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Darwin’s peppered myth: Turns out, peppered moths take care to protect themselves

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A Darwin cult (the peppered myth) developed during the twentieth century around the peppered moths, with the recent “resounding triumph” that it turns out that pollution effects do favour dark coloured moths over light coloured ones in the same species, with no important changes.

Whoop whoop. That is all Darwinism can come up with, in real life, after all this time.

But so? Snowbelt effects explain why the Canadian Groundhog Day groundhog is white and the American one is brown. No evolution was ever harmed in the making of the diverting nonsense.

In “Peppered Moths Without Evolution” (July 31, 2012), Creation-Evolution Headlines comments , noting a recent, more detailed study,

Kettlewell and Majerus didn’t take into account the moths’ behavior. They treated moths as passive creatures that would alight on tree trunks at random. They placed the selective power in the environment, with lower contrast producing greater camouflage, leaving the high-contrast moths vulnerable to birds.

The South Korean researchers found, instead, that moth behavior plays a vital role in the camouflage. They “found out that moths are walking on the tree bark until they settle down for resting; the insects seem to actively search for a place and a body position that makes them practically invisible.” A video clip embedded in the article shows the moths doing this.

The article avoids superstitious homage to Darwin as well, apparently. That’s a start  in the right direction.

We always thought that the moth had more interest in protecting its hide than the researchers did, and guess what? But how do the moths know if, when they feel invisible, they really are invisible?

See also: US Darwinists (US ranked 14th) wail over South Korea (ranked 1st), supposedly “not able to compete”

Comments
a few 'non-random' notes:
Genome-wide characterization of non-reference transposons in crops suggests non-random insertion - 2 August 2016 Results We identified 13,066, 23,866 and 35,679 non-ref TEs in rice, maize and sorghum, respectively. Genome-wide characterization analysis shows that most of non-ref TEs were unique and non-ref TE classes shows different among rice, maize and sorghum. We found that non-ref TEs have a strong positive correlation with gene number and have a bias toward insertion near genes, but with a preference for avoiding coding regions in maize and sorghum. The genes affected by non-ref TE insertion were functionally enriched for stress response mechanisms in all three crops. Conclusions These observations suggest that transposon insertion is not a random event and it makes genomic diversity, which may affect the intraspecific adaption and evolution of crops. https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-016-2847-3 Non-random distribution of transposable elements in the nuclear genome of plants. - 1993 Excerpt: We have studied the genomic distribution of five different families of plant transposable elements by analyzing their location in DNA fractions from maize and tobacco genomes fractionated according to base composition. The results show that each family of elements is preferentially integrated in one specific fraction of its respective host genome. This demonstrates that the distribution of transposable elements in the nuclear genome of plants is not random but compartmentalized,,, https://www.ncbi.nlm.nih.gov/pubmed/8389439 Integration specificity of the hobo element of Drosophila melanogaster is dependent on sequences flanking the integration site - 1999 http://link.springer.com/article/10.1023%2FA%3A1003712619487 We analyzed the integration specificity of the hobo transposable element of Drosophila melanogaster. Our results indicate that hobo is similar to other transposable elements in that it can integrate into a large number of sites, but that some sites are preferred over others, with a few sites acting as integration hot spots. Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements - 2009 http://nar.oxfordjournals.org/content/38/5/1515.full We first discovered that most TEs insert within specific ‘hotspots’ along the targeted TE… Finally, we performed a global assessment to determine the extent to which young TEs tend to nest within older transposed elements and identified a 4-fold higher tendency of TEs to insert into existing TEs than to insert within non-TE intergenic regions. Our analysis demonstrates that TEs are highly biased to insert within certain TEs, in specific orientations and within specific targeted TE positions. TE nesting events also reveal new characteristics of the molecular mechanisms underlying transposition. A Key Evidence for Evolution Involving Mobile Genetic Elements Continues to Crumble - Cornelius Hunter - July 13, 2014 Excerpt: The biological roles of these place-jumping, repetitive elements are mysterious. They are largely viewed (by Darwinists) as “genomic parasites,” but in this study, researchers found the mobile DNA can provide genetic novelties recruited as certain population-unique, functional enrichments that are nonrandom and purposeful. “The first shocker was the sheer volume of genetic variation due to the dynamics of mobile elements, including coding and regulatory genomic regions, and the second was amount of population-specific insertions of transposable DNA elements,” Michalak said. “Roughly 50 percent of the insertions were population unique.” http://darwins-god.blogspot.com/2014/07/a-key-evidence-for-evolution-involving.html Non-Random and Targeted Mutations (Environmentally induced changes to the level of DNA, 6:34 minute mark of video) - video http://www.youtube.com/watch?v=qTChu5vX1VI Evolution Is Not Random,,, - Tanya Lewis, - 02 October 2014 Excerpt: "So in the end, most mutation is not random, at least for the DNA sequences we analyzed here," http://m.livescience.com/48103-evolution-not-random.html?cid=514636_20141002_32724136 WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Fully Random Mutations - Kevin Kelly - 2014 Excerpt: What is commonly called "random mutation" does not in fact occur in a mathematically random pattern. The process of genetic mutation is extremely complex, with multiple pathways, involving more than one system. Current research suggests most spontaneous mutations occur as errors in the repair process for damaged DNA. Neither the damage nor the errors in repair have been shown to be random in where they occur, how they occur, or when they occur. Rather, the idea that mutations are random is simply a widely held assumption by non-specialists and even many teachers of biology. There is no direct evidence for it. On the contrary, there's much evidence that genetic mutation vary in patterns. For instance it is pretty much accepted that mutation rates increase or decrease as stress on the cells increases or decreases. These variable rates of mutation include mutations induced by stress from an organism's predators and competition, and as well as increased mutations brought on by environmental and epigenetic factors. Mutations have also been shown to have a higher chance of occurring near a place in DNA where mutations have already occurred, creating mutation hotspot clusters—a non-random pattern. http://edge.org/response-detail/25264 "It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns” James Shapiro - Evolution: A View From The 21st Century - (Page 82) Duality in the human genome - Nov. 28, 2014 Excerpt: The results show that most genes can occur in many different forms within a population: On average, about 250 different forms of each gene exist. The researchers found around four million different gene forms just in the 400 or so genomes they analysed. This figure is certain to increase as more human genomes are examined. More than 85 percent of all genes have no predominant form which occurs in more than half of all individuals. This enormous diversity means that over half of all genes in an individual, around 9,000 of 17,500, occur uniquely in that one person - and are therefore individual in the truest sense of the word. The gene, as we imagined it, exists only in exceptional cases. "We need to fundamentally rethink the view of genes that every schoolchild has learned since Gregor Mendel's time.,,, According to the researchers, mutations of genes are not randomly distributed between the parental chromosomes. They found that 60 percent of mutations affect the same chromosome set and 40 percent both sets. Scientists refer to these as cis and trans mutations, respectively. Evidently, an organism must have more cis mutations, where the second gene form remains intact. "It's amazing how precisely the 60:40 ratio is maintained. It occurs in the genome of every individual – almost like a magic formula," says Hoehe. http://medicalxpress.com/news/2014-11-duality-human-genome.html
etc.. etc...bornagain77
November 24, 2016
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wd400 @119,
wd400: I think Hunter probably didn’t read (or at least didn’t understand) the paper so didn’t realise how improbable his scenario was.
Do not simply state your opinions, but provide arguments for your views. For instance, when you wish to talk probabilities, you should take example from dr. Hunter, who does provide arguments:
… evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through. It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen. [Darwin's God]
Origenes
November 24, 2016
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Amazing! I have now read through most of these posts. Nick and wd400 both explain that a single mutation(or perhaps an 'insertion', not sure) caused a gene which governs the production melanin (I think)to produce more pigment in a single, perhaps several moths. The mutation was random and unguided, the process of selection that followed, was anything but random. This happened before, or in and around the fifties. Britain at this time was highly polluted and many buildings were covered in soot. The mutation allowed the dark moths to be camouflaged against predators, escape predation, and successfully pass on this advantageous mutation. Now as Britain is a much less polluted place, the few moths that have another mutation reducing melanin, means the process is being reversed. Easy, logical, evidence based, supported by years of patient research. Not being a scientist but genuinely interested in letting scientists explain their work, this explanation is clearly the correct one. I have no idea what all the other sciencey babble is about. I do know it is incredibly difficult to read, illogical, God based, and supported by exactly zero research. Which idea will win through I wonder?rvb8
November 23, 2016
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I think Hunter probably didn't read (or at least didn't understand) the paper so didn't realise how improbable his scenario was.wd400
November 23, 2016
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WD400: Do you really think a this is response is “directed” to occur in a single moth?
Do you really (really) think that that is what dr. Hunter proposes when he writes:
A much more likely explanation, and one that has been found to be true in so many other cases of adaptation (in spite of evolutionary pushback), is that the peppered moth coloration change was directed. The environmental change and challenge somehow caused the peppered moth to modify its color. This suggests there are preprogrammed, directed adaptation mechanisms, already in place that are ready to respond to future, potential, environmental changes, which might never occur.
?Origenes
November 23, 2016
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Insertions are a type of mutation, I'm not sure what you think this adds? It remains the fact we are talking about a single insertion. Do you really think a this is response is "directed" to occur in a single moth?wd400
November 23, 2016
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WD400: In this case we are talking about a single mutation.
For clarity, we are not talking about a single point mutation, therefore it would be helpful to say: "we are talking about a single insert". From the paper:
We conclude that the large insert is the carbonaria mutation. The carbonaria insert is 21,925 nucleotides long and is composed of a roughly 9-kb essentially non-repetitive sequence (except for approximately 370 nucleotides at the repeat unit junctions) that is tandemly repeated approximately two and one-third times, with only minor differences among the repeats (Fig. 1c). The insert bears the hallmark of a class II (DNA cut-and-paste) transposable element ...
Hunter:
This observed mutation (the insertion of a long sequence of DNA into an intron), is much more complicated than a single point mutation. ... and the fact it was inserted into an intron suggests that additional molecular and cellular mechanisms are required for the coloration change to occur. None of this fits evolutionary theory. For example, evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through. It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen. A much more likely explanation, and one that has been found to be true in so many other cases of adaptation (in spite of evolutionary pushback), is that the peppered moth coloration change was directed. The environmental change and challenge somehow caused the peppered moth to modify its color. This suggests there are preprogrammed, directed adaptation mechanisms, already in place that are ready to respond to future, potential, environmental changes, which might never occur.
Origenes
November 23, 2016
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I’m sure the authors will invoke “selection” somewhere along the line, and then bow down to Darwinism; but, that proves nothing other than they only have one paradigm out of which to look at and analyze things.
They show strong evidence of selection.
Up until this paper, let’s say from the “1920’s” on, was this thought to be anything other than some “random” mutation, and likely a SNP?
No one knew what a SNP was in the 1920s. You are the only person how said anyting about a SNP in this thread.
TE’s are not ‘random.’
You keep saying this, but it's not true. In this case we are talking about a single mutation. Is you claim really that this is a directed response, programmed to occur in a single moth then take over the population?
As to the paper, if you would like to direct my attention to something there, please do.
You are the one making the claims. Please demonstrate something in this paper requires a whole new paradigm to understand. Or perhaps just admit that you wrote this post before you even read the paper, you didn't understand the results and you made a mistake in necroing this thread?wd400
November 23, 2016
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wd400: I'm sure the authors will invoke "selection" somewhere along the line, and then bow down to Darwinism; but, that proves nothing other than they only have one paradigm out of which to look at and analyze things. Up until this paper, let's say from the "1920's" on, was this thought to be anything other than some "random" mutation, and likely a SNP? Here, for example, is what Nick Matzke wrote early on:
As for the mutational change from light to dark in the peppered moth, we don’t quite know the exact mutational change yet, but it could well be just a point mutation. It’s not exactly hard for a mutation to push up the amount of melanin in an organism.
TE's are not 'random.' That's the whole upshot. Here's a snippet from a report on the paper:
Saccheri and colleagues compared that region in one black moth and three typical moths. The researchers found 87 places where the black moth differed from the light-colored moths. Most of the differences were changes in single DNA bases — the information-carrying chemicals in DNA. Such genetic variants are known as SNPs for single nucleotide polymorphisms. One difference was the insertion of a 21,925-base-long stretch of DNA into the region. This big chunk of DNA contained multiple copies of a transposable element, or jumping gene. Transposable elements are viruslike pieces of DNA that copy and insert themselves into a host’s DNA. By examining the DNA of hundreds more typica moths and ruling out mutations one by one, the team ended up with one candidate: the large transposable element that had landed in the cortex gene. But the jumping gene didn’t land in the DNA that encodes the protein. Instead it landed in an intron — a stretch of DNA that gets chopped out after the gene is copied into RNA and before a protein is made.
So, the insert is in "junk DNA," and it's not a SNP If you can't accept that as a new starting point, I can't do anything about it. But just throwing the same old bromides at me, and insisting that I'm wrong; well, this gets us nowhere. That this "mutation"---all 22 kbases of it---started at some point in time, and was handed down meiotically. And, yes, they've located this as occurring around 1820. None of that amounts to a hill of beans. What matters is HOW did this mutation arise. The rest is mumbo-jumbo. Time will prove one of us right. I'm confident. What about you? As to the paper, if you would like to direct my attention to something there, please do. I may, or may not, respond, depending on whether I deem it a worthwhile use of my time. I'm not going to beat a dead horse here.PaV
November 23, 2016
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Phenotypic plasticity exists, of course. But it's not relevant to the peppered moth example, where the phenotype is encoded by a single dominant allele (as has been known since the 1920s).wd400
November 23, 2016
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PaV, Does anything happen to the RBC count of people living in low lands traveling to very high altitudes? That kind of adaptation is possible because the biological systems have a built-in framework that is conducive to such adaptation. That kind of adaptation is called phenotypical plasticity. There are many examples like that. Biological systems were designed with those built-in features.Dionisio
November 23, 2016
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Taken together, this simply means that RM+NS means almost nothing here
You still haven't read the paper, have you?wd400
November 23, 2016
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Dionisio: No, I had only read the abstract, and I didn't see the paper until you linked to it. You stated this: "Note they’re referring to “mechanism underpinning rapid adaptation.” They’re talking about “adaptive evolution”, i.e. micro-evolution, which is possible because the biological systems are designed with a built-in framework that is conducive to such adaptation mechanisms, which explain the observed phenotype variety within each kind of biological systems. What else is new? That’s all. Same old, same old. Don’t we all agree on that?" The "classic" story surrounding the peppered moth is that because of industrial pollution and the concomitant darkening of tree barks, the moth, subject to 'selection pressure,' changed its allele frequencies. That's the classic story. And, within the traditional pop. gen. way of thinking, this would mean some point mutation occurred, or that some kind of recombination occurred. So, either a protein was itself changed (SNP), or, expression of a protein was changed. And, of course, all of this would be "random." This is the critical remark. We are NOT dealing with a "random" event, just as your statement above implies. And, I invoked Barbara McClintock because she was run out of the academy (let's just say that she no longer felt comfortable in the pop. gen. community, much like what happened to Sternberg at the Smithsonian, and to Duesberg at Berkeley) precisely because she was claiming that TE's were responsible for rapid adaptive events AND that they were "non-random." No one in their right mind would quibble with adaptation occurring. What is at stake, always, is the mechanism that's involved. From this paper we know that a TE is involved, and, that it is nicely fitted into an intron region, which, of course, should not affect the protein involved in any way. Taken together, this simply means that RM+NS means almost nothing here. But, this is an ICON of evolution. If neo-Darwinism fails to explain its origin, then neo-Darwinism is dead! But, of course, many in the evolution camp are already saying this. Against all of this, wd400 is holding out to the end. I personally don't think that there is much to traditional evolutionary thinking. I believe that what has historically been called "microevolution" is not really that at all, but simply built in mechanisms at work using environmental cues. If you've paid attention over the years, you'll see that I've asked wd400 on many occasions to explain the very rapid change in phenotype that occurred in Pod podicarus, an Adriatic lizard transplanted to another island. He says he can't explain it. I said that the only way it can be explained is that the changed diet of the lizards brought the dramatic phenotypic changes, viz, cecal valves, about. I suggested 4 or 5 years ago that an experiment be run in which the diet was changed/controlled. Such an experiment was conducted, and, in fact, when the diet of the lizards were changed in the lab, the 'exact' changes took place in the lab specimens. I have every right to feel vindicated in my thinking. And it is, of course, 'intelligent design' that informs my thinking. So, not only do I think it is impossible to explain "macro-evolution" using Dawinian thought, I don't even think that "microevolution" will hold up to scrutiny once the genome's regulatory mechanisms are more fully explored. But, we'll just have to 'wait and see' on that one.PaV
November 23, 2016
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bornagain77: After opening the link you posted @106, with an interesting article by Dr. Hunter, I looked at another recent article he posted in his own blog: http://darwins-god.blogspot.com/2016/11/about-that-genetic-code.html In that article Dr. Hunter refers to this paper by two scientists from Kazakhstan, who apparently don't care much about being as "politically correct" as their western colleagues or simply didn't realize their title choice for their paper may be prone to different interpretations. Well, that could happen to any title anyway. :) Here's the paper (>3yo) by the two scientists from Kazakhstan: https://arxiv.org/pdf/1303.6739v1.pdfDionisio
November 23, 2016
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bornagain77 @106: Thank you for sharing that interesting report. Every new scientific research report is bad news for Neo-Darwinian ideas.Dionisio
November 23, 2016
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#104 addendum http://isyeb.mnhn.fr/joron/nadeau15nature.pdfDionisio
November 23, 2016
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PaV and Dionisio, this is of related interest to epigenetic mechanisms:
Yale's Steven Novella Argues with Michael Behe -- Here's Why Novella Is Wrong - Cornelius Hunter - November 23, 2016 Excerpt: the press release informed the public that the (MEGA) experiment provided "A powerful, unvarnished visualization of bacterial movement, death, and survival; evolution at work, visible to the naked eye." Likewise, Novella called it "a nice demonstration of evolution at work in a limited context." There's only one problem: The experiment did not demonstrate evolution, it falsified evolution. http://www.evolutionnews.org/2016/11/yales_steven_no103309.html
bornagain77
November 23, 2016
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#104 addendum http://www.genetics.org/content/204/1/3.full.pdf BTW, I think on several occasions gpuccio has expressed his interesting opinion on the transposons in relation to ID.Dionisio
November 23, 2016
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PaV @100:
I looked quickly at the date and thought I saw 2014. Simple as that. And, yes, that is the paper.
Thank you for clarifying this to me. I appreciate it. BTW, that may happen to anyone, not a big deal. It happens to me often. Just wanted to make sure there wasn't another more recent discussion between you and your politely dissenting interlocutor that I was not aware of. Didn't want to comment on your discussion with your politely dissenting interlocutor before seeing all the related comments. Please, note that the following two questions are mainly for my own research study, hence they're not directly related to this discussion with your interlocutor:
1. When you saw Dr. Hunter's reference to that paper, did you see the entire paper or just the abstract? 2. Had you seen the text of the entire paper before the link to the PDF copy of that paper was posted @99?
Now, back to your discussion with your politely dissenting interlocutor. The referenced paper has this paragraph in their conclusion:
The carb-TE is a spectacular example of an adaptively advantageous transposon; its discovery fills a fundamental gap in the peppered moth story and furthers our appreciation of the mechanism underpinning rapid adaptation. A consensus on the general importance of transposable elements for adaptive evolution has yet to emerge.
Note they're referring to "mechanism underpinning rapid adaptation." They're talking about "adaptive evolution", i.e. micro-evolution, which is possible because the biological systems are designed with a built-in framework that is conducive to such adaptation mechanisms, which explain the observed phenotype variety within each kind of biological systems. What else is new? That's all. Same old, same old. Don't we all agree on that? You're on target. Your politely dissenting interlocutor isn't. Just let's be gracious to them. They don't know what they're talking about. You may tell them to read better the entire paper next time they want to discuss with you. I try not to discuss directly with them. My time is very limited. Can't afford to squander it on trolling nonsense. PS. Please correct any inaccuracies in my comments. Thank you.Dionisio
November 23, 2016
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"Feel free to point out anything in this paper (and not your own imagination or misunderstanding of it) that requires a new paradigm." Says the man who himself, given naturalism, is a merely a figment of imagination with no free will.
The Confidence of Jerry Coyne - Ross Douthat - January 6, 2014 Excerpt: then halfway through this peroration, we have as an aside the confession that yes, okay, it’s quite possible given materialist premises that “our sense of self is a neuronal illusion.” At which point the entire edifice suddenly looks terribly wobbly — because who, exactly, is doing all of this forging and shaping and purpose-creating if Jerry Coyne, as I understand him (and I assume he understands himself) quite possibly does not actually exist at all? The theme of his argument is the crucial importance of human agency under eliminative materialism, but if under materialist premises the actual agent is quite possibly a fiction, then who exactly is this I who “reads” and “learns” and “teaches,” and why in the universe’s name should my illusory self believe Coyne’s bold proclamation that his illusory self’s purposes are somehow “real” and worthy of devotion and pursuit? (Let alone that they’re morally significant:,,) Read more here: http://douthat.blogs.nytimes.com/2014/01/06/the-confidence-of-jerry-coyne/?_r=0
bornagain77
November 23, 2016
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Feel free to point out anything in this paper (and not your own imagination or misunderstanding of it) that requires a new paradigm.wd400
November 23, 2016
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wd400: I said that if you didn't admit you were wrong here, you never would. You're stuck in an old paradigm.PaV
November 22, 2016
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Dionisio: I looked quickly at the date and thought I saw 2014. Simple as that. And, yes, that is the paper.PaV
November 22, 2016
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PaV @92: Why did you write "...two years later..."? From Aug 6 2012 to Nov 20 2016? BTW, is this the paper Dr Hunter referred to? http://rnajc.ucsf.edu/sites/rnajc.ucsf.edu/files/nature17951.pdfDionisio
November 22, 2016
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"I don’t know if it’s just your ignorance or motivated reasoning, but neither seems curable…" Says the man who adamantly believes, without one shred of evidence, that unguided material processes can out program and engineer our best programmers and engineers. A few notes to that effect:
“a one-celled bacterium, e. coli, is estimated to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 10^12 bits of information. In comparison, the total writings from classical Greek Civilization is only 10^9 bits, and the largest libraries in the world – The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library – have about 10 million volumes or 10^12 bits.” – R. C. Wysong ‘The information content of a simple cell has been estimated as around 10^12 bits, comparable to about a hundred million pages of the Encyclopedia Britannica.” Carl Sagan, “Life” in Encyclopedia Britannica: Macropaedia (1974 ed.), pp. 893-894 HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that,, E. coli contain(s) over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance. http://www.pathlights.com/ce_encyclopedia/Encyclopedia/20hist12.htm
Moreover, the regulatory network of a e-coli is found to be much more elegant than the operating system of Linux:
The Multi-dimensional Genome–impossible for Darwinism to account for– by Dr Robert Carter – video (15:52 minute mark: Comparing the Computer Operating Systems of Linux to the much more sophisticated operating systems of Regulatory Networks in e-coli) https://youtu.be/K3faN5fU6_Y?t=952 Comparing genomes to computer operating systems – Van – May 2010 Excerpt: we present a comparison between the transcriptional regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) in terms of topology,,, http://www.ncbi.nlm.nih.gov/pubmed/20439753 regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) – Picture of comparison http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2889091/figure/F1/
Along that line, it is also found that bacteria ‘solve optimization problems for collective decision making that are beyond what we, human beings, can solve with our most powerful computers’
Learning from Bacteria about Social Networking (Information Processing) – video Excerpt: I will show illuminating movies of swarming intelligence of live bacteria in which they solve optimization problems for collective decision making that are beyond what we, human beings, can solve with our most powerful computers. http://www.youtube.com/watch?v=yJpi8SnFXHs
And here is, according to a Darwinist, a ‘horrendously complex’ metabolic pathway chart of a ‘simple’ cell:
ExPASy – Biochemical Pathways – interactive schematic http://biochemical-pathways.com/#/map/1
Even the most stripped down bacteria imaginable, gives us every indication that life was Intelligently Designed
Microbe with stripped-down DNA may hint at secrets of life – Mar 24, 2016 Excerpt: The newly created bacterium has a smaller genetic code than does any natural free-living counterpart, with 531,000 DNA building blocks containing 473 genes. (Humans have more than 3 billion building blocks and more than 20,000 genes). But even this stripped-down organism is full of mystery. Scientists say they have little to no idea what a third of its genes actually do. “We’re showing how complex life is, even in the simplest of organisms,” researcher J. Craig Venter told reporters. “These findings are very humbling.”,,, The genome is not some one-and-only minimal set of genes needed for life itself. For one thing, if the researchers had pared DNA from a different bacterium they would probably have ended up with a different set of genes.,,, The genome is “as small as we can get it and still have an organism that is … useful,” Hutchison said.,,, http://hosted.ap.org/dynamic/stories/U/US_SCI_SKINNY_GENES Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information – David L. Abel and Jack T. Trevors – Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8 “No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms’ genomes programmed?” http://www.biomedcentral.com/content/pdf/1742-4682-2-29.pdf To Model the Simplest Microbe in the World, You Need 128 Computers – July 2012 Excerpt: Mycoplasma genitalium has one of the smallest genomes of any free-living organism in the world, clocking in at a mere 525 genes. That’s a fraction of the size of even another bacterium like E. coli, which has 4,288 genes.,,, The bioengineers, led by Stanford’s Markus Covert, succeeded in modeling the bacterium, and published their work last week in the journal Cell. What’s fascinating is how much horsepower they needed to partially simulate this simple organism. It took a cluster of 128 computers running for 9 to 10 hours to actually generate the data on the 25 categories of molecules that are involved in the cell’s lifecycle processes.,,, ,,the depth and breadth of cellular complexity has turned out to be nearly unbelievable, and difficult to manage, even given Moore’s Law. The M. genitalium model required 28 subsystems to be individually modeled and integrated, and many critics of the work have been complaining on Twitter that’s only a fraction of what will eventually be required to consider the simulation realistic.,,, http://www.theatlantic.com/technology/archive/2012/07/to-model-the-simplest-microbe-in-the-world-you-need-128-computers/260198/
And yet wd400, although he has not one shred of evidence that unguided material processes can produce such unfathomable complexity, has the audacity to label those who disagree with him as ignorant. The truth is, the willful ignorance manifested in wd400s false bravado towards PaV makes rocks appear as genius in comparison!bornagain77
November 22, 2016
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You're wrong about almost everything here, I'm afraid. I don't know if it's just your ignorance or motivated reasoning, but neither seems curable...wd400
November 22, 2016
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"A simple Mendelian trait." Is a 'transposon' a "simple Mendelian trait"? That the transposon is handed down from one generation to the next is almost entirely immaterial. What matters is how it arose. Now your pet theory, really hypothesis, is RM+NS. I argued that, to the contrary, it was likely some directed effect caused by some kind of environmental cue. As I mentioned, Barbara McClintock's work with "jumping genes" (transposons) led her to the conclusion that these transposons were NOT random mutations. IOW, RM+NS is off the table. So, you were wrong. (Point mutations were ruled out as being causitive in this paper) There is likely some kind of set of internal mechanisms that react to the environment, with the transposons being part of these mechanicsms. That means we're dealing with an 'epigenetic' origin of the mutation. You are simply wrong here--other than your assertion that changes brought about in one generation are then transmitted to the next. What a surprise assertion that is! Does the transposons have any choice in being handed down? And, if this insertion occurs in an intron, I think terming this a Mendelian trait misses the mark. As to Haldane, I invite you to look it up yourself if you're interested. It's up to you to prove that what I stated is wrong. Otherwise, what I said stands.PaV
November 22, 2016
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The link you provide is the very same link you’ll find in the link I provided to Dr. Hunter’s “Darwin’s God” blog.
Yes. I know. In this thread I said that the black colouration was a simple mendelian trait that arose from a single mutation which rapidly spread to near-fixation. The paper says the same thing. You said a lot of confused things about epigenetics and directed mutation. The paper doesn't say anything about that. It's that simple (Do you have a citation for the Haldane thing -- I think you've probably mis-remembered this)wd400
November 21, 2016
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Ummmm.....yes. The link you provide is the very same link you'll find in the link I provided to Dr. Hunter's "Darwin's God" blog. This from an article about this finding:
By examining the DNA of hundreds more typica moths and ruling out mutations one by one, the team ended up with one candidate: the large transposable element that had landed in the cortex gene. But the jumping gene didn’t land in the DNA that encodes the protein. Instead it landed in an intron — a stretch of DNA that gets chopped out after the gene is copied into RNA and before a protein is made.
Should I bring up the ignoble history of Haldane driving Barbra McClintock out of population genetics because "she didn't know what she was talking about"? And what made Haldane make this claim? McClintock said that 'transposable elements' are "non-random." How dare her? Well, as we know, she went on to receive the Nobel Prize for her work on transposons. Therefore, we can definitively say that if they were "non-random" in 1953, they're still "non-random"; you know, "directed." And you can take that to the Nobel Prize award ceremony. If you can't admit here, in this instance, that you were wrong, then you never will.PaV
November 21, 2016
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Ummmm.... no.wd400
November 21, 2016
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