Another Day, Another Bad Day for Darwinism

_{June 23, 2010

Evolutionary biology, Intelligent Design}

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In the latest issue of Nature, a definitive role for pseudogenes is established. In the last sentence of the Abstract the authors conclude:

These findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs.

Haven’t read the full article* (no time at present), but there’s a related link at PhysOrg.com that gives an overview.

Yes, “junk” DNA now “communicates” with itself. A new “language”, an RNA language, is discovered. Another 30,000 pieces of functional information (over and above proteins) are part of cell architecture. And even more for Darwinists to explain per RM+NS. And the old standard explanation, of gene duplication and pseudogenes ‘evolving’ new function, takes a hit. You’ve got to feel bad for these Darwinists. What’s tomorrow going to bring!?!

*BTW, somehow I gained access to the pdf version of the article.

Comments

Joaozinho, Your friend says that my claims are exaggerated. Gpuccio has defended my position, and the ID position, admirably. I agree with every point he makes, and would have made the same points myself (although not quite as nicely). I'm reminded of what is said of Winston Churchill. (I could very easily be wrong about it being Churchill) It is said that he once got into a discussion with a woman who made the comment that no amount of money would get her to sleep with another man. He asked her if she would sleep with him for a million dollars. She said, "Well, for a million dollars, yes." Then he asked her if she would sleep with him for 50 dollars. She said to him, "What kind of a woman do you think I am?" He answered that he already knew what kind of a woman she was, and that they were simply haggling over the price. Even if, right now, the amount of pseudogenes that have function is small (per A Hunt's calculation), neo-Darwinian theory is nevertheless under duress since even a 23 bp miRNA doesn't just happen by chance---which is exactly the neo-Darwinian understanding of how gene duplication + RM(=neutral drift) + NS = a new, "coding" gene. Did the 23 bp regulatory function come about by chance? (The odds are 1 in about 10^14; ie, 1 in 100 trillion) Not only that, if the pseudogene has a function while being transcribed, though not translated into a protein, then the translation process would likely lead to a loss of the miRNA function. And, if the miRNA, small as it may be, is involved in gene regulation, that could easily have catastrophic effects for the organism. You have heard of the proverbial "tip of the iceberg," well, this finding, most likely, is just that. It represents a severe blow to Darwinian story telling. But, of course, the Darwinists don't see it that way.PaV_{June 28, 2010
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Joaozinho, though you and "your friend" may laugh at this following paper as well, I find it very indicative of the great divide as to how IDists approach the genome and how evolutionists approach it: Human Genome “Infinitely More Complex” Than Expected - April 2010 Excerpt: Hayden acknowledged that the “junk DNA” paradigm has been blown to smithereens. “Just one decade of post-genome biology has exploded that view,” she said, speaking of the gene regulation was a straightforward, linear process of gene coding for regulator protein that controls transcription. “Biology’s new glimpse at a universe of non-coding DNA – what used to be called ‘junk’ DNA – has been fascinating and befuddling.” If it’s junk, why would the human body decode 74% to 93& of it? The plethora of small RNAs produced by these non-coding regions, and how they interact with each other and with DNA, was completely unexpected when the project began.,,, In the heady post-genome years, systems biologists started a long list of projects built on this strategy, attempting to model pieces of biology such as the yeast cell, E. coli, the liver and even the ‘virtual human’. So far, all these attempts have run up against the same roadblock: there is no way to gather all the relevant data about each interaction included in the model.,,, The p53 network she spoke of is a good example of unexpected complexity. Discovered in 1979, the p53 protein was first thought to be a cancer promoter, then a cancer suppressor. “Few proteins have been studied more than p53,” she said. “...Yet the p53 story has turned out to be immensely more complex than it seemed at first.” She gave some details: "Researchers now know that p53 binds to thousands of sites in DNA, and some of these sites are thousands of base pairs away from any genes. It influences cell growth, death and structure and DNA repair. It also binds to numerous other proteins, which can modify its activity, and these protein–protein interactions can be tuned by the addition of chemical modifiers, such as phosphates and methyl groups. Through a process known as alternative splicing, p53 can take nine different forms, each of which has its own activities and chemical modifiers. Biologists are now realizing that p53 is also involved in processes beyond cancer, such as fertility and very early embryonic development. In fact, it seems willfully ignorant to try to understand p53 on its own. Instead, biologists have shifted to studying the p53 network, as depicted in cartoons containing boxes, circles and arrows meant to symbolize its maze of interactions. Network theory is now a new paradigm that has replaced the one-way linear diagram of gene to RNA to protein. That used to be called the “Central Dogma” of genetics. Now, everything is seen to be dynamic, with promoters and blockers and interactomes, feedback loops, feed-forward processes, and “bafflingly complex signal-transduction pathways.” http://www.creationsafaris.com/crev201004.htm#20100405a as well Joaozinho, I noticed you nor "your friend" have picked a number for Junk DNA yet.bornagain77_{June 28, 2010
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Joaozinho, Did you say you're a religious studies major? Who is this "friend" of yours? A friend from Stanford?Clive Hayden_{June 28, 2010
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Art Hunt, In order to support this "dated" assertion with full integrity,,, "a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis." ,,,,You must also address the more recent evidence presented for cortical inheritance, i.e.,, live memory, instead of just presenting very interesting experiments done exchanging genetic material between closely related sub-species: Cortical Inheritance: The Crushing Critique Against Genetic Reductionism – Arthur Jones – video http://www.metacafe.com/watch/4187488 “Live memory” of the cell, the other hereditary memory of living systems – 2005 Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2K-4FJXNG6-1&_user=10&_coverDate=06%2F30%2F2005&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1273117547&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0bfa74d6bb0937402472343daa6bdef8 I am not saying DNA does not have a very important role in form and function, I am just saying that you are completely missing the point that DNA is, by far, not the whole story for form and function! Which is exactly the main point that Wells and company make! as a side note Art Hunt,, Dr. Sanford is the one who developed the "gene gun" that is a major technique that is used to exchange genetic material between closely related plants in the first place, even "before" he wrote his book on Genetic Entropy, so do you think that he just might have noticed if your examples went against the overriding principle for biology he established in his book?bornagain77_{June 28, 2010
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Joaozinho: Just to be precise: gpuccio admitted that PaV’s post wasn’t accurate What I wrote is what I wrote, and can be read by anyone. The above statement is your statement, and not mine. You know, that's just to remind you that I am not "your friend", and that I can speak for myself if I want.gpuccio_{June 28, 2010
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veilsofmaya, Sorry for the late reply, sometimes it takes me a few days before I can come back. Anyway, here is the full New Scientist quote: Myth: Junk DNA is not junk after all Once the vast majority of our DNA was dismissed as junk, but now we know it is important - or so you might have read recently. In fact, it still appears likely that 85 to 95 per cent of our DNA is indeed useless. While many bits of DNA that do not code for proteins are turning out to have some function or other, this was predicted by some all along, and the overall proportion of our DNA with a proven function remains tiny. You wrote @49: Darwinsts clearly do not claim that “DNA is junk” and also: Again, they do not suggest it is “useless” in it is universally non-functional. Nor do they suggest we may not find other functions for non-coding DNA. You seem to be conflating the class of junk DNA with universal non-function. Let's talk about nothing but the plain reading of the NS article. I think that title implies that junk DNA is indeed junk. Later it says that it is "likely ... indeed useless". Putting everything together, this article does not orientate the reader to do more research into unknown functionality. Instead, it makes a statement that 85 to 95 percent of our DNA is useless. The solid opinion of the author is clear from the title. Nevereless, later it uses the word "likely" to provide an exit clause. Does this article seem to be conflating the class of junk DNA with universal non-function? :) To me it seems highly unlikely that such gross inefficiency was at the base of life. Especially because living creatures can vastly outperform our best technology, like the humble fruit fly. We have never created autonomous flying vehicles with optical, mechanical and chemical sensors that can seek out various targets, avoid dangers and re-fuel when needed. The fruit fly does in in a few cubic mm of volume. I bet my money that we will find function for the vast majority of DNA. For me, the context implies it so.Alex73_{June 28, 2010
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Phaedros, In what way is the definition naive? bornagain, Where did you get the idea that because most of the transcription is nonfunctional, that anyone's declaring anything to be junk? This has been a real education for me…gpuccio admitted that PaV's post wasn't accurate, but when I contrast what my friend says with what the rest of you are saying, my friend has a lot more credibility. He points me to evidence, while you point me to what people say about the evidence.Joaozinho_{June 27, 2010
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1. One report (of hundreds or thousands) that describe the regeneration of normal plants from isolated somatic cells. 2. The cybrid example is one that shows that, contrary to the claims of Wells et al., the nuclear DNA does indeed determine form. It's entirely consistent with, oh, a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis. ID proponents need to give up on this failed assertion - it only leads to very puzzling claims (such as some of the suggestions about plants and animals that we are seeing here). Facts are facts - there is an exorable and unbreakable link between "the DNA" and multicellular growth and development, a link that is positively affirmed in systems that are amenable to appropriate experimental study. 3. "Genetic entropy" as laid out in Sanford's book is a concept that is utterly irrelevant to this discussion, as well as biology in general. And it most certainly does not apply to the example I gave that refutes Wells et al. in no uncertain terms.Arthur Hunt_{June 27, 2010
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Art Hunt,, I'm finding the link you listed to fall within Genetic Entropy: Agricultural Applications of Plant Protoplast Fusion David A. Evans1 Abstract Plant protoplasts can be fused and the fusion products cultured to produce somatic hybrid plants. This technique has been used to produce germplasm previously unavailable to the plant breeder. Several researchers have emphasized production of hybrids between distantly related, sexually incompatible species, but many of these hybrids are sterile, precluding incorporation into a breeding program. Hence, to transfer traits such as disease and herbicide resistance, emphasis has shifted to production of hybrids between more closely related species. Novel variation has been observed in such somatic hybrids due to segregation of mixed organelles, cytoplasmic and nuclear gene recombination, and somaclonal variation. The unique gene combinations made possible by protoplast fusion ensure that new plant varieties will soon be derived from somatic hybridization. http://www.nature.com/nbt/journal/v1/n3/abs/nbt0583-253.html Do you disagree with that assessment Art Hunt?bornagain77_{June 27, 2010
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Can you or your friend pick a percent number for just how much Junk DNA you think is present as I asked earlier Joaozinho? as well Can you or your friend cite any studies as to declaring protein coding genes (of all things) to be junk?bornagain77_{June 27, 2010
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Joaozinho- That's a naive definition of functional and can you please have your friend speak for himself and you speak for yourself.Phaedros_{June 27, 2010
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bornagain, In answer to your claim that transcription = function for noncoding dna, my friend laughed again and pointed out that there is massive evidence that most transcription of most protein encoding genes that have been studied is nonfunctional, and we know this from studying mutants, even humans. He defines functional as "having any detrimental effect on the organism when it is not present."Joaozinho_{June 27, 2010
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Art Hunt, I'm wondering just how much weight you should give to your link,,, for the plants seem to be related: Solanum, the nightshades, horsenettles and relatives, is a large and diverse genus of annual and perennial plants. http://en.wikipedia.org/wiki/Solanum Nicotiana (pronounced /?n?k??i?e?n?/)[3] is a genus of herbs and shrubs of the nightshade family (Solanaceae) http://en.wikipedia.org/wiki/Nicotiana i.e. has one descended by means of genetic entropy from the other? The reason I ask is because quite a bit a variability can be found in plants from just one parent stock: Evolution? - The Deception Of Unlimited Variation - video http://www.metacafe.com/watch/4113898 i.e. variation within kind! Now Art if you put the DNA from say a dog into a cat and had a dog develop then you will have saved the DNA dogma. But as it sits I am not impressed.bornagain77_{June 27, 2010
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Art, why don’t you provide a link to your final claim in #56? I would be interested, too.gpuccio_{June 27, 2010
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When a similar experiment is done in plants, the results refute Wells et al. in no uncertain terms.
But plants are not animals, and that could be a hasty extrapolation. Replacement of some genes in some plants does not necessarily result in observing ill effect, but we can't extrapolate that to all plants and animals in all reasonable contexts. And here earlier you were objecting to making extrapolations from limited observation, and the argument you put forward does exactly that. But the bottom line is, do you believe "genes alone control all development" or do you believe information apart from genes is necessary to effect development, such as pseudogenes? I think that will help clarify the discussion. Do you beleive pseudogenes serve function in development? Do you think this would be a worthy area of research?scordova_{June 27, 2010
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Art, why don't you provide a link to your final claim in #56?PaV_{June 27, 2010
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veilsofmaya [52 and 53]: Try to be more clear about what you're saying. For example, what is this supposed to mean? As such, wouldn’t this be a “very bad day” for those who continually, perpetuate, these claims, despite research such as this which clearly suggests otherwise? You seem to be suggesting that IDists are the one suggesting that there is no function to junk DNA, which is, of course, quite the opposite. So who are these people who "continually, perpetuate, these claims"? And why is there a comma between continually and perpetuate, and one following perpetuate? I shouldn't be expected to make sense out of all of this. And, as to #53 and this quote:
it draws an arbitrary boundary beyond which human reason and understanding has no access and problem solving can no longer increase knowledge.
I'll presume you're the author of this quote. Can't you see that this applies exactly to neo-Darwinists who continually state: "Well, who is this Designer? We know what humans are capable of, but we don't know anything about this Designer. So how can we possibly detect his design." Doesn't this exactly draw "an arbitrary boundary beyond which human reason and understanding has no access and problem solving can no longer increase knowledge." When you start pointing fingers, you ought to be careful.PaV_{June 27, 2010
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Another fact that flies in the face of the mistaken claims of IDists that there is some mysterious, ethereal factor or force that plays roles in multicellular development.
I know of no IDist of any repute who makes that claim for the devlopment (as in cell to mature individual) of organisms in existence today. Development follows a developmental program. Multicellar evolution (as in when the first unicellular organism became multicellular) is different from multicelluar development. I invite the readers to do a google search to see how many times the phrases: "intelligent design" and "multicellular develpment" and "ethereal force" come up together. :-)scordova_{June 27, 2010
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Re: gpuccio @ #45 I think it needs to be pointed out that the sort of duplication event that yields pseudogenes such as PTENP1 does not involve merely the protein-coding sequence; all of the gene, including promoter, 3’ UTR, and miRNA target site (the decoy site in the pseudogene-encoded RNA) come from the original gene, and they are all duplicated. And, as I have stated before, and as countless ID proponents have insisted every time they are asked about gene duplication as it relates to the origins of new proteins, the ID party line is that this is not a change in information. Thus, when you say:
My point is, if we believe that transcription and translation of the original gene are finely regulated by a complex network, including miRNAs (and many other regulatory modalities), then the duplication-mutation event must be finely tonuse to integrate in such a network. The point is not that the event in itself is “possible” through known random biochemical mechanisms. It certainly is, exactly as the mutations which can bring to a new functional protein are certainly “possible” from a biochemical point of view.
you seem to miss the simple point that the duplicate gene will automatically be “finely tuned” to co-express with the original gene. It’s unavoidable, and a natural consequence of the random duplication event.
The ID point is that such events are rare functional examples among a huge majority of non functional possible events.
I don’t believe you have any data to support the ID position that such events are so impossibly rare as to be beyond the bounds of normal evolutionary processes. Indeed, the deep sequencing that is being done in humans reveals just the opposite – that all manner of genetic alterations, such as deletions and duplications, are not impossibly rare.
The ID point is that, exactly as obtaining a new functional protein is empirically impossible through RV and NS alone,
This ID point is clearly not correct.
in the same way obtaining a finely tuned duplication, or set of duplications, and the coordinated mutations both in the coding and non coding sequence and in the related regulatory sequences, which perfectly integrates in a complex regulatory system involving many different agents, is empirically impossible through RV and NS alone.
The problem is that, in the case under discussion here, all of this fine tuning is an unavoidable consequence of a single random event.
We have no evidence that those “typical biochemical processes” are random and unguided, any more than we have evidence that all single point mutations are random and unguided.
We know that all of these processes involve well-understood chemical rules, and that no “hand of God” (with all apologies to football fans, and especially those aggrieved by the alluded-to event) need be invoked to understand the past, present, or future when it comes to gene duplication. If you have positive, repeatable and controlled experimental data that suggests otherwise, please discuss it. Until then, the suggestion that something other than chemistry is behind gene duplication must be considered as idle fancy.
Moreover, many pseudogenes are the result of transposon activity, and transposon activity is a very good candidate as an interface for guided variation.
The pseudogenes of interest here have nothing to do with transposons (which are not guided in any ways, other than the substrate preferences, as determined by chemistry, of the enzymes that catalyze transposon duplication and movement). To reiterate, we are talking about something here that is at best information-neutral, and at worst involves a loss of information. And it is the result of a common and random process.Arthur Hunt_{June 27, 2010
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“There is now considerable evidence that genes alone do not control development. For example when an egg’s genes (DNA) are removed and replaced with genes (DNA) from another type of animal, development follows the pattern of the original egg until the embryo dies from lack of the right proteins. (The rare exceptions to this rule involve animals that could normally mate to produce hybrids.)
When a similar experiment is done in plants, the results refute Wells et al. in no uncertain terms. Then there is the fact that single, isolated plant cells that have a completely deprogrammed cytoskeleton and have been removed from all maternal influence can grow into normal, fertile plants. Another fact that flies in the face of the mistaken claims of IDists that there is some mysterious, ethereal factor or force that plays roles in multicellular development.Arthur Hunt_{June 26, 2010
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bornagain77 (#46): Thank you for the link to the interesting paper: I am looking at it.gpuccio_{June 26, 2010
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veilsofmaya (#50 - 51): 1) First of all, the lungfish (and other similar giant genomes). The C enigma is, as far as I know, still an enigma. If you are aware of recent literature which has detailed in some way the composition of the lungfish genome (or of any other giant genome), I will be very grateful if you can point that to me. I have found this paper of 2005: "NfCR1, the first non-LTR retrotransposon characterized in the Australian lungfish genome, Neoceratodus forsteri, shows similarities to CR1-like elements" which analyzes a retrotransposon in the lungfish genome, and finds it to be account for 0.05% of the genome (the same % as in chicken). That's interesting, but is really too little. Beware, I am not underestimating the importance of these giant genomes. Though they are certainly more an exception than the rule, they can probably give us important insights about some unsolved problems (and, in general, help us understand better the C enigma). I have been waiting for years to know more about those genomes. But my point is, until we know something substantial about those genomes, and their structure, we cannot even begin to discuss why they are so big. So, I don't think you can use them as evidence of any sort of principle in any discussion about the functions of DNA, be it coding or non coding. 2) About your other remarks, I would say that I am drawing no arbitrary boundary. The difference between harmful traits and useful new functions is extremely objective, and Behe has discussed that in great detail in TEOE: harmful tracts are simple, new functions are complex. Take, for instance, mendelian genetic diseases: they are ususally due to a single point mutation, which reduces or abolishes some important protein function. we all agree (darwinists and IDists) that random single point mutations do occur. That they are frequent. Living cells have a whole set of complex functions to try to deal with negative simple mutations. I would not even agree to call them "unplanned errors on the part of nature", because nature, if considered blind, does not make errors: it just proceeds through unmeaningful events. The thing is very different for complex functions. Functional proteins are both specified and complex. They cannot emerge form random noise, not even with the help of necessary NS. That's the whole point of ID. So, I am drawing no arbitrary boundary, except for the very natural and logical one between what is complex and what is simple, what specifies a completely new function, and what simply and accidentally destroys an existing one. A very simple example can show the difference. Sometimes darwinists discuss experimental models where bacteria undergoe a mutation, usually induced by the researcher, which inactivates a protein. In those cases, in the appropriate context, microevolution can, with some relative ease, reintegrate the previous function through random mutation. Now, some darwinists argue: isn't that evidence that CSI can be acquired through one simple mutation, and therefore it is not complex? After all, the non functional protein changes to the functional one through one single mutation. Bit it's obvious that that's not the case. The non fucntional protein still keeps the whole functional structure except for one aminoacid which has been accidentally changed. From that position, it is obvious that it is relatively easy to go back to the full functional structure by one appropriate substitution, which is perfectly in the reach of the probabilistic resources of a bacterial model. But, if the harmful mutations are two, we can already see that the difficulties increase exponentially. Indeed, two coordinated mutations are almost a natural boundary which is traversed very rarely and only through huge probabilistic resources, as shown by Behe. If they are not the edge of unguided evolution, they are very near. And three mutations? Four? Five? Please consider that basic protein domains differ one from the other for tens, up to hundreds, of AAs. That's the boundary. It's not me who am drawing it. It's reality itself.gpuccio_{June 26, 2010
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@Pav (#12) You wrote:
You didn’t respond to this point I made. Instead, you sped forward to the Copernican revolution (BTW, you do know, of course, that Copernicus was a Catholic cleric? See here) and now want to infer that it is perfectly permissible to draw an analogy between that paradigm shift and the current one taking place, implying that ID thinkers are blinded in some way.
If you actually read the comments I linked to, you'd find…. Now that we actually have two theories – one explicit and on implicit – was there a way we could have differentiated between them at the time? I’m going to suggest that [A] there is such a thing as a bad explanation and [B] there really are ways we can identifying them. [...] Again, as a critical rationalist, I realize intuition, observations and induction are insufficient on their own as any theory can make any prediction. Ultimately, It’s the arguments and explanations behind them which makes one tenable over another. […] In other words, to understand planetary motions via the Inquisition’s implied theory it’s essential to reference Heliocentrism. It’s a cosmology that can be only understood in terms of a different cosmology which it contradicts but faithfully mimics. The result is that Inquisition’s theory does not actually explain planetary motion without having to introduce the complication of Heliocentrism first. As such, we can rightfully say that the Inquisition’s implied theory is a convoluted elaboration of Heliocentrism. […] In case it’s not clear, I’m suggesting that we can rightfully say ID’s implied theory is a convoluted elaboration of and a response to TOE. Furthermore, it shares the following with The Inquisition’s implied theory and even Solipsism: it draws an arbitrary boundary beyond which human reason and understanding has no access and problem solving can no longer increase knowledge.veilsofmaya_{June 26, 2010
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@Pav (#12) You wrote:
“PaV says that the bias of Darwinism blinds researchers to the function of junk DNA. Yet the researchers are studying junk DNA. If they thought it had no function, then why are they studying it.”
First, As I read it, your suggesting was it was "a bad day for Darwinism" because of the specific details of the discovery. That is, because you thought Darwinism could not explain it. While you may have made such an argument elsewhere or you thought it was implied, it was not explicitly present in your post. This is why I wrote.. if the claim that biologists commit the fallacy of assuming genes with no currently known function really are universally functionless was true, it’s unclear why anyone bothered to study these psuedogenes in the first place. … and linked to specific arguments ... As such, wouldn’t this be a “very bad day” for those who continually, perpetuate, these claims, despite research such as this which clearly suggests otherwise? … rather than making a blanket statement of ID as a whole. As such, your most effective response would have been to point out that the “bias of Darwinism” supposedly preventing researchers from studying junk DNA was a misrepresentation of your position. However, this particular argument was not explicitly present this particular position in this post.veilsofmaya_{June 26, 2010
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@gpuccio (#45) You wrote:
The ID point is that such events are rare functional examples among a huge majority of non functional possible events. The ID point is that, exactly as obtaining a new functional protein is empirically impossible through RV and NS alone, in the same way obtaining a finely tuned duplication, or set of duplications, and the coordinated mutations both in the coding and non coding sequence and in the related regulatory sequences, which perfectly integrates in a complex regulatory system involving many different agents, is empirically impossible through RV and NS alone.
Gpuccio, How is this not a convoluted elaboration of TOE? The complexity of biological life is just like neo-darwinsts suggest in that the arrival of harmful traits are unplanned errors on the part of nature, while the appearance of useful traits, including those that only appeared to be neutral or unhelpful on their own but add up to an advantage when put together, are really the work of an intelligent being. In other words, it's like evolution, except an intelligent designer must have occasionally stepped in because useful traits represent information and information is defined as resulting from an intelligent agent, or you simply can't imagine a way these traits formed naturally (personal incredulity.) Again, your'e drawing what appears to be an arbitrary boundary. We can understand how harmful traits appear, but no amount of problem solving or reasoning can explain how positive traits can appear.veilsofmaya_{June 26, 2010
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@gpuccio (#20) Thanks for your response. I have a few follow-up questions. You wrote..
- I have never considered credible that 95% or more of the human genome is non functional. That concept seems so ridiculous that I have never seriously considered it as true. Call it an argument for incredulity A good argument form incredulity.
First, when you say non-functional are you referring to universal non-function or having some indirect role in expression? If the former, then the 95%+ figure your using here is not applicable. Again, this really is non-controversial. However, I'm guessing you'd also find the idea that a even the rough estimation such as any significant part of the human genome was is universally non-functional is ridiculous as well. Correct? If so, it's here that we would being to diverge. Given that the lungfish as 130 billon bases compared to the roughly 3 billon bases in human beings, what is the purpose of, lets say 70 billon of the 127 lungfish bases which humans being lack? That is, if your argument is from incredulity, what other "credible" explanation does Intelligent Design provide for why lungfish have 40 times the number of bases than we do?veilsofmaya_{June 26, 2010
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@Alex73 (#35) You wrote:
Why is it then, that Darwinists trumpet that DNA is junk?
Alex, You're back to making ambiguous statements again. Darwinsts clearly do not claim that "DNA is junk". Again, they use the term "junk DNA" to describe a specific class of bases that we currently think are not directly involved in coding.
Why is it that they blatantly allow unjustified leaps of logic to declare something useless, when the we just simply do not understand it?
Again, they do not suggest it is "useless" in it is universally non-functional. Nor do they suggest we may not find other functions for non-coding DNA. You seem to be conflating the class of junk DNA with universal non-function. Are you sure this isn't just a reaction to being offended by even the hint of any sort of non-functionality in DNA?veilsofmaya_{June 26, 2010
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A little more clarity: This inability of body plans to be reduced directly to the DNA code is clearly shown by Cortical Inheritance. Cortical Inheritance: The Crushing Critique Against Genetic Reductionism - Arthur Jones - video http://www.metacafe.com/watch/4187488 “Live memory” of the cell, the other hereditary memory of living systems - 2005 Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2K-4FJXNG6-1&_user=10&_coverDate=06%2F30%2F2005&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1273117547&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0bfa74d6bb0937402472343daa6bdef8bornagain77_{June 26, 2010
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Arthur Hunt, On top of the penetrating questions gpuccio brings to you for the inadequacy of neo-Darwinism to account for the origination of "higher level" regulatory functions in the genome, my question is much more foundational to your position: How in blue blazes do you, as a neo-Darwinist, justify your belief that mutations to DNA is the main catalyst of the morphogenesis of new species, when genetic reductionism is falsified in the first place? And since genetic reductionism is falsified as being the "cause" of morphogenesis, how do you justify using purported genetic similarities as evidence for common ancestry? notes: Stephen Meyer - Complexity Of The Cell - Layered Information - video http://www.metacafe.com/watch/4798685 ...Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection." - Jonathan Wells http://www.evolutionnews.org/2008/08/inherit_the_spin_the_ncse_answ.html#footnote19 Darwin's Theory - Fruit Flies and Morphology - video http://www.youtube.com/watch?v=hZJTIwRY0bs Hopeful monsters,' transposons, and the Metazoan radiation: Excerpt: Viable mutations with major morphological or physiological effects are exceedingly rare and usually infertile; the chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event. These problems of viable "hopeful monsters" render these explanations untenable. Paleobiologists Douglas Erwin and James Valentine “Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find the information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing that there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype (Body Plan)." Michael John Denton page 172 of Uncommon Dissent "There is now considerable evidence that genes alone do not control development. For example when an egg's genes (DNA) are removed and replaced with genes (DNA) from another type of animal, development follows the pattern of the original egg until the embryo dies from lack of the right proteins. (The rare exceptions to this rule involve animals that could normally mate to produce hybrids.) The Jurassic Park approach of putting dinosaur DNA into ostrich eggs to produce a Tyrannosaurus rex makes exciting fiction but ignores scientific fact." The Design of Life - William Dembski, Jonathan Wells Pg. 50 Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 A comparative approach for the investigation of biological information processing: An examination of the structure and function of computer hard drives and DNA – David J D’Onofrio1, Gary An – Jan. 2010 Excerpt: It is also important to note that attempting to reprogram a cell’s operations by manipulating its components (mutations) is akin to attempting to reprogram a computer by manipulating the bits on the hard drive without fully understanding the context of the operating system. (T)he idea of redirecting cellular behavior by manipulating molecular switches may be fundamentally flawed; that concept is predicated on a simplistic view of cellular computing and control. Rather, (it) may be more fruitful to attempt to manipulate cells by changing their external inputs: in general, the majority of daily functions of a computer are achieved not through reprogramming, but rather the varied inputs the computer receives through its user interface and connections to other machines. http://www.tbiomed.com/content/7/1/3 Arriving At Intelligence Through The Corridors Of Reason (Part II) - April 2010 Excerpt: In fact the term ‘junk DNA’ is now seen by many an expert as somewhat of a misnomer since much of what was originally categorized as such has turned out to be pivotal for DNA stability and the regulation of gene expression. In his book Nature’s Probability And Probability’s Nature author Donald Johnson has done us all a service by bringing these points to the fore. He further notes that since junk DNA would put an unnecessary energetic burden on cells during the process of replication, it stands to reason that it would more likely be eliminated through selective pressures. That is, if the Darwinian account of life is to be believed. “It would make sense” Johnson writes “that those useless nucleotides would be removed from the genome long before they had a chance to form something with a selective advantage….there would be no advantage in directing energy to useless structures”. further note: Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness - May 2010 Excerpt: Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.2 This following paper reveals that there is a "cost" to duplicate genes that further precludes the scenario from being plausible: Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence. http://www.springerlink.com/content/vp471464014664w8/ Fearfully and Wonderfully Made - Glimpses At Human Development In The Womb - video http://www.metacafe.com/watch/4249713 As you can see Arthur Hunt there are many intractable problems with your genetic reductionism scenario coming from multiple angles.bornagain77_{June 26, 2010
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gpuccio, I think you may find this paper that just came out interesting: Messenger RNAs are regulated in far more ways than previously appreciated, study finds Excerpt: A team of molecular biologists from Cold Spring Harbor Laboratory (CSHL) has now discovered that mRNAs can be targeted for destruction by several modes and molecules, highlighting a previously unanticipated complexity in the control and regulation of the cell's genetic messages. http://www.physorg.com/news196687864.htmlbornagain77_{June 26, 2010
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