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Here’s this snippet from a Phys.Org entry.

The most remarkable part of it is that they link “cell-type” evolution to the repression of genes, making one wonder if all the necessary genes needed for all of life was somehow present in an original genome.

Obviously there are problems with this thesis in terms of genome length and type, bacterial genomes being ciruclar, while animals generally have discrete chromosomes, but, it’s entirely possible that multi-cellular life represents a complete break with bacteria, and that what we’re seeing here is the ultimate in “front-loading,” where everything is in place, yet, per Behe’s first law of adaptation, we see “loss of function” leading to novelties.

And, it should be a little troubling, if not greatly troubling, to Darwinists, since we don’t see differing cell-types being produced by the onset of new genes, but, rather, what they generally see in the study is, as I already mentioned, a ‘turning-off’ of genes as different cell-types emerge.
Just another, almost daily, contradiction of Darwinian expectations.

KLF/SP genes belong to an important class of genes, called transcription factors, which either turn on or turn off the expression of other genes. The findings show a clear increase in repressor domains (domains that turn off the expression of other genes) as the KLF/SP gene family has expanded. This expansion mirrors increases in cell type diversity among animals and demonstrates that the transition from single-cell life to multicellular life occurred largely by “tinkering” with existing genes.

“This is interesting because it supports the idea that the appearance of new types of cells in a lineage of organisms as they evolve may be, more commonly, a consequence of turning off genes in unique temporal and spatial combinations,” Browne said. “Large numbers of unique cell types are required to support the development of complex tissues and organs.”

For the study, the researchers looked at 48 different genomes ranging from plants; single celled organisms including slime molds, fungi, and choanoflagellates; early branching multicellular animals including ctenophores, sponges, and jellyfish; invertebrates including insects and sea urchins; to vertebrates such as sharks, fish, and mammals including humans.

Too bad they don’t have a link to the study.

Comments
so… evolution doesn’t require new information?
Articles have been published in peer-reviewed journals that have been generated by a computer algorithm that searches other papers, and sources on the web, IIRC, and then patches them together into the final product. Now, I ask two questions of those who find themselves laughing: (1) Does the published paper represent "new information"? and, (2) Did the program that searched and pasted the paper together arise by "chance," or, did it involve "intelligence." I'd be happy if you answered either question.PaV
August 21, 2015
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so… evolution doesn’t require new information?
It's just ATCG all the way down. I think we have a new form of information: PaV-information. For any discrete state space with a binary representation and at least one 0 and one 1, the information is always constant. The proof of this involves showing that one can get to any state from the state 01 simply by shuffling and duplication, and using the PaV-information property that shuffling and duplication don't change information.Bob O'H
August 20, 2015
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so... evolution doesn't require new information?wd400
August 19, 2015
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You might want to read the paper.
If you have a computer program that moves around where and when the subroutines will be utilized, the program will run differently, and produce different results, but no real information would have been added.PaV
August 19, 2015
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This “cell-type” evolution and the link to the repression of genes is an amazing process. Totally detached from NS and RM and drift and niches. Has to be guided. You just can't make this stuff up. Leopard stalking it's niche is guided too. Every level of Nature is guided. Design stacked on design stacked on design. And it's Design all the way down:)ppolish
August 19, 2015
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Bob O’H asks
had you missed this paragraph? The analysis reveals that the primary mechanisms for the expansion and diversification of the KLF/SP gene family, during evolution of animals occurred as a complex intersection of domain shuffling (where segments of a gene that code for specific domains are shuffled between genes during evolution), gene duplication (the process by which an entire gene is duplicated), and de novo domain evolution (the emergence of gene sequences with novel functional protein domains).
Only problem is that it is, as PaV pointed out, a 'just so' story. In other words, as has been repeatedly pointed out to you, you don't have any actual empirical evidence that it is possible for unguided material processes to produce functional proteins (and/or functional genetic information). As to this unsubstantiated claim:
de novo domain evolution (the emergence of gene sequences with novel functional protein domains)
Yet, 'de novo domain evolution' is precisely the area that Doug Axe, Ann Gauger and others have worked in and shown to be fantastically beyond the reach of unguided Darwinian processes:
Evolution vs. Functional Protein Domains ("Mount Improbable") - Doug Axe and Stephen Meyer – Video https://www.youtube.com/watch?v=7rgainpMXa8 Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences. http://www.toriah.org/articles/axe-2004.pdf The Case Against a Darwinian Origin of Protein Folds - Douglas Axe - 2010 Excerpt Pg. 11: "Based on analysis of the genomes of 447 bacterial species, the projected number of different domain structures per species averages 991. Comparing this to the number of pathways by which metabolic processes are carried out, which is around 263 for E. coli, provides a rough figure of three or four new domain folds being needed, on average, for every new metabolic pathway. In order to accomplish this successfully, an evolutionary search would need to be capable of locating sequences that amount to anything from one in 10^159 to one in 10^308 possibilities, something the neo-Darwinian model falls short of by a very wide margin." http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.1
Even evolutionists themselves, though they refuse to accept their own experimental results, also come up with such ridiculously large numbers for finding functional protein domains by unguided Darwinian processes:
Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact - Cornelius Hunter - July 2011 Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude. per Darwin's God
Even subtle changes in proteins to new similar functions are found to be far beyond the reach of unguided Darwinian processes
Following the Evidence Where It Leads: Observations on Dembski's Exchange with Shapiro - Ann Gauger - January 2012 Excerpt: So far, our research indicates that genuine innovation, a change to a function not already pre-existent in a protein, is beyond the reach of natural processes, even when the starting proteins are very similar in structure. http://www.evolutionnews.org/2012/01/observations_re055171.html When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://www.biologicinstitute.org/post/18022460402/when-theory-and-experiment-collide Bill Nye, Nicholas Wade, and the Origin of Human Color Vision - Stephen C. Meyer - January 6, 2015 Excerpt: as the researchers tried to produce a protein with the properties of human eye proteins from the allegedly ancestral protein (in mice), they found that changing any one of the amino acids by itself did not affect the protein's function. To get anywhere, they discovered that they had to make sure that two or more specific mutations occurred together in concert to make it progressively more like the one found in human eyes.,,, (Yet) the calculated "waiting times" for the occurrence of coordinated mutations (i.e., multiple mutations occurring together) far exceeds the available time for the transition from a mouse-like common ancestor and the emergence of humans. Per Evolution News and Views
Dr. Axe challenges a Darwinist to create a single new gene by Darwinian processes:
Show Me: A Challenge for Martin Poenie - Douglas Axe August 16, 2013 Excerpt: Poenie want to be free to appeal to evolutionary processes for explaining past events without shouldering any responsibility for demonstrating that these processes actually work in the present. That clearly isn't valid. Unless we want to rewrite the rules of science, we have to assume that what doesn't work (now) didn't work (then). It isn't valid to think that evolution did create new enzymes if it hasn't been demonstrated that it can create new enzymes. And if Poenie really thinks this has been done, then I'd like to present him with an opportunity to prove it. He says, "Recombination can do all the things that Axe thinks are impossible." Can it really? Please show me, Martin! I'll send you a strain of E. coli that lacks the bioF gene, and you show me how recombination, or any other natural process operating in that strain, can create a new gene that does the job of bioF within a few billion years. http://www.evolutionnews.org/2013/08/a_challenge_for075611.html
As to the proposed mechanism of 'domain shuffling', that is also shown to be unfeasible, to put it mildly:
Exon Shuffling, and the Origins of Protein Folds - Jonathan M. - July 15, 2013 Excerpt: A frequently made claim in the scientific literature is that protein domains can be readily recombined to form novel folds. In Darwin’s Doubt, Stephen Meyer addresses this subject in detail (see Chapter 11). http://www.evolutionnews.org/2013/07/exon_shuffling074401.html Exon Shuffling: Evaluating the Evidence - Jonathan M. - July 16, 2013 The Problems with Domain Shuffling as an Explanation for Protein Folds Excerpt: The domain shuffling hypothesis in many cases requires the formation of new binding interfaces. Since amino acids that comprise polypeptide chains are distinguished from one another by the specificity of their side-chains, however, the binding interfaces that allow units of secondary structure (i.e. ?-helices and ?-strands) to come together to form elements of tertiary structure is dependent upon the specific sequence of amino acids. That is to say, it is non-generic in the sense that it is strictly dependent upon the particulars of the components. Domains that must bind and interact with one another can't simply be pieced together like LEGO bricks. In his 2010 paper in the journal BIO-Complexity Douglas Axe reports on an experiment conducted using ?-lactamase enzymes which illustrates this difficulty (Axe, 2010). http://www.evolutionnews.org/2013/07/an_evaluation_o074441.html
as to the proposed mechanism of gene duplication, that also leaves much to be desired:
Biologic Institute's Groundbreaking Peer-Reviewed Science Has Now Demonstrated the Implausibility of Evolving New Proteins - Casey Luskin January 22, 2015 Excerpt: one of their citations makes a compelling case that the gene duplication step poses a major obstacle to gene recruitment via gene duplication and mutation. They cite a paper from PLOS Genetics, "The Extinction Dynamics of Bacterial Pseudogenes," which notes: In bacteria, however, pseudogenes are deleted rapidly from genomes, suggesting that their presence is somehow deleterious. The distribution of pseudogenes among sequenced strains of Salmonella indicates that removal of many of these apparently functionless regions is attributable to their deleterious effects in cell fitness, suggesting that a sizeable fraction of pseudogenes are under selection. It concludes, "Although pseudogenes have long been considered the paradigm of neutral evolution, the distribution of pseudogenes among Salmonella strains indicates that removal of many of these apparently functionless regions is attributable to positive selection." Don't miss the profound importance of this. What it means is that there is very likely a fitness cost associated with carrying an extra, useless copy of a gene, and therefore it can be advantageous to delete duplicate version. This has major implications for the co-option model of protein evolution, because it shows that producing a new protein does not involve "neutral evolution," but rather requires steps that very likely will impose a deleterious effect upon the organism. http://www.evolutionnews.org/2015/01/biologic_instit_1092941.html
bornagain77
August 19, 2015
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Shuffling and duplication don’t get you any new information...
You might want to read the paper.wd400
August 19, 2015
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Bob OH, And you believe what, that this all happened by accidents?phoodoo
August 19, 2015
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Bob O'H Shuffling and duplication don't get you any new information. The de novo events are "rare". We don't see anything really new, just a shutting down of this or that. It has parallels to venom. Venom is made up of proteins that are not normally expressed; i.e., genes that were turned off, get turned on. REC: That increases in organismal complexity (more cell types doing more specialized things) requires more gene repression modules isn’t shocking. Nothing "shocks" a Darwinist; there's always a "just-so" story ready to be fashioned. That's the problem.PaV
August 19, 2015
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True, software can't write itself directly. But all you need is a little program that keeps trying random code and it can get better. Plus this software is mostly commented-out gibberish. So it's junk and it must have written itself. Oh, in some versions the comments are removed and the gibberish turns out to be more code. Hm... Ah but you see these particular programs sometimes rearrange existing code so it works differently. So you see they're not all that impressive. And would you look at that--sometimes they borrow code from each other! There you go, that was how it must have happened, more or less. Phew! Now, what's all this hogwash about programmers? If you teach that to your children you're evil and the state should take them away for their own good.englishmaninistanbul
August 19, 2015
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REC:
Front-loading of genetic information not used by the organism would only result in the degradation of that information.
Not if the design said to keep it from degrading.
From the sequence analysis, it seems that by de novo evolution, domain shuffling and duplication and divergence, these modules evolved.
If gene duplication was involved then they evolved via intelligent design as there isn't enough time in the universe for natural selection to A) duplicate a gene, B) build it a new binding site and C) change it such that it has a new function.Virgil Cain
August 19, 2015
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Front-loading of genetic information not used by the organism would only result in the degradation of that information. That increases in organismal complexity (more cell types doing more specialized things) requires more gene repression modules isn't shocking. After all, expressing liver genes in the brain (or vice versa) would be quite lethal. From the sequence analysis, it seems that by de novo evolution, domain shuffling and duplication and divergence, these modules evolved.REC
August 19, 2015
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Bob O'H- Until they can test the claims made in that paragraph it isn't science. For one no one can show how it was determined that gene duplication is an accident, error and/ or mistake. Also it isn't enough to merely duplicate the gene- it needs a binding site, promoter, repressor, etc., otherwise it is useless.Virgil Cain
August 19, 2015
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PaV, when you wrote
And, it should be a little troubling, if not greatly troubling, to Darwinists, since we don’t see differing cell-types being produced by the onset of new genes, but, rather, what they generally see in the study is, as I already mentioned, a ‘turning-off’ of genes as different cell-types emerge. Just another, almost daily, contradiction of Darwinian expectations.
had you missed this paragraph?
The analysis reveals that the primary mechanisms for the expansion and diversification of the KLF/SP gene family, during evolution of animals occurred as a complex intersection of domain shuffling (where segments of a gene that code for specific domains are shuffled between genes during evolution), gene duplication (the process by which an entire gene is duplicated), and de novo domain evolution (the emergence of gene sequences with novel functional protein domains).
Bob O'H
August 19, 2015
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. . . so the turning off of these genes in these cells is indeed the result of a change in DNA sequence. . . .
And the change is trivial.PaV
August 18, 2015
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mapou: The study goes back to before the Cambrian Explosion in terms of species type, and we're not seeing new cell types come about by something new developing, but, so it seems, by something that is present, but which is no longer expressed. We've seen a lot this kind of stuff over the last 10 years or so since genome sequencing has become fairly accurate and inexpensive.PaV
August 18, 2015
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Since when can “evolution” happen without a change in the base code of dna?
The paper is about new represaor domains, so the turning off of these genes in these cells is indeed the result of a change in DNA sequence.wd400
August 18, 2015
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"Free Will - The Power of No" chapter 2 of "Being as Communion" What a profound book by Dr. Dembski! I know free will / free won't does not apply at the atomic level. Or maybe it does:)ppolish
August 18, 2015
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"This is interesting because it supports the idea that the appearance of new types of cells in a lineage of organisms as they evolve may be, more commonly, a consequence of turning off genes in unique temporal and spatial combinations,” Browne said. ----------- (I used to post as VH) Since when can "evolution" happen without a change in the base code of dna? Futuyma: "There cannot be evolution without genetic variation in the first place. So there must be mutation and often recombination to generate the different genotypes or the different versions of the genes, known as alleles, which then may or may not make a difference in the ability of an organism to survive and reproduce. You can’t have any evolutionary change whatever without mutation, and perhaps recombination, giving rise to genetic variation." http://www.actionbioscience.org/evolution/futuyma.html ---- aside from that, by allowing "evolution" to happen without a change in dna, it essentially invalidates phylogenetic comparisons in regards to relationships. I mean if dna is not the only cause of difference between organisms then why should we put any stock in a method of classification that only tells a partial story?tommy hall
August 18, 2015
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“This is interesting because it supports the idea that the appearance of new types of cells in a lineage of organisms as they evolve may be, more commonly, a consequence of turning off genes in unique temporal and spatial combinations,” Browne said.
Why can't novelty also be the result of turning on dormant genes or a combination of both? I guess I'm not seeing the reason for the emphasis on OFF.Mapou
August 18, 2015
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Study is available: http://gbe.oxfordjournals.org/content/early/2015/07/30/gbe.evv141.full.pdf+htmlturell
August 18, 2015
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