutionists thought that these rapidly-evolving unique genes must not code for functional or important proteins. But again, many of the unique proteins were in fact found to play essential roles. (Chen, Zhang and Long 1010; Daubin and Ochman; Pilcher) As one researcher explained, “This goes against the textbooks, which say the genes encoding essential functions were created in ancient times.” (Pilcher) https://sites.google.com/site/darwinspredictions/similar-species-share-similar-genes
For wd400 to try to turn around and say that widespread ORFans are a successful prediction of evolution, is yet another shining example of the non-falsifiable, pseudo-scientific, nature of the religion of neo-Darwinism, which wd400 apparently believes in with all his heart, mind and soul.bornagain77
August 27, 2015
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wd400: Wow, you guys have really lost it… Some of us never had it in the first place!Mung
August 27, 2015
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That may be the strangest ID argument I've ever seen. Best of luck with it, I guess.wd400
August 27, 2015
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wd400: It’s just biochemistry. Nope. You are not seeing the wood for the trees. Gene expression employs rules as well as the laws of nature. So when you appeal to gene expression and other sophisticated functionality in the cell, be careful to distinguish rules from the laws of nature. There is logic implemented using biochemistry on all levels of biological organization. Biochemistry alone cannot explain the presence of if-then-else rules. The same laws of nature act upon a switch in either position ON or OFF. Biochemistry is about constraints, not rules. Rules can apply where biochemistry is indeterminate. The same biochemistry will apply in any of the biochemically indeterminate states. Biochemistry cannot account for the existence of logic circuitry. Likewise, electromagnetism alone cannot account for the existence of television or sound waves cannot account for the existence of speech. Logic is irreducible to the laws of nature. Logic traces back to choice contingent causation and, ultimately, to agency (which manifests itself in decision making in the context of planning with forethought) because naturalistic means are limited to chance and necessity and consequently are not capable of explaining the existence of logic. It is clear that you have a few major flaws in your current understanding of biology. Removing those flaws is dependent on you understanding the following: (i) logic is not the same as the laws of nature; (ii) biological organization is replete with built-in decision making; (iii) the decision making capability can plausibly only be a result of prior decision making, planning and forethought (intelligent causation); (iv) intelligent causation is irreducible to the limited naturalistic causation; (v) naturalistic causation is incapable of explaining the origin of life.EugeneS
August 27, 2015
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I should add, SA, the idea that sequence space will have more function than previously thought if de novo genes are common is also a prediction of evolutionary biology. If they are really performing biological functions, there is good reason to think they will be less biochemically specific functions, and use shorter amino acids sequences to get them done.wd400
August 27, 2015
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SA, Leaving out the childish concern trolling
You’re claiming that by merely adding more junk (more scrabble letters) this increases the likelihood of spelling out a coherent sentence.
Right. Are you seriously claiming that's not true? The question though is what is the equivalent of a "coherent sentence" in sequence space. If you'd read what I said to start with, it's hard to see an ID explanation for what we know about existing de novo genes. As I said, it's hard to imagine that humans are carrying around a sequence homologous to Poldi because it was designed to later become a gene in mice! i.e. A sequence that is very close to the functional poldi gene exist in your intergenic DNA. Box, Without selection lineages would not be able to explore sequence nearly as efficiently, so I think it does makes sense to say selection creates functional sequences. If you'd like some sophmoric philosophical debate about the meaning fo teh word create you'll have to find someone else. The rest of your post is the classic retreat to the origin of life tactic. All I can say is that we know that function is much denser is the space of short RNAs than typical proteins. There are many unanswered questions about the origin of life, but, again, selection and recombination (and, in fact HGT!) mean that even rare events can be amplified and shared across species.wd400
August 27, 2015
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WD400: I think biologically functional sequences don’t arise from one-of random sampling sequence space but by natural selection (…).
Box: Natural selection needs biologically functional sequences in order to have something to select on. It doesn’t make sense to say that natural selection produces biologically functional sequences.
WD400: (...) it is true that selection only works on a sequence once it exists.
Thank you for acknowledging my point. So functional sequences arise by chance (random sampling sequence space) — given unguided evolution.
WD400: But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.
I'm not sure I get your point. Starting with LUCA I see an obvious problem: the finding of biological function cannot always have been an exceedingly rare event in the evolutionary narrative. Right?Box
August 27, 2015
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wd400
Nope. I literally can’t see anything in there that relate s to anything I’ve said.
Ok, I thought I made at least a few points that were quite clear, but I guess not. I'll try again on your comment following.
But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.
If de novo genes are not common, then they're an exceedingly rare event, but you're using a statistical approach to explain their origin. You already said this, that where there is more junk (complexity) there will be more opportunity for the emergence of de novo genes. But you've said nothing about how the junk produces specified order. From the article ...
Yet creating a gene from a random DNA sequence appears as likely as dumping a jar of Scrabble tiles onto the floor and expecting the letters to spell out a coherent sentence.
This is pretty simple and I think every IDist here understands it. Unfortunately, you haven't understood it at all. You're claiming that by merely adding more junk (more scrabble letters) this increases the likelihood of spelling out a coherent sentence. Try it with scrabble some time. Beyond that, you're looking at the pile of letters and noticing a sentence (a de novo gene). Now you calculate the odds based on the presence of one sentence appearing in a pile of letters. This you're considering "an exceedingly rare event". However, if there were several paragraphs of complete, coherent sentences, you say "It's a lot easier to create function this way than we thought". Again, if there's any IDist on this site that doesn't understand the problem you have stumbled into, I'd really like to hear it. Amazingly, you simply can't understand this at all. You're dealing with an entirely stochastic process. Selection is not going to help you. For de novo genes, their origin remains as difficult to explain if they appear rarely or if they're extremely common (although more remarkable if common). You're fond of modelling evolutionary scenarios. All you have to do is start with random junk and show us the specified order that arises out of it, and then explain why it has done that. So far, you're willing to accept that fully-formed coherent sentences can simply arise from a pile of scrabble letters (which is a vastly simpler task than what we're talking about). After that, you've basically said nothing. I'll add that you did admit there was a surprise here, but you seem to think that any wildly conflicting data from observations can be imported into your theory without negative consequences. To make it simple: 1. You assume evolutionary theory is correct and will absorb conflicting observations into the theory without admitting that the theory has been falsified. 2. Your assumption that "things evolved that way" is used as an explanation for every observation. Again, I mentioned that I was concerned for you because anybody can see what you've been doing. You're totally blind to the issues. I don't think you even realize what you've been saying and it's pretty clear you don't know what ID is, even after the many hours you spend here. Again, I find that very sad. You need to come to grips with this -- at the very least -- for the sake of whatever personal integrity you want to have for yourself.Silver Asiatic
August 27, 2015
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