evidence that intelligent design can't explain

Dear Monkenstick,
I already overthrew this fallacy, but for your updating I will show it once more. (As demonstarted in the thread: Pseudogenes & retrotransposons)"In the evolutionary community the shared retroviruses are commonly regarded as evidence of common descent. However, this may only be superficial.First there is the claim that they do not serve any purpose. That should be scientifically proven. Maybe their function cannot be deduced from knocking them out, but that does not say anything about their function, since you can knock out genes with an open reading frame without any effect on the organism (genetic redundancies). Secondly, I would like to see the complete DNA sequences within the species and between the species before jumping to conclusions.I checked one claim about the GLO pseudogene (the gene that catalyses the final step in vitamin c synthesis) that has been inactivated in the same spot in primates and is taken as proof for common ancestry. And, indeed a superficial look would immediately convince any evolutionist. However, if you have a careful look at the presented sequences you will discover that the replacement of nucleotides is not at random between the distinct species. Secondly, you will discover that it does not make a difference for the mutation rate of this gene whether it is functional or not, in contrast to what evolution theory would predict. Thirdly, it violates population genetics: why would the inactivated gene become fixed in the entire population, while the active gene conveys longivity. In addition, evolution never compensated for vitamin C uptake in the gut, and, finally, the gene is redundant anyway since the third step in vit c synthesis already yields vitamin C by spontenaous oxidation and is sufficient to avoid vit c deficiency. Also not unimportant, at least 2 primates are able to synthesise vitamin c in the liver, indicating the presence of an intact GLO gene (I once had a discussion about this gene with Dr D. Theobald (Talk Origin) so I know a bit about pseudogenes).
However, at this level it is mostly speculation since we do not know a lot about it, yet.In analogy to vestiges (appendix, tonsils) that shouldn't have a function according to evolution theory, it is far too early to say that this is proof for common descent. Show me the DNA sequences of these retroviruses in chimp and man, and I will respond in more detail.Retrotransposons may have a function in epigenic regulation of gene expression (actually there is some proof for that. See: Dr. E. Max's website Talk Origin. Another one regulates the aghouti colour of fur in mice). It is thought that they may also play a role in eye colour (human), and some diseases like schizophrenia, and B.-W.-syndrome.
Evolutionists are free to claim these genes as evidence for common descent (as they did -- and still do -- for genetic redundancies, but which has actually contributed to the fall of natural selection as I will substantiate with scientific evidence in my forthcoming posting on genetic redundancy).
I foresee that ultimately there will be an unexpected (regulatory or stabilizing) function for these "vestiges".Furthermore, read Spetner's book carefully on what he has to say on transposons. It makes sense. It will pay off to read opposite opinions. In summary, it is not an argument to take DNA sequences of which we do not know the function of as evidence for evolution. Our lack of knowledge described 98% of the DNA in the genome as "junk". This vision is increasingly proven to be wrong."Best wishes,
PeterAlso read Dr Max's "rebuttal" to Spetner's book on the true-origin website.

dear mark24,
The reference you have to study carefully is: Ohta et al Biochim Biophysica Acta 1472 (1999), 408-411. Study the presented DNA and protein sequences carefully with an unbiased mind. My biological intuitaion told me that something is wrong with the sequences. It took me months to figure out exactly what it was. If I were you I would calculate a bit on it.If you have a close look you will see that the rate of change between rat and human, chimp, orang and macaque is almost constant 26/164, 25/164, 26/164 and 29/164, respectively. If we compare human with chimp, orang and macaque one finds 4/163, 7/163 and 15/163, respectively. However, if we compare chimp and orang, and chimp and macaque we find 9/163 and 15/163. Thus, while we observe 4/163 between human and chimp, human and chimp are equally similar to macaque. Thus if we reason from the macaque's position human and chimp coincide. Still, we "know" there is time difference of 6 million years.If we assume 1% variation per million years (in primates this is reasonable), this implicates that the common ancestor for both human and chimp lived around 10 million years ago. Thus, this pseudogene example violates the descent of primates. (the authors choose their references so that it is in accord with the accepted vision, but there are references of neutral rates in primates that would support my vision). Even the authors admit that the orangutan does not fit in what they expected.If it is allowed to compare these primates and assuming paleontological time scales to be right, the neutral rate observed in primates is actually 15/163:25 = 3.6exp-3= 0.36% per million years. Similarly, the change since the divergence of rats and primates is 26/164:50 = 0.31% per million years. Thus, it doesn't matter whether the gene has been inactivated or not, it still changes with the same rate. And so we have another violation.Finally, it is no secret hat the GLO pseudogene violates Darwinian Evolution Theory (it is an example of non-darwinian evolution) and population genetics. I presume you know that.Of course I agree with you on the common single nucleotide deletion, but it may have been directed.Furthermore, you state:"Furthermore, & most importantly, in addition to the two primates, other orders & classes have fully functional vit c genes that haven’t been wrecked by your hot spot, why?"You are wrong. Throughout all orders and classed in the animal kingdom vit c synthesis has been inactivated randomly. For instance, the whole family of bats -- irrespective whether they are fruit eating or carnivorous -- do not synthesise vit c. It remains to be established which genes in the vit c biosynthesis have been inactivated, and where. Maybe there are several "hotspots".You also wonder:
"Functioning transposons are just as good an evidence of common descent as functional gene sequences. Why does them having function represent a falsification?"As mentioned before, you cannot take DNA sequences in the same spot of the chromosome that we do not know the function of as proof for common descent. Maybe it is not a falsification, but you are not allowed to do this. If you do that, than I will take alle homologue DNA sequences in human and chimp that are not in the same spot as proof against common descent. And, I think you will not like that since it is a tremendous amount.Finally, "WHY-questions" are irrelevant in science, it is metaphysics.
Best wishes,
Peter

dear mark,You say:
"I really don’t see the relevance of whether the wrecking site was on a hotspot or not, the point surely is that you couldn’t predict where the next mutation would occur, this is entirely a separate question as to the fixation of the gene. For your information, there was one family of the order Chiroptera (bats) that had at least one species that could produce trace amounts of vit c in the liver, the other 6 families tested were blank."This is not significant. Vit c synthesis requires the activity of four proteins. Thus, theoretically four gene defects can give rise to vitamin C deficiency. In human we see two genetic defects. A defective lactonase gene completely abolishes vitamin C synthesis. Defects in L-gulonolactone oxidase, which is the final step in vitamin C synthesis does not completely abolish vitamin C synthesis (your bat example shows trace amounts vit c), because the substrate, L-gulonolactone, spontaneously decomposes to 2-keto-gulono-gamma-lactone (=vitamin C) in the presence of oxygen. Remember that there was a considerable amount of sailors who survived the long 16th century overseas voyages. The survivors were still able to synthesise vitamin C, albeit in very low concentrations through the action of lactonase, and they did not have to take vit c. (In some human populations, for instance the desert nomads of the Sahara the non-synthesisers are completely removed from the gene pool.)Question remains how this (redundant) enzyme evolved, while it was not absolutely required for survival (lactonase is already sufficient to produce the amount of vit c to survive)?
The GLO enzyme ensures longevity. Why than was selected for non-producing primates (=non-darwinian evolution)? It is obvious that the longevity must have been a redundant trait. It is an evolutionary riddle how a defective gene improved reproductive success: it was spread throughout the complete population of primates.If the GLO enzyme was inactivated 25 million years ago there was ample opportunity to improve vit c uptake in the gut. Still, humans are very lousy uptakers. (Levels of vit C uptake reach levels that can also be generated by lactonase activity alone).Your questions:1/ How do you know the replacement between species is not random?Have a look at the predicted protein sequence in the article I refered to.2/ At what GLO sites are the hotspots? You need to know this in order to attribute the wrecking to the hot spot(s) at all.We do not know yet, since the mechanism is not known. There may be several hotspots. Have a close look at the 1g5 gene in Drosophila.3/ Which two primates specifically CAN synthesise vit c?
Two prosimians, don't know what species. Maybe you can look it up.best wishes
Peter

Dear john,
Indeed scurvy was a huge problem, but not everyone died during these voyages. It is reasonable to assume that the vit c synthesizer (via sponteneous oxydation) were the survivers. Thus, there was selection during these voyages for the intact galactonase enzyme. Similarly, desertnomads all have this intact gene. Do a search on internet and you will find the answer to your questions.
best wishes
Peter

Dear John, Don't give up so fast.
It took me along time to find all relevant information. But here I have a link for you:
http://yarchive.net/med/vitamin_c.html
Have a good one,
Peter

Dear Mark,In response to:
"Interesting. Nishikimi thinks the substitutions are random in exon x of this pseudogene."If you have a very careful look at the protein sequence you will discover that they do not change at random. The article of Ohta and Nishikimi is discussed according to the paradigm of common descent.
If you objectively study the presented sequences, i.e without this paradigm in mind, you will see that some changes are non-random. In the presented protein sequence this is most obvious. From orangutan to chimp 2 aa changed, and 2 aa changed afterwards (from chimp to human). I find it very surprising that the aa at position 11 (from the righthand side) was two times involved, since it is a non-functional protein. I wouldn't have expected that by chance alone. So I think there is a (non-random) mechanism involved.
Cleared things up?Best wishes,
Peter

Dear mark,
You write:
"Your going to have to do better than a couple of mutations on the same spot. I've seen sequences where most sites have a couple of mutations, & one or two have hundreds."Show me the references. (And you weren't even surprised?)And:
"They ARE hot spots. Such studies are concuded from thousands of mutations on particular genes."Than I expect thousands of references. More importantly, what do you think hotspots are?Best Wishes
Peter

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[This message has been edited by peter borger, 07-24-2002]

dear mark,You write:
"A hot spot is a site that exhibits a NON-RANDOM occurrence of mutation."EXACTLY!Peter

dear Mark,
You say:
"C'mon Peter B, I only mention what I do in the postscript of the last post, because, if you are claiming that we need to know function of alleged "junk" DNA in order to apply phylogenetic analysis (or anything else), then you can't make ANY judgements yourself about vit c pseudogenes & any inherent sequences therein."Ultimately, we are not able to make judgements. The only thing we can do is to have faith in a paradigm. Whether it should include design and/or a creator or not is up to you.best wishes
Peter

Dear Peter,You write:
"Random in the sense of ToE means we cannot predict when
the mutatation will occur i.e. it is not directed."If we do not know the mechanism how can you speak of "not directed". If the mutation is induced by the environment it is reasonable to expect a non-random mechanism. Since we do not know the mechanism the introduction of mutations seems to be at random. I think we might compare it to immunoglobulin-antigen affinity improvement. Here, it seems that a random mechanism introduces the mutations. At present we do not know all ins and outs about this process, but it might well be non-random. As soon as we elucidate the underlying mechanism(s) we may also discover that the introduction of mutations is non-random (or maybe semi-random). Maybe we are even able to predict the exact location of mutations.
(It should be noted that not all mutations are directed, but I already mentioned that in previous mails.)
Best wishes
Peter

Dear Peter,You state:
"Random in the sense of ToE means we don't know when it will
happen. It is not a direct response to the environment, but
a happy circumstance if it's a benefit."I say:
'When' and 'where' are completely different questions. I say that a mechanism introduces the mutations observed in the 1G5 gene (and maybe also in other genes). It maybe in response to the environment (this answers the when question).For instance.
Q: WHEN do antibody genes start to mutate to improve affinity?
A: When the immune cells (B cells) that produce the immunoglobulins encounter antigen that can be bound by the antibody.Elucidating the underlying mechanism will answer the WHERE question. But at present it is certain that it is protein mediated and therefor cannot be at random.Peter

dear Mark,You say:
"Good grief, this isn’t in dispute!!!"If mutations can be non-randomly introduced how can the NDT still be around? Once more, how do you conceive hot-spots in the DNA? Is a mechanism involved, or not? If not, how do you conceive hot-spots in the DNA? I am really interested in your opinion.And:
"1/ That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab."First of all, the GLO gene is an inactive gene since it has been interupted at several sites. The sequence shown in the paper is the sequence of exon X. It is of interest since it demonstrates a non-sense mutation (introduction of a stop codon). Since the protein is not expressed at all, all positions in the DNA are completely neutral. This means that natural selection does not act on the sequence since the protein is not expressed. So, mutations should be introduced completely at random according to NDT (and according to Kimura with a neutral rate). If not, than a hot-spot is present in the DNA. It tells me that a mechanism drives the mutations. Since we presently do not know the mechanism we cannot say where exactly the mutations will occur.
For the 1G5 gene there are much more data than the GLO gene and the hotspots are pretty clear. One may even be able to predict future mutations in the gene of Drosophila melanogaster. If you have a close look at the figure in Schmidt and Tautz article you will notice that some nucleotides change in different subpopluations at the same spot in the DNA, idependent from selection. Since we do not yet have such extended data for subpopulations of primates it is too early to say something about it. However, there are such data for human subpopulations, but these are not yet thoroughly scrutinised.
I am sure we will find the mechanism of non-random mutation.And you state:
"Common descent & genetic drift remains the best explanation for non-vit c synthesis in primates, particularly given that the two prosimian primates that can synthesise vit c, fit in nicely at the bottom of the primate phylogeny, where they would be expected if evolution & common descent were responsible. That is, that vit c gene wrecking occurred after the prosimian divergence, leaving them unnaffected. A remarkable coincidence, don’t you think?"You are free to believe that common descent and genetic drift are the best naturalistic explanations. However, if mutations are non-random these conclusion cannot be drawn. As observed in the 1G5 gene of D. simulans even indel-mutations may be non-random. As long as we do not know this, your conlusion is unwarranted. I can imagine that you -- as an evolutionist-- are eager to take the GLO gene as proof for common descent. However, then I could take all genes that violate the species tree as evidence against common descent. So, it doesn't proof anything. Common descent is merely a believe.And:
"2/ That you are able to attribute the existence of hot spots to design, when the cause of hot spots is UNKNOWN. God-Of-The-Gaps."I (and others) have already explained that if the information is already present in the genome it makes it hard not to believe in design. Maybe you know a naturalistic explanation. I am very curious to hear about it.3/ That non-random means directed, or pre-programmed in the sense of design, with regard to spontaneous mutations. If you think it does, rather than not-an-equal-chance-of-mutation-at-each-site, then you need to back this up. Remember, you have already told me you aren’t conflating the statistical & colloquial definitions of random/non-random."At present the only well presented gene in subspieces of an organism is the 1G5 gene of D. mel. I invite you to study the sequences of the 13 subspecies extensively and have a careful look at the site of the mutations, and the type of substitutions. (Please do, since I am becoming a bit tired of repeating myself.)And, what exactly did I tell you about conflating the statistical and colloquial definitions of random/non-random?Best wishes,
Peter

Dear WI,You say:
"Let me get some clarification on Peter Borger's frequent self-aggrandizing declarations in various threads about the demise of NDT. Does his whole argument boil down to
unequal frequency of mutations at all loci = non-random mutation = directed mutation by mechanism unknown = genomes designed to mutate in (enhancing) response to external evnironmental factors = evidence for intelligent design by designer unknown (don't say god) = demise of NDT ?"I consider this a pretty concise summary, with a conclusion I don't object to,
Peter

dear Taz,
I invite you to read all my mail to Mark24, since there I addressed all your comments.And you say:
"Did you get this from another reference. I do not remember it from Ohta's paper"No, Ohta did not show it but the data he showed are sufficient to get the mutations rates before and after inactivation of the gene. Sometimes it pays off to do a bit of research yourself with data that are present in literature anyway.best wishes
Peter