More non-random evolution

Hi Quetzal,
If you go to the "Endosymbiotic theory wrong" thread, Peter has fleshed out a bit more of his hypothesis, though the spurious defintion he uses of "non random" persists. Just to give you a heads up. The posting traffic here is increasing and it is getting harder (for me at least) to keep up with the various threads.Cheers,
M

So as to let Quetzal continue this without distraction from me, I want to address only one point here. Your theory of repair based "non-randomness" is falisfied for mtDNA which do not have an established DNA repair machanism.It also occurs to me that if you use your definition of non-randomness (though it has changed from time to time) , I should be able to pinpoint exactly the mutation in every somatic cell I have (germ cells as well of course) for any mutation just before it happens. Can you do this...where will the next mutation in my genome occur Peter if it is non-random? Easier question, where will the next mutation in my mtDNA HVI region occur?Cheers,
M

quote:

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Originally posted by peter borger:
Dear Mammuthus,

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You say:
So as to let Quetzal continue this without distraction from me, I want to address only one point here. Your theory of repair based "non-randomness" is falisfied for mtDNA which do not have an established DNA repair machanism.

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I say:
So, the mechanism is nucleus dependent and/or similar to 5-methylcytosine hostpots. Both would result in alignment of non-random mutations.

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You say:
It also occurs to me that if you use your definition of non-randomness (though it has changed from time to time) , I should be able to pinpoint exactly the mutation in every somatic cell I have (germ cells as well of course) for any mutation just before it happens. Can you do this...where will the next mutation in my genome occur Peter if it is non-random? Easier question, where will the next mutation in my mtDNA HVI region occur?

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I say:
Most likely it would involve position 223 or position 311.

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Best wishes,
Peter

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*********************Hi Peter,Quetzal's post above addresses questions that I would also like to see answered so I won't post more than to ask the following.Likely positions 223 or 311? If it is non random than why not with absolute certainty? There are individuals with mutations outside of these positions. How do you explain those?Your definition of non-random just became one of randomness cheers,
M

This is actually a reply to Peter Borger but I am using the reply to Quetzal as I wanted to expand on a few things he brought up. I also want to know Peter if you are thinking about responses to the points I have brought up or just ignoring me.Originally posted by Quetzal:

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You don't have to be a genomic researcher. It is obvious from the sequences of the 1G5 gene and the mtDNA in subpopulations.

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It is quite easy to make assertions. Anyone — expert or not — can do that. However, to counter the assertions it is often necessary to have in-depth expertise. This is one of those times. I simply don’t have the background necessary to argue this point. I’m sure someone else does.

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Q: You are aware, of course, that one of the most common point mutations is C-->T deamination? It's usually repaired fairly easily by glycosylase. There are at least 8 different kinds of glycosylase for example - each one repairing a particular kind of base damage. Basically, every single mutation requires a distinct, seperate mechanism for repair. Only when these already-present repair mechanisms fail or are overwhelmed is there mutation that carries over. IOW, repair means it puts the DNA strand back together just like it was. OF COURSE it introduces the same nucleotide during repair - or the same sequence of nucleotides. There's no other way it CAN repair. I think you're missunderstanding how DNA repair works.

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PB: In addition to this mechanism that always introduces C-->T tranversions, there is also the mechanism of C--> tranversions due to 5-methylcytosine conversions. After reading your reference, I realised there is another mecahnism involved in generation of oxidative stress induced mutations. As described by Hatahet et al (PNAS 1998, 95:8556) there is a consensus sequence that modulate the frequency of misincorporation 8-oxoguanine by DNA polymerase. This mechanism is also likely to contribute to the illusion of common descent. In particular in mtDNA sequences. Finally, it is becoming increasingly evident that junk DNA may be used to repair DNA (Nature Genetic JUNE 2002, if I recall properly) and may also lead to the introduction of the same nucleotide on th same spot.

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Actually, the mechanism repairs C-->T deamination errors. If you’ll check, I think you’ll find that 5-methylcytosine is implicated in G-->T mispairing. The glycosylases TDG or MBD4 are the specifics for repair of this particular error. You seem to be confusing repair mechanisms such as the glycosylases with the mutagens that cause the problem in the first place. On another note, here’s a good article on the repair of 8-oxo-G errors: Substrate specificity and Reaction Mechanisms of Murine 8-Oxoguanine-DNA glycosylase.Please provide the full reference for the article you cite. If you're going to use something as evidence, we need to be able to check it.
******************************************************M: I wanted to add that mitochondrial DNA has a primitive repair system at best (for which the evidence of any repair at all is limited). Similarly, there is no "junk DNA" in mitochondria thus it cannot be postulated as a repair mechanism for mtDNA. Thus, your premise is falsified on this count.Second, that transitions are more common than transversions is basic chemistry and hardly constitutes and novel discovery. However, you still cannot pinpoint where the next mutation will occur in a given portion of any DNA sequence thus, non-randomness is falsified.PB: No evidence? Whole families of new genes show up in the genomic record. If I'm correct, this is Tranquility Base's major point. The sudden appearance of such new gene families in organisms should be sufficient evidence.M: If you read the "kinds" thread where I debated TB on this topic for every example he provided I could find primitive versions of the gene families he claimed appeared spontaneously. He was fixated on hemoglobin and I found data demonstrating its presence in bacteria. This propostion of sudden appearance is not supported.PB continued:
If you really want me to completely falsify and overturn evolution theory, let me know, and I will present the example of an organism that are gentically identical without being a clone. So, this organism can be interpreted as being created yesterday, last year, last century, whenever. It hasn't been published in peer reviewed journals (for the obvious reason), but a book on the topic was published in 2000. It is the final blow to evolution theory, and strong support for the hypothesis of 'creation of a multipurpose genome'M: Two fallacies in this statement, genetically identical organisms are by definition clones. If you are referring to twinning this is also natural cloning and twins are actually not 100% identical.
Second fallacy, even if evolutionary theory were to fall, it would neither provide evidence for creationism or for your multipurpose genome idea.Q:
You are merely repeating your assertion. I wouldn’t bank too much on TB’s sudden appearance, as he has yet to show any evidence for this. I’d say the obvious reason your amazing discovery hasn’t been published in the literature is because it doesn’t exist. What book? And why a book and not a journal? The great Evilutionist Conspiracy again?PB:
You have failed to answer the question, so I’ll repeat it:

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There is absolutely no evidence for this assertion. Please show one single study, with references, on any population of any organism, where the introduction of a new pathogen, mutagen, or environmental factor produced fortuitous variation that allowed the population to adapt to the new conditions.

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M: Look up Richard Lenski. He has published extensively on this subject. I listed two of his papers in the Punctuated Equilibrium thread yesterday. In addition there were the E. coli experiemnts demonstrating that those with retrotransposons were better able to adapt to selection than those without. If YOU would look this stuff up for yourself rather than asserting it does not exist you might gain some credibility.PB:
I supported my assertions several times. However, evolutionism also seems to have an 'explanation'. So, it will be my explanation against evolutionism's explanation.M: It will be your falsified assertions against a theory with supporting evidence.Q:
You have consistently failed to support your assertion. You’ve merely repeated it ad nauseum and then dragged in pointless details that have no bearing on your contention. If there’s evidence, present it. Reveal your magical organism. I promise I won’t steal your Nobel Prize.M: Ig nobel prize perhaps You know, the one for non-reproducible science and unsupportable theories like the origin of belly button lint.PB:
In the multipurpose genome 'all' genes that contribute to variation are already present. Variation is induces by genetic elements that affect gene regulation --and therefore gene expression--, and probably shuffle from one place in the genome to another.M: However, you have ignored my questions with regards to extinction and heredity. Also why there should be any variation at all and why any two organisms should be more similar than any others if all mutation is non-random.PB:
All observations of population genetics can be explained since it only involves (regulation of) frequencies of alleles. If populations get isolated they may 'speciate' due to loss and/or shuffling of genes.M: Do you believe that you are related to your parents Peter or do you believe that storks brought you? If you pick up any book on the genetics of disease you can observe specific alleles segregating in families (not just the disease allele)...this is transmission genetics and is what you are denying occurs. You are stating that at each birth, the genome is reformed poof bang de novo and "created" to appear like the genomes of the parents in some sort of "designed" attempt to mimic hereditary similarity. This is completely unsupported. Genetics in general, Lenski's studies of 10,000 generations of bacterial evolution, and 100 years of hereditary study falsify your contentions as well.PB:
Furthermore, entropy acting on the genome can account for all degenerative observations in the genome (for instance, the inactivation of genes that are more or less redundant).M: This sounds like an L.Ron Hubbard statement. Inactivation of genes can occur by methylation, histone acetylation, insertional mutagenesis, point mutation, deletion etc. Where is entropy involved?PB:
Finally, mechanisms that introduce mutations non-randomly can explain the illusion of common descent.M: This has been falsified by myself, others on this board, and thousands of other researchers who actually know what random means.Q:
Once again, you’re simply repeating your assertion concerning multipurpose genomes without evidence. Your first part is simply a restatement (simplistically, and leaving out a number of different mechanisms btw) of the random mutation part of RM&NS. The last bit about entropy and degenerative observations doesn’t make any sense. Finally, you have NOT shown that non-random mutations exist — only that you have absolutely no idea what random means in statistics.
Q: Nope, it doesn't, unless you plan on completely redefining statistical probability along with your redefinition of random.PB: Maybe we have to do that.M: If you have to mis-define random for your hypothesis to be valid then it was falsified from the beginning without us wasting effort to show the other reasons why it is falsified.Q: Wow — you’re really reaching now, Peter. Gonna re-invent mathematics as well as evolution? Okay — please show the probability equations you propose that overturn current understanding of statistics.M: I would like to see the equations to...and I am still waiting for him to tell me exactly where in HV1 will my next mutation occur? I am making it easy Peter...make it a somatic cell mutation.cheers,
M

Yet another problem for your sudden appearance of gene duplications..Hidden gene duplications
10 October 2002 - Proc. Natl. Acad. Sci. U.S.A.
Arabidopsis thaliana offers botanists a model plant genome. As in other advanced forms of life, the genome of Arabidopsis has experienced gene duplications on a large scale. These may even have included the duplication of all of the plant’s genes. Duplicated genes, however, are often lost, making it difficult to document gene duplication. A new report demonstrates that it is possible to recognize blocks of duplicated genes, despite gene loss, if indirect comparisons are made with other gene segments. In this way, researchers are able to get a good idea of how many times genes have been duplicated during the course of the plant's evolution.Reference: Simillion, C., Vandepoele, K., Van Montagu, M.C.E. et al. 2002. The hidden duplication past of Arabidopsis thaliana. Proc. Natl. Acad. Sci. U.S.A. (online), October 8.

sorry that should have read sudden appearance of novel gene families

In fact mtDNA ONLY appears to have BER for DNA repair and is exposed to much higher oxidative stress. Thus nuclear DNA repair and mtDNA are qualitatively and quantitatively different....where is the next mutation going to occur in my HV1 region? If you cannot tell me then it is a random mutation.1: Prog Nucleic Acid Res Mol Biol 2001;68:257-71 Related Articles, LinksEnzymology of mitochondrial base excision repair.Bogenhagen DF, Pinz KG, Perez-Jannotti RM.Department of Pharmacological Sciences, SUNY at Stony Brook, Stony Brook, New York 11794, USA.A number of laboratories have shown that those types of DNA damage that are generally reparable by base excision repair are efficiently repaired in mtDNA. In contrast, most types of damage that require other sorts of repair machinery are not effectively repaired in mtDNA. We have shown that a set of highly purified mitochondrial proteins, including AP endonuclease (APE), DNA polymerase gamma, and mtDNA ligase, is capable of efficiently repairing abasic (AP) sites in mtDNA. These three enzymes appear to conduct all four steps in a conventional BER mechanism: incision, removal of the 5'-deoxyribosephosphate by dRP lyase, polymerization, and ligation. Both DNA polymerase gamma and mtDNA ligase possess some dRP lyase activity. DNA polymerase gamma is a member of the family A of DNA polymerases, with clear homology to DNA pol I of E. coli, while mtDNA ligase is an alternatively expressed form of DNA ligase III. The dRP lyase activities discovered in these mitochondrial enzymes are not unique, but are found in all representatives tested of the family-A DNA polymerases and of the ATP-dependent DNA ligases. These dRP lyase activities have low turnover rates that may have important implications for the overall process of BER. All proteins involved in maintenance of mtDNA are encoded in the nuclear genome and must be directed to mitochondria in order to act on mtDNA. Thus, it is evident that the scope of DNA repair activities undertaken within mitochondria is determined by the set of nucleus-encoded DNA repair enzymes that are capable of being imported into the organelle. A review of DNA repair proteins that may be imported into mitochondria in various organisms will be presented.

OOps,
I miscredited the quote of Quetzal's to Peter as I read the quote to mean that random mutation cannot produce beneficial mutations that by selection can become frequent in a population which would be consistent with other statements of Borger's.I see that the request was actually for an example of spontaneous genome adaptation that Peter is stating is obvious. In any case, the Lenski publications further falsify Peter's claims.My apologise to both Peter and Quetzal for mis-crediting the quote....doh!Cheers,
MPB:
You have failed to answer the question, so I’ll repeat it:quote:
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There is absolutely no evidence for this assertion. Please show one single
study, with references, on any population of any organism, where the
introduction of a new pathogen, mutagen, or environmental factor produced
fortuitous variation that allowed the population to adapt to the new
conditions.
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----M: Look up Richard Lenski. He has published extensively on this subject. I
listed two of his papers in the Punctuated Equilibrium thread yesterday. In
addition there were the E. coli experiemnts demonstrating that those with
retrotransposons were better able to adapt to selection than those without.
If YOU would look this stuff up for yourself rather than asserting it does
not exist you might gain some credibility.

Hi PeterDear mammuthus,I think that you are a bit confused now. It was Quetzal's question. But anyway, Quetzal will be happy (?) I guess.M:If I am not mistaken I pointed out that I mis-credited Quetzals question to you and posted my error and an apology to both you and Quetzal.PB:
However, I am aware of these studies and the authors conclude that "three lines of evidence suggest that they [genomic changes] are mostly due to IS-transposition and other types of chromosomal rearrangements. First, [..], point mutations are NOT [caps are mine, PB] abundant in these evolving populations. Second, the extent of genomic change [..] was similar among lines that had become genetic mutators and those that had wild-type point-mutation rates. [..] Finally, we observed significant changes in the copynumber of certain IS-elements [..], most easily explained by transposition and deletion events that produce gains and losses of copies, respectively" (Papdopoulos et al, PNAS 1999, 96:3807)MY RESPONSE:
Thus, although populations change over time, this is not due to the change of nucleotides and therefore not due to changing DNA sequences. The only changes are the ORDER of the sequences, the order of transposable elements and therefore --in my opinion-- gene expression is altered. That is all what is required for distinct phenotypes. No information added or gained. All information was already present. It has been shuffled due to exision and reintegration of DNA through specific proteins (endonucleases, integrases, ligases etcetera). The only thing that was added to the genome in certain cases were additional copies of transposable elements. All this after 10.000 generations! This is NO evolution, it is VARIATION INDUCTION generated by a genetic mechanism already present in the original cells. Similar observations have been done in Enterococcus (Nature 2002, 13 june), that is able to actively shuffle genes on a DNA island in response to antibiotics. Apparently, bacteria have a very plastic genome.
It perfectly fits in the multipurpose genome hypothesis.M: Actually Peter, it does not. When a retrotranposon transposes it leaves the original copy behind and inserts new ones in other parts of the genome. Thus, it is novel variation. In addition, novel infections lead to new classes of retrotransposons that can then infect, integrate, and diverge i.e. HERV-W family present in Old World monkey but absent from New World Monkeys and strepsirhines.You are also presenting a logical fallacy in saying that the change does not count because the source of the mutation i.e. transposon was already present. That is like saying that all mutations are not novel because there is DNA in the cell or a C-T is not novel because there are other C's and T's. New content comes in via horizontal transfer, infection, etc. and then is mutated or shuffled. This is the mutation resources that drive evolution.I will ask again if you are going to respond to my other points I brought up? I would like to believe that you are contemplating responses or just missed them. If so I look forward to your response and continued debate.best wishes,
M

PB:
That is correct. C-->T tranversion will be repaired. However, it is important to realize that cytosince methylation can affect mutations through other mechanisms. These occur because 5-methyl cytosine is itself mutagenic. It can undergo spontaneous hydrolytic deamination to cause C-->T tranversions. This enhanced mutagenesis is seen in the germ line of all organisms that methylate their DNA. Furthermore, approximately 50% of inactivating pointmutations in the coding region of p53 in somatic cells occur at methylated cytosines (Science, 249:1288-90). That is half of the mutations! This mechanism will assuredly contribute to the illusion of common descent.M: However, which C-T occurs is still a random process. And when one compares the tranversion rate it is also not insignificantly small. None of this can logically "assuredly contribute to the illusion of common descent."Again, if you find that your mtDNA sequence is identical to your mothers is this assuredly an illusion of parentage? This is of necessity if your hypothesis is correct....and think of the benefits..no more having to remember to send mothers day (or fathers day) cards .)

quote:

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Originally posted by peter borger:
dear mammuthus,

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You say:

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I will ask again if you are going to respond to my other points I brought up? I would like to believe that you are contemplating responses or just missed them. If so I look forward to your response and continued debate.

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I say:

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I forgot about them but I will certainly respond to them next week.

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best wishes,
Peter

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***********************Hi Peter,
Looking forward to it. I basically put down a bunch of things that came to mind a few posts ago regarding your hypothesis and would like to debate them with you.cheers,
M

Hi Peter,
Post 42 to 45 in this thread for example went unanswered.
Unfortunately, others are buried in other threads but at least I could easily find the ones in this thread. I think the rest are in the "Endosymbiotic thoery is wrong thread"cheers,
M

found some more...posts 30, 36, 37 (Quetzals post) and 40 in the Endosymbiotic theory is wrong thread...