ID/Creationism - Comparison of Human and Chimp Genomes

Hi eggasai, Could you give us an unnatural explanation, then? The transposable elements have been perfectly well characterized (review aricle). The interesting question is really a) why you would think that 8% of the human genome is too much, since population genetic models predict extremely high frequency of such elements under conditions such as small population size, and more importantly, b) why should humans and chimps share the SAME transposable elements? Question b is really the key here, one you failed to address. You have completely missed the point here - why do chimps and humans BOTH have the same pseudogene with the same deactivating mutation? Sure, pseudogenes degenerate because there is no natural selection keeping them faithful to the original copy. That is obvious. But why would humans and chimps have the SAME pseudogene, if they did not share a common ancestor in which that pseudogene arose and degraded? Do you have an alternative explanation or not? Since you appear to read the literature, I have to wonder whether you have done this sleight of hand on purpose. The number of point mutations is not equal to the number of nucleotide differences between two species. There are two classes of point mutation: substitution and indel (the latter is an abbreviation of insertion/deletion). A substitution involves one nucleotide being replaced with another, and results in exactly one nucleotide difference between an individual who has the mutation and an individual who does not have it. An indel, on the other hand, changes every nucleotide downstream of the mutation until a further indel puts an end to the frame shift. For example, consider a sequence, and a variation caused by a single substitution:

original sequence: ACTAGGACT
mutated sequence:  ACGAGGACT
ONE MUTATION = ONE NUCLEOTIDE DIFFERENCE

Now imagine that a deletion occurs at the first position, removing letter A:

original sequence: ACTAGGACT
mutated sequence:  CTAGGACT
ONE MUTATION = SEVEN NUCLEOTIDE DIFFERENCES

Now let's look at your numbers.Phylogenetic and palaeontological studies suggest that humans and chimps share a most recent common ancestor around six million years ago. Generation time for chimpanzees is around 20 years. Assuming that that generation time is a reasonable approximation for the intervening primate species, and given your rate of 123 mutations per generation, we would have nearly 37 million mutations in each of the human and chimpanzee lineages in that time, i.e. a total of 74 million mutations (since there are two lineages, protochimp and protohuman, which both accumulate mutations).So it seems that we are missing 70 megabases of mutations? Well, only if ALL mutations are substitutions. That's the implicit assumption of your argument that the mutation rate is too small. In reality, the researchers who published the new analyses of chimp versus human DNA found that around three times more nucleotide differences were caused by indels than were caused by substitutions. Indeed, from a Science Editorial it is reported:

quote:

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as suggested by earlier work on portions
of the chimp genome, other kinds of
genomic variation turn out to be at least as
important as single nucleotide base changes.
Insertions and deletions have dramatically
changed the landscape of the human and
chimp lineages since they diverged. Duplications
of sequence “contribute more genetic difference
between the two species”70 megabases
of material”than do single base pair
substitutions,” notes Evan Eichler, also of UW,
Seattle, who led a team analyzing the duplications.
“It was a shocker, even to us.”

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Could that be your missing 70 megabases?It would help to know where the 145 megabase number comes from, so we can examine your source more carefully. Could you give a reference? The results reported in the Science editorial were: 35 million single nucleotide substitions, and 5 million indels. We know that the indels gave rise to 70 megabases of divergent positions, so the authors appear to be reporting a total of 105 megabases, rather than 145, of divergent nucleotide positions caused by point mutation.More importantly, the total number of point mutations reported is 40 million, well within the bounds of the number of possible mutations according to your own figures.MickEdited by M, : No reason given.Edited by M, : No reason given.Edited by M, : No reason given.Edited by M, : Sorry for editing so many timesEdited by M, : okay that's the last edit, i promise

Hi eggasai,How about loss of the nocicepin receptor: Facilitation of long-term potentiation and memory in mice lacking nociceptin receptors.

quote:

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The peptide nociceptin (also named orphanin FQ) acts in the brain to produce various pharmacological effects, including hyperalgesia and hypolocomotion. The nociceptin receptor uses guanine-nucleotide-binding proteins to mediate the inhibition of adenylyl cyclase, the activation of potassium channels and inhibition of calcium channels. It has been shown using knock-out mice that the nociceptin receptor is not required for regulation of nociceptive responses or locomotion activity, but modulates the auditory function. Here we show that mice lacking the nociceptin receptor possess greater learning ability and have better memory than control mice. Histological analysis revealed the expression of both the nociceptin precursor and the nociceptin receptor in the hippocampus, thought to take part in aspects of learning and memory. Moreover, the receptor-deficient mice showed larger long-term potentiation in the hippocampal CA1 region than control mice, without apparent changes in presynaptic or postsynaptic electrophysiological properties. These results show that the loss of the nociceptin receptor results in a gain-of-function mutation in both the memory process and the long-term potentiation mechanism in CA1, perhaps as a result of altered intracellular signal transduction systems in neurons.

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Or, the KvB1 gene

quote:

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To further investigate the relationship between learning and memory, neuronal excitability, and synaptic plasticity, we have carried out experiments with aged mice that lack the auxiliary potassium channel subunit KvB1.1. In aged mice, the deletion of the auxiliary potassium channel subunit KvB1.1 resulted in increased neuronal excitability, as measured by a decrease in the post-burst afterhyperpolarization. In addition, long-term potentiation (LTP) was more readily induced in aged KvB1.1 knockout mice. Finally, the aged KvB1.1 mutants outperformed age-matched controls in the hidden-platform version of the Morris water maze.

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Of course, the 18 mutations you described in your post are also examples, unless you consider them to have been deleterious, which is inconsistent with evidence of positive selection at the so called HAR loci.MickEdited by mick, : No reason given.Edited by mick, : added bold to the quotes

This is certainly the standard approach of creationists, but it is not actually the first step in effecting a paradigm shift in science. One would really want to forge a superior theory that can explain everything explained by evolutionary theory, plus some other things that evolutionary theory cannot explain. If all you want to do is "deconstruct Darwinism" but have not a single theory with which to replace it, that is hardly a constructive enterprise.Why not give us the Intelligent Design explanation for the origin of characteristics unique to the human brain, and let us see how it stands up against the evolutionary explanation?This thread is about the ID response to the human/chimp genome comparison, but we have heard not a single non-Darwinian hypothesis explaining the observed genome data. All we get is the standard creationist bluster, which is to claim that evolutionary theory is collapsing (just that no scientists have noticed, yet). If you have your way, and "Darwinism" is one day tossed into the grime at the back of history's fume cupboard, how are we going to explain the similarites and dissimilarities of the human and chimp genomes?Mick

Hello again eggasai, Well, that remains to be seen . Really, I do appreciate your contributions and I do not wish to typecast you. I am debating with you on quite similar material on two separate threads, so I just want to make it clear at the outset that I do not want to give the impression that I am hounding you or anything like that. This is a bit of a red herring. First, natural selection is not the "default explanation for absolutely everything in evolution". In reality, neutral models of evolution are often considered to be the null hypothesis and the existence of natural selection must be inferred by departures from the predictions of that null model. Second, because the exclusion of God does not make the evidence "secondary" in any way; scientists also exclude fairies, unicorns and Satan from their causal models for the simple reason that their existence cannot be empirically falsified and therefore cannot offer much in terms of material causation. So please don't feel that (the Christian?) God is being excluded because evolutionary biologists have some sort of religious axe to grind; at least, to no more an extent than all scientists have a methodological prejudice against pixies, fairies, Valhalla and elephant-headed gods playing a role in causal explanation. I have serious reservations about your statement, mainly because you don't reallly define what you mean by "observed". Prehistoric events can be directly observed in the sense that they leave behind physical traces of their existence (fossils, geological formations, corpses, written documents, radiation, etc). But I assume you have a problem more generally with the concept of inference used by evolutionary biologists. It is my opinion that inference is the cornerstone of science. Astronomers infer the existence of stars which they cannot directly observe, based on electron degeneracy; oil engineers infer the existence of oil fields which they cannot observe based on geology; chemists infer the strength and existence of chemical bonds based on the temperature required to effect a change in state of a substance; etc. etc. Evolutionary biology is no different in inferring the existence of an evolutionary process from existing observable data. However that process can also be directly observed in the laboratory, as you may know.If you really want to get rid of inference in biology, I'm not sure what we would be left with other than a collection of statistical descriptions of the patterns evident in nature. There would certainly be no possible causal explanation of anything. But this really does appear to be what you are suggesting: First, it is a bit rich to claim that creationists or ID proponents are in some way hindered by the a priori assumptions of evolutionary biology. There is nobody stopping them from abandoning such assumptions, "simply looking at what happens in living systems" and reporting what they find. Indeed I have specifically invited you to do precisely this! hence my request for an ID explanation of the genome data. I am perfectly happy to concede arguendo that evolutionary biology is a load of bunkum that cannot explain the first thing about chimpanzee genomes; that God or the divinity or intelligent agent of your choice has been monitoring and modifying the universe since its creation; and that exclusively naturalistic forces cannot explain the patterns we see in nature.So, let us look together at the patterns you have described:1. human and chimp DNA is extremely similar
2. human DNA contains a large number of repeated units of great similarity to viral DNA
3. the number of nonsynonymous nucleotide differences beween chimp and human DNA is smaller than the number of synonymous differencesWhen I look at these facts without any inferential framework I have a great deal of difficulty working out what they signify. How many identical aligned nucleotides should we expect to find between human and chimp? Is 8% a high proportion or a low proportion of apparently viral DNA in the human genome? Why does it look like viral DNA?Since I have dropped what you define as the a priori assumptions of biology, could you explain to me what is supposed to have become clear?Mick

Hi eggassai,In post number 26 you said deconstructing darwinism is the necessary first step for its opponents because "natural selection is the default explanation for absolutly everything in evolution".I replied that "In reality, neutral models of evolution are often considered to be the null hypothesis and the existence of natural selection must be inferred by departures from the predictions of that null model"You replied as follows: Your quote supports MY position that natural selection is not the "default explanation" or null hypothesis for biologists. The example you give clearly shows biologists NOT inferring the importance of natural selection. You appear to be arguing against yourself.You are arguing against the evolutionary explanation of human/chimp genome similarities and dissimilarities. I have asked you repeatedly to provide an alternative explanation. Your response to my request is: My proposed mechanism would consist of mutation, selection and drift. The parameters involved in these processes are described in the nature paper you keep citing.Now perhaps it is your turn to describe an alternative mechanism? Last time I asked you, I got the following: That is not an alternative explanation, it is a critique of the existing one.Please permit me to repeat myself. I will save you the trouble of debunking evolutionary theory. I am perfectly happy to concede arguendo that evolutionary biology is a load of bunkum that cannot explain the first thing about chimpanzee genomes; that God or the divinity or intelligent agent of your choice has been monitoring and modifying the universe since its creation; or that no such intelligent agency was involved.You don't need to convince me that evolutionary theory can't explain the observed patterns. I am saving you the trouble! This is your chance to present an alternative hypothesis explaining the patterns of similarity and dissimilarity in the chimp and human genomes. I would be very interested to hear it.