The Origin of Novelty

No to the first part, but you're right about loss of diversity through spreading. The Middle-Eastern groups are sub-groups of other groups. Just in your model. They would have spread so quickly from the Middle East that they would be very homogeneous all over the world, surely.

Why is it ridiculous to point out that chemical phenomena are formed by chemical processes? Do you know of any exceptions? Why is what we can readily observe ridiculous? Obvious to whom? The discussion is perfectly civil on my part. I thought you were aware of the examples of novel protein coding genes that I gave on the peanut gallery. There was one in the Douc Langur monkey and one in an Antartic fish. They are paralogs. I'll repeat them here if you really want me to when I've got time. There's nothing subjective about pointing out that natural processes are the best explanation for natural phenomena. The conclusion is based on observations we can all make.

[Copied from the peanut gallery on mindspawn's great debate].There are various theoretical models of how gene duplications can produce new function, and there's considerable evidence that this can happen in several different ways.One interesting way is the "Escape from Adaptive Conflict" model, known as "EAC". This is based on the fact that some genes perform more than one function. This could hypothetically cause "adaptive conflict", because the ideal allele for one function may not be the same as the ideal for the other. Duplication of such genes, says the theory, could lead to subfunctionalization of each paralog, and to enhanced or new function as each copy of the gene is free to perform only one of the original functions, thus ending the conflict.Here's a recent research paper which presents very good evidence of an example of neofunctionalization arriving in this way. AbstractArticle based on paper

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Abstract

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The evolutionary model escape from adaptive conflict (EAC) posits that adaptive conflict between the old and an emerging new function within a single gene could drive the fixation of gene duplication, where each duplicate can freely optimize one of the functions. Although EAC has been suggested as a common process in functional evolution, definitive cases of neofunctionalization under EAC are lacking, and the molecular mechanisms leading to functional innovation are not well-understood. We report here clear experimental evidence for EAC-driven evolution of type III antifreeze protein gene from an old sialic acid synthase (SAS) gene in an Antarctic zoarcid fish. We found that an SAS gene, having both sialic acid synthase and rudimentary ice-binding activities, became duplicated. In one duplicate, the N-terminal SAS domain was deleted and replaced with a nascent signal peptide, removing pleiotropic structural conflict between SAS and ice-binding functions and allowing rapid optimization of the C-terminal domain to become a secreted protein capable of noncolligative freezing-point depression. This study reveals how minor functionalities in an old gene can be transformed into a distinct survival protein and provides insights into how gene duplicates facing presumed identical selection and mutation pressures at birth could take divergent evolutionary paths.

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Paralogs are identified by sequence similarity. Many paralogs with differing functions have been identified in many different species. Mindspawn faces the daunting task of demonstrating that all of these genes which look like functional coding paralogs are actually not (which is essentially what he is claiming).When something looks like a duck and quacks like a duck, the default is that it's a duck. The onus is not actually on RAZD to show that apparent ducks (or paralogs) are what they appear to be, but on mindspawn to support his extraordinary claim that they are not what they appear to be.Rather him than me!Note the significant added function of the new gene described in the article. "Unlike the SAS enzymes, which remain inside the cell, the AFP III proteins are secreted into the blood or extracellular fluid, where they can more easily disrupt the growth of invading ice crystals."

You, the churches, and the Bibke people have NOT satisfatorily discredit Modern Science with your science arguments. In the mean time, you all agree in the Spontaneous Generation of first life which is identical to Abiogenesis.Why NOT stop there, and claim god did it as far as the Bible and Science can tell.
First life was an Act-of-God.Why do you place the Bible on the fence with public ridicule on one side and the whole Institution of Religion on the otherside while atheists and devils throw rocks at it?It doesn't even make god look very intelligent, that he had to personal utilized Spontaneous Generation over and over again for every little germ and creature.His Natural Laws might well have created everything by using the initial life forms, and evolving them as science is so ready to accept.

Hi, Mindspawn Well, I can see why you'd think that. But, the problem is that "increased complexity" (however you define it) isn't a mechanism: it's a phenotype. There's no reason to think every class of phenotype has to have a different mechanism. For example, unequal crossing-over is a type of mutation that can cause both gene deletions (decreased complexity) and gene duplications (increased complexity). So, we don't need two separate mechanisms.However, it's incontrovertible that you require a mechanism for microevolution, and a mechanism for creation.----- Can you explain exactly what you think is happening here? Because, I think you've been duped by an offhand comment about the human nervous system (or its genetic components) being found in a coral. This is not what they found.A "homolog" is a gene that two groups of organisms have in common. Homologs are not identical to one another: they are just similar enough in sequence and (sometimes) in function to be considered related in an evolutionary worldview. So, it's not like two unrelated airplanes both having Rolls-Royce Merlin engines: it's like two unrelated airplanes both having piston engines.These researchers sequenced a bunch of genes (or, actually, sections of genes), and found that corals have more homologs with humans than with insects or nematodes. It doesn't say that corals have human genes or that humans have coral genes: it says that insects and nematodes are more different from other animals than other animals are from each other.----- Okay, now I need some clarification. I thought "increased complexity" and "additional coding genes" were the same thing, in your argument. This statement suggests that they are not always. Was I wrong?

Hmm, let's see. We either have:(a) The known processes of genetics.
(b) The known processes of genetics, plus an invisible creator.Unless there are a negative number of invisible creators, that would be one more, not one less.

Are you sure about that? How does God create animals without some process that adds complexity?Animals are complex, even if the process is magically poofing them into existence, it still adds complexity.

We have already done that on multiple occasions. Here is the pocket mouse example AGAIN.Just a moment...At least 4 mutations in the MC1R gene resulted in a gain of fuction which caused a darker fur color phenotype. In areas with black lava this was a very beneficial trait which was further supported by the lack of the mutations in populations directly surrounding the lava areas, populations that were living in brownish dirt and shrubs where the black fur color sticks out. From the paper:

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Third, the dark allele is dominant over the light allele, consistent with observations of Mc1r mutations in the mouse (11, 16) and other organisms (21—25). In the laboratory mouse, loss-of-function mutations at Mc1r are recessive and result in light color, whereas gain-of-function alleles are dominant and result in dark color (16).

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It does matter in that we are using the phylogenies that are informed by fossils to reconstruct the genetic history of species.Also, you would need to show that this interpretation is contradicted by the evidence. If evolution is NOT true then it should be pretty simple to point to fossils that violate the nested hierarchy, such as fossils with three middle ear bones and feather impressions. The fact that the fossils also fall into the same nested hierarchy constructed on both genetics and the features of living species only further demonstrates that the interpretation is correct. Again, they look evolved because they fall into a nested hierarchy. When we look at automobiles we find that they do NOT fall into a nested hierarchy like life does. There is simply no reason why ID should predict a nested hierarchy, unless the designer actually went through the additional effort of making it look like life evolved. Perfect example. We may find the exact same radio in a Landcruiser and an Avanza, but a different radio in a Corolla. We may find the same exact paint on both a Corolla and a Forerunner, but different paint on an Avanza. There are clear violations of nested hierarchies in designed things because there is simply no reason a designer would limit itself to such a hierarchy. None.All of this gets back to your question of why biologists think that genomes look evolved. Again, it goes right back to this nested hierarchy. The nested hierarchy is the central pillar of evolution. How so? Let's look at ERV's as an example. The retroviral genome looks something like this:LTR---viral genes---LTRThe LTR's, or long terminal repeats, are the bookends of the viral genome. Due to the way that the virus inserts into the host genome the LTR's have identical sequences at the time of insertion. LTR's are much longer than what I will show, but here is just a mock up of what I am talking about with some made up sequence:AAAA----viral genes----AAAAOver time, random mutations will occur in the genome which will cause the LTR's to become less similar over time, say something like this:AATA----viral genes----GAAAIn this case, we see that we have a mutation in each of the LTR's causing them to lose similarity. So how does this tie in with the nested hierarchy? An ERV shared by all apes (including humans) would have inserted into the common ancestor of all apes while an ERV shared by just humans and chimps would have inserted into the more recent common ancestor shared by just humans and chimps. Therefore, the ERV shared by all apes has been accumulating mutations longer than the ERV shared by just humans and chimps, that is if evolution is true. So what do we see? The ERV's that inserted into a more distant ancestor (as shown by the phylogeny) have more LTR divergence than ERV's that inserted into a much more recent ancestor just as the theory of evolution predicts.This is just one tiny example of millions that have led scientists to accept evolution as being accurate.

Oh yes, you have really identified many examples of random mutations and natural selection causing new complexities of functions haven't you? I guess if you really really want to believe something, you are going to aren't you.If you are going to rest your entire case of Darwinian evolution on pocket field mice colors, you are going to have a lot of problems.First, the study you are quoting is a better condemnation of the evidence for your theory than it is a support. Your eyes seemed to have glazed over some of the quotes, but I am not surprised frankly, as you also believe that the term "accidental" means intent. Here some things you should have read in the study: Gee, what are they saying here? With all of the supposed heaps of evidence for the theory of evolution being caused by slow step mutations, added on top of one another, they are being forced to admit that actually we don't know genetic pathways for virtually ALL of life's adaptive functioning. Really we know none. And why do we know none-because there is no one chain of events that leads to a new functioning, exactly the opposite of what we would expect to be true if Darwinism really was true.In the study itself it points out that there are at least several pathways that lead to hair coloration. Why should there be several? In fact, there at at least 80 genes that are responsible for hair coloration! 80! In a one mutation equals one new possible variation that is likely to spread because of an advantage paradigm?? Doesn't this at least cause you to raise your eyebrows? I guess not if you really need to believe something.What else do we know about coloration? We know that in most animal populations, light colored hair is really just a loss of function of dark colored hair. When you have a white dog coming from a wolf species, all you have is a dog that has lost its ability to produce melanin. Is there anything much more going on here in the pocket mice? Have the dark mice adapted a new function-like say be able to produce melanin in a population of animals that was never able to produce melanin before? Weren't all the ancestors of the mice able to produce melanin? What tree of life did these mice come from??Not only does this study not tell much of a story, since it concludes that there isn't just one reason or one mutation which accounts for the variation in hair color, but the worst part of this study is that its THE BEST YOU HAVE! Doesn't that tell you that you have a very serious problem with your theory? That the only infinitesimally small study that you can point to which you believe supports the theory of evolution, concludes that well, actually there are so many causes of coloration adaption, that we really only know one small part of a complex net of adaptive pathways that point to numerous mutations leading to convergent evolution.So we find nothing in the study which shows the mutations are random. Nothing in the study which shows we are talking about a one point mutation leading to a new novel function, and finally we have evidence that even with all the different mutative pathways, we still end up converging in the same place-dark mice.Does the theory of evolution that you believe in say "No matter what mutations an animal develops, it will still lead to exactly the same animal in the end, one who gets exactly the functions it needs exactly when it needs it regardless of what path it takes?" Is that how Darwin explained it? Did he say convergent evolution is virtually inevitable? Through random mutations and natural selection? This describes how your theory works? I thought if we unwind the clock, and make any small change, the results are supposed to come out differently. Whoops, sounds like its teleological afterall!But to understand so, first you have to get past the notion that accidental means intent!!!!!Believe me, I can certainly understand why Bluegenes is so shy about talking about the evidence. Edited by Bolder-dash, : No reason given.Edited by Bolder-dash, : No reason given.Edited by Bolder-dash, : My head swells at the notion that someone could consider this good evidence for the theory of Darwinian evolution.

We don't know all of the the SPECIFIC mutations that give rise to SPECIFIC phenotypes, that much is true. What we do know is that the differences in DNA sequence is what produces the differences seen between species, and that the pattern of divergence between species is entirely consistent with random mutations and natural selection. In fact, you have been incapable of even pointing to a single genetic difference between species that could not be produced by random mutations. Why should it raise eyebrows? Please explain. We have known for quite a while that there are many genes involved for many phenotypes, hair coloration being one of them. A mutation in any of those genes can cause a change in hair coloration, just as it appears to be the case in pocket mice. As the old saying goes, there's more than one way to skin a cat. The dark color did appear in a population of light colored mice which again indicates that these mutations resulted in a gain of function. It tells the entire story for one population of black mice. They found the mutations in that population that gave rise to the dark coloration. They discussed when the new environment and niche appeared. They discussed the selective pressures that were placed on the allele. They have the entire story right there. The study shows how random mutations result in a gain of function that is then selected for through natural selection. Yes, we do. We find that in other populations they also evolved dark coloration through other mutations demonstrating that the mutations were not triggered by the needs of the organism. Instead, the mutations were random with respect to fitness. The study demonstrates exactly what you claim it doesn't. And they did come out differently. Did you read the article or not? There were different mutations in each of the populations. When you have an accident it implies that you intended one outcome, but another happened. Accident implies intent. It always has.Edited by Taq, : No reason given.

Really? So what would the pattern look like if it wasn't random mutations and natural selection which caused the divergences of species?If a theory says that a mutation is random, and then if that mutation causes some of survival advantage the random mutation will slowly become the norm in a population, and then later that mutation will progress further through another random mutation-then what you would expect to see is functions in the organism which are controlled by 80 different genes? Did all 80 genes get mutated, and all 80 caused some type of slight survival advantage?And what if a function needs 7 different mutations before it even displays any difference in its functioning-why would the first six mutations be preserved in the populations before the seventh came about? I asked you what species of animal do you think the pocket mouse evolved from, which didn't have the function of producing melanin? You think it evolved from a creature which didn't have this function before? See its new and novel? Why are you so naive? This is again another one of your reading comprehension problems. They didn't come out differently at all. The mice had many different kinds of mutations and yet they ALL came out the same-with black fur! Is that complicated to get? Different mutations same results-not different results!Goodness gracious.

Could you kindly post your evidence for your claims please.Are you claiming that diversity of haplogroups are not directly related to genetic diversity? I didn't understand your points here. The map showed the widest range of haplogroups in the Middle Eastern/Asian region.

I don't really understand your point here. Small groups can often be homogenous, and can also often be highly diverse due to isolation. Societies can retain behaviours and also rapidly change behaviours, our culture is nothing like 100 years ago. I've heard this argument before, that the cultural differences between races are so strong that it couldnt have occurred over 4500 years. History however shows continuously rapidly changing cultures making that point null and void.There was an initial spurt of homogenous civilizations about 3800 years ago, this is sometimes referred to as the early pyramid cultures. All having a high degree of architectural ability combined with similar "birdman" myths.

Maybe you can discuss this in a more related thread?