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Author Topic:   molecular genetic evidence for a multipurpose genome
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 1 of 317 (20534)
10-23-2002 1:57 AM


Dear All,
As demonstrated on this site evolutionism can readily be falsified on the level of the genome and thus cannot be the right hypothesis to explain life on earth in all its variation. Why? Evolutionism supposed to have its foundations in molecular biology and genetics, and when the theory can be falsified at this level it lacks a proper foundation and thus cannot be a good theory. Therefore, I introduced the concept of the multipurpose genome.
The concept of a multi purpose genome is not entirely new since a similar concept has been introduced by P. Scheele in his book ‘Degeneration’ (http://www.evolution-is-degeneration.com) and by L. Spetner in his book ‘Not by Chance’.
In my opinion their hypotheses cannot explain all biological observations --like sequence similarities/shared mutations within related species-- and so it cannot be complete.
Therefore I also introduced and provided scientific evidence for non-random mutations. The non-random mutations should be conceived as non-random with respect to nucleotide and position. At present they should not be conceived as deliberately introduced as a response to environmental change, since that cannot be scientifically proven. In genetics non-random mutations are generally referred to as hot-spots. This type of mutations may have important implications for common descent (see my mailing # 184 in ‘molecular genetic evidence against random mutation’ and is still open for discussion). In conjunction with non-random mutation the idea of a multipurpose genome are able to explain all biological phenomena, including genetic redundancies and phylogenetics.
The concept 'multipurpose genome' holds that:
1) DNA sequences —although plastic-- are stable throughout time,
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,
3) mechanism for adaptive phenotypes and variation are preexisting and due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes, and through RNA editing,
4) the function of natural selection is to remove degenerate organisms, and
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).
Predictions:
1) predicts that within species we do not see abundant variation with respect to genes, and usually such genetic alterations are neutral or degenerate (although distinct alleles can be expected through the principle of degeneration, which is in effect the action of entropy).
It also predicts that all organism --even the simplest-- have an elaborate and accurate mechanism to counteract mutations.
2) predicts that a considerable part of the genes of any organism can be knocked out without being lethal.
3) predicts that adaptive phenotypes of organism do never demonstrate new genes.
4) predicts that organism lacking vital DNA elements are selected against.
5) predicts that there should be organisms that have not undergone genetic changes (yet).
Falsification:
The concept will be falsified by the observation of the evolution of new genes unrelated to preexisting genes.
Predictions 1-4 can easily be verified. In fact it is what we see in contemporary biology all the time, but is always explained in an evolutionary fashion.
Prediction 5 could be hard to proof. However, I recently encountered a species that is in accord with this criterion, so I am able to proof all these points. The organism is the Wollemia nobilis, a huge pine of the Araucaria family recently discovered in the Wollemi National Park 100 kilometer north of Sydney. Below follows the amazing story on this organism. The passages are extracted from the book by James Woodford (The Wollemi pine. 2000. The Text publishing Company, Melbourne, Victoria, Australia. ISBN: 1-876485-48-5)
The Wollemi pine (book summary)
In 1994, the bushwalker David Noble and a couple of friends stumbled upon a cluster of majestic trees with an unfamiliar, bubbly bark, while exploring a remote canyon covered with dense rainforest. Maybe I was the first one to see them, he remembered. I picked up the leaf litter and said, ‘that looks a bit different. I went over and had a look at the tree it came from’. [] He broke of a peace of juvenile foliage as big as his hand and stuffed it into his bumbag. (p14).
The next day he took the cutting to his mentor at work, Wyn Jones, a naturalist with 25 years of experience in the field of determining Australian plants. Jones recalls: So the thing landed on my desk. I didn’t know what it was. [] Certainly it was in the group of lower plants. (p17). Jones began planning to make a trip to the canyon where Noble discovered the trees. They arrived in the canyon on October 1994, about an hour before dusk, which in the bowels of the Wollemi is getting pretty close to dark. [] ‘I saw it straight away’, Jones said. ‘It was quite different from all the other rainforest trees around it; its shape and the type of the foliage and the patterning of the branches. I took a photograph straight away of that particular tree’. (p19).
Jones noted that the massive organisms were multi-stemmed. He also observed that seedlings were scattered through the forest, which meant that the trees were reproducing. Only months later, after new expeditions to collect female cones from the tree tops for identification purposes, it became evident that David Nobles had discovered a new species, in fact a complete new genus of the conifer family of Araucariaceae. It was named the Wollemia nobilis, partly because of the tree’s noble stature and partly after its discoverer.
The genus of the Wollemi pine was well known from the fossil record, but referred to as Araucarioides, and considered to have become extinct thirty million years ago. Palaeobotanist professor Bob Hill puts it like this: If there are any fossil leaves buried in Australia that belong to the genus of Wollemia than the Araucarioides may be it. It’s either Wollemia or a fourth extinct genus — it’s not Araucaria or Agathis. If someone looked at Araucarioides and decided that is was a species of Wollemia then, if we were applying the naming rules, we would have to change the name of the Wollemi pine to Araucarioides nobilis. (p102).
Despite the abundance of fossilised Araucarioides, the fossil record does not contain an exact match of Wollemia nobilis. The closest relative yet found is between Wollemi pollen and fossilised pollen known as Dilwynites. [Dilwynites] had been considered as part of an ancient conifer family of Araucariaceae, but no one could agree on which genus. The pollen is abundant in the fossil record of Australia, New Zealand and Antarctica from about 94 million years ago until the middle of the tertiary period. Its range and diversity plummets after Australia’s split from Gondwanaland and its drift north 30 million years ago. The last known occurrence of the pollen in the records comes from oil drilling in the waters between northern Tasmania and the Australian mainland, dated at two million years ago. From then on the fossil record is silent (New Scientist December 1997). Until David Noble discovered a stand in the Wollemi park in 1994.
The Wollemi pine’s genus can be traced back till the Cretaceous, approximately 100 million years ago, when dinosaurs were dominating the earth. Or, as the science writer of the Sydney Morning Herald, James Woodford, and visitor of the secret Wollemi canyon, explained in his book ‘The Wollemi Pine’: The clearest evidence that I could see that this was a tree with a Cretaceous heritage was its conical crown — that crown was its most striking characteristic and my strongest first impression. Wollemia had evolved when continental Australia was in low light conditions at Antarctic latitudes and the trees in those times had vertical canopies that ran parallel to its trunk which maximises the amount of low-light available. Trees that have evolved more recently [i.e. at higher geographical latitudes] have canopies that are parallel to the ground, designed to catch sunlight higher in the sky. (p177). In other words, during the last one hundred million years or so, continental Australia had drifted approximately 30 degrees to the north, but the tree never adapted to this shift in geographical altitude. It still clings to its original appearance, designed for lower latitudes! This would only be possible if the Wollemi’s DNA is remarkably stable! Fortunately, the Wollemi pine has been discovered in the era of molecular biology and, as will be become evident in the next paragraph, it is a very remarkable organism.
Since the pine’s discovery, the park has been scoured for more stands of the trees. Only one additional stand of trees was found in the same canyon, an even more secluded spot approximately one kilometre upstream of the first stand. Why the pine has survived the ages in apparently one of a number of similar gorges in the Wollemi National Park is unknown. According to plant pathologist Brett Summerell of the Royal Botanic Gardens in Sydney: It’s just there, and we have no real understanding of why. It’s a very deep gorge, but there are others next door that are just as deep and just as inaccessible; there are similar soils, similar light regimes and similar creeks running in the same direction. [] It’s very puzzling (New Scientist 1997).
Whatever the history of Wollemi pine, there is no doubt that the remaining trees have been isolated for ages. To find out exactly how long, ecological geneticist Robert Peakall and his colleagues at Canberra’s Australian National University studied the genetic diversity of the trees. Because of the isolation of the trees, inbreeding may theoretically reduce genetic diversity over time. Establishing the amount of genetic variation between members of a particular group allows scientists to estimate the how long a species has been reproducing within that narrow population.
Paekall’s team started analysing the genetic variability of the trees. In the outline of the project Peakall wrote: This ancient lineage has presumably survived as an extremely small and isolated population(s) for many generations. Under these conditions, theoretical models predict a significant loss of genetic diversity over time as a result of genetic drift and inbreeding. Genetic drift is a technical term which means that if a population stays small enough it will loose variability until individuals almost become the same. This species may thus provide a rare opportunity to test the theory of natural populations. Furthermore, it is widely assumed that genetic diversity is essential for evolutionary success, hence the goal of conservation to maximise the preservation of genetic variability. (p155-156).
For a proper understanding for what is going to come next it should be realised that all but identical twins and clones have differences in their DNA - due to recombination and neutral mutations - that are immediately detected when subject to sensitive molecular analysis. The offspring of sexual reproduction between a pair of clones or identical twins, however, will be genetically different from the two identical parents (p158).
Paekall’s team first results demonstrated that Wollemia nobilis is genetically distinct from the other genera in the family, Araucaria and Agathis. Surprisingly, when two Wollemi pines from the first stand were compared the DNA of both trees was indistinguishable. Or as Peakall says: When the DNA graphs from the two different trees are overlaid they are absolutely identical. [] It indicates that the tree is either highly inbred or else an impossibly perfect clone. We may still find some variation but we have not been able to yet. (p159). Then, fifty seedling obtained from 5 different mothers were analysed. With the same result: None of the trees in the first discovered site showed any variation! This was an extraordinary finding since the team had analysed a region of the tree’s genome that in other plant species demonstrate the most variation (lookup which region). Complete lack of genetic variability has never been witnessed before and it is unknown in the scientific literature (p161). This may be so for plants, but as demonstrated previously absence of genetic variability has also demonstrated for certain regions of the human sex chromosomes.
For Peakall’s team the problem further deepened as soon as they analysed the same DNA region from the trees of the second stand. It was expected to find variation between the two sites. Incomprehensibly, no genetic variability could be demonstrated between any trees of both sites. Mature trees, juveniles or seedlings alike, the DNA of all trees was completely identical.
According to James Woodford: If no variability can be found in a Wollemi pine then only two explanations can be put forward — evolution in the trees has ceased or it has slowed to the point where it is no longer detectable.
But, that is an evolutionary paradox! Molecular evolution demands genetic variation on neutral positions. At least between trees of the two separated sites. Let’s have a look how this story that apparently confounds the theory of evolution unfolds.
It is imaginable that the two sites are genetically identical because the Wollemi pine is a giant clone. Or as Peakall assures the readers of New Scientist: There is no doubt with the Wollemi pine, there’s local cloning caused by root coppicing. The question is whether it goes beyond that: is there an underground root system, and were they once all the same organism? At the time this was published, in 1997, Peakall still must have been under the impression that both sites consisted only of teenage or adult trees: There was no evidence given to him that any seedlings were reaching a reproductive age. According to theory, if this were happening he ought not to have got the results that he did: when two genetically identical clones reproduce with each other their offspring should have DNA different from its clonal parents. Even if two identical seedlings had reproduced then Peakall would expect to find variability in the population. The only other possibility was that Wollemia was growing by apomixis — this means that the female cone is able to produce seeds without pollen. But this has never before been observed in any conifer in the world (p163-164).
Peakall’s results were so awkward [i.e. violating molecular evolution] that he asked permission to visit the Wollemi canyon in order to determine whether he was something missing or not understanding about the trees. As he arrived on the site he was expecting to find a organism struggling to survive. When he went into the site he thought this is not like other rare species which are on the brink of extinction. I think the Wollemi pine is functioning normally. [] There is no obvious evidence to suggest that the tree has a serious problem, and if it’s been in the canyon for a long time, the opposite is the case (p165). He also convinced himself that young new trees were being recruited to the adult population and that these should therefore produce genetically distinct offspring. But, as his team had previously demonstrated they were not. In every other respect these seem like normal rainforest trees (p165).
The other shock of the visit of the Wollemi canyon came when Peakall flew two kilometres upstream to the second stand of the Wollemi pine. In his own words: While the distance between the sites is not that great ’as the crow flies’, it now seems to me that genetic exchange among the populations via pollen flow is very unlikely given the convoluted pathway required and the density of the intervening vegetation. For similar reasons, while it can never be ruled out, the likelihood that site one has been derived from site two also seems unlikely (p166). Thus, the pines were not likely to have become genetically identical in the canyon, but were already identical long before they became isolated!
James Woodford explains it as follows. They must have been extraordinary similar before climate change forced them in [the canyon] and this low variability, over thousands of years, has been further exaggerated by cloning in one big stand of pines that had somehow been split in two. However, this ad hoc explanation is exactly the opposite of what would be expected from molecular biological rules, and violates molecular evolutionary rules. According to the principles of wobble and neutral evolution it is inevitable for the Wollemi pine to accumulate mutations over time at neutral positions in the DNA. Ultimately, Peakall and Woodford agree that evolutionary theory did not sit comfortable (p170). Evolution is founded on selection of the best adapted organisms and this demands genetic variability. But, they reason that over a long time [] these plants have developed an all purpose genotype. Despite that this may be so, it still does not explain the complete absence of mutations in the plants DNA, and therefore they decide that Wollemi is probably an exception that disproves a rule (p170).
Previous examples already demonstrated that invariability of DNA sequences is not exceptional, but rather the rule on this planet. In my opinion it is more likely that the Wollemi pine is the extreme example of a multipurpose genome, and all the multipurpose genome requires is DNA shuffling.
Contemplating the extraordinary findings on the tree, I realised that if someone claimed the Wollemi pine had been created only last century neither geneticists nor palaeontologists or dendrologists would be able to falsify it!
Best wishes,
Peter
[This message has been edited by peter borger, 10-23-2002]
[This message has been edited by peter borger, 12-17-2002]
[This message has been edited by peter borger, 01-15-2003]

Replies to this message:
 Message 5 by Quetzal, posted 10-23-2002 4:09 AM peter borger has replied
 Message 6 by Mammuthus, posted 10-23-2002 5:08 AM peter borger has replied
 Message 7 by Syamsu, posted 10-23-2002 5:13 AM peter borger has not replied
 Message 19 by Mammuthus, posted 10-24-2002 8:18 AM peter borger has replied
 Message 21 by Mammuthus, posted 10-24-2002 12:13 PM peter borger has not replied
 Message 22 by Mammuthus, posted 10-24-2002 12:14 PM peter borger has not replied
 Message 289 by Fred Williams, posted 11-21-2002 1:34 PM peter borger has replied
 Message 316 by judge, posted 12-20-2002 9:53 PM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 3 of 317 (20538)
10-23-2002 3:21 AM
Reply to: Message 2 by monkenstick
10-23-2002 2:36 AM


Dear Monkenstick,
You say:
quote:
--------------------------------------------------------------------------------
Predictions:
2) predicts that a considerable part of the genes of any organism can be knocked out without being lethal.
--------------------------------------------------------------------------------
there are a whole bunch of genes classed as embryonic lethal borger - you might want to check it out
I say:
These mutations will be selected against (point 4).
Best wishes,
Peter

This message is a reply to:
 Message 2 by monkenstick, posted 10-23-2002 2:36 AM monkenstick has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 10 of 317 (20623)
10-23-2002 8:24 PM
Reply to: Message 4 by monkenstick
10-23-2002 4:02 AM


Dear Monkenstick,
The fact that all organism have numerous genes that can be knocked out and do NOT have an association with gene duplication and do NOT mutate with an increased rate compared to essential genes falsifies evolutionism.
Rebuttals are always annoying, but that's how it works: every rebut has its rebut.
Best wishes,
Peter
[This message has been edited by peter borger, 10-23-2002]

This message is a reply to:
 Message 4 by monkenstick, posted 10-23-2002 4:02 AM monkenstick has not replied

Replies to this message:
 Message 13 by Itzpapalotl, posted 10-23-2002 9:35 PM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 11 of 317 (20625)
10-23-2002 8:31 PM
Reply to: Message 9 by Andya Primanda
10-23-2002 12:23 PM


Dear Andya,
You say:
'Just concentrate on your predictions. Even if there are many potentially lethal genes if knocked out, your prediction can hold good. Maybe we can prove this--lets say, get 100 zygotic mice and knock some 10% of their genome out and if you're right, then many will survive the experiment. To the lab! "
I say:
These experiments have been carried out in E coli. Scientists were able to reduce the E coli genes by appoximately 9.3% without any effect on the organism.
REFERENCE:
1: Genome Res 2002 Apr;12(4):640-7 Related Articles, Links
Engineering a reduced Escherichia coli genome.
Kolisnychenko V, Plunkett G 3rd, Herring CD, Feher T, Posfai J, Blattner FR, Posfai G.
Institute of Biochemistry, Biological Research Center, H-6701 Szeged, Hungary.
Our goal is to construct an improved Escherichia coli to serve both as a better model organism and as a more useful technological tool for genome science. We developed techniques for precise genomic surgery and applied them to deleting the largest K-islands of E. coli, identified by comparative genomics as recent horizontal acquisitions to the genome. They are loaded with cryptic prophages, transposons, damaged genes, and genes of unknown function. Our method leaves no scars or markers behind and can be applied sequentially. Twelve K-islands were successfully deleted, resulting in an 8.1% reduced genome size, a 9.3% reduction of gene count, and elimination of 24 of the 44 transposable elements of E. coli. These are particularly detrimental because they can mutagenize the genome or transpose into clones being propagated for sequencing, as happened in 18 places of the draft human genome sequence. We found no change in the growth rate on minimal medium, confirming the nonessential nature of these islands. This demonstration of feasibility opens the way for constructing a maximally reduced strain, which will provide a clean background for functional genomics studies, a more efficient background for use in biotechnology applications, and a unique tool for studies of genome stability and evolution.
PMID: 11932248 [PubMed - indexed for MEDLINE]

This message is a reply to:
 Message 9 by Andya Primanda, posted 10-23-2002 12:23 PM Andya Primanda has replied

Replies to this message:
 Message 27 by Andya Primanda, posted 10-25-2002 5:49 AM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 12 of 317 (20636)
10-23-2002 9:26 PM
Reply to: Message 5 by Quetzal
10-23-2002 4:09 AM


Dear Quetzal,
YOU WRITE:
This is the magical, mystical organism you've been tantalizing us with for the last several weeks? Wollemi nobilis??!!! You have got to be kidding me!
I SAY:
NO, I am not kidding you.
YOU SAY:
Look at the reality:
1. The species is clonal. (I thought you said your magic organism wasn't a clone?) The miniscule population (39 individuals) represents the descendents of a single tree - the ultimate in population bottlenecks, hence refuting your #5 - the very point you thought it proved.
MY RESPONSE:
If you know so much about this tree why don't you write a letter to Dr Peakall (University of Canberra), and explain to him how it all works. I think he will be pretty pleased, so he can publish his work --at last-- in a peer reviewed scientific journal.
Furthermore, the species is NOT clonal, and does not reproduce by coppicing. I recommend to order the book, so you can read it yourself. It is a highly interesting book, albeit a bit biased by evolutionism, but you will not mind that, I presume.
Actually there are two populations of the tree, both were analysed and demonstrated exactly the same DNA (as mentioned in letter #1). Surviving populations with invariable DNA points in the direction of a stable multipurpose genome, not in the direction of evolution.
2. The species propagates by coppicing - roots grow out from the main tree, then send up shoots. IOW, it isn't a sexually reproducing organism in the wild. Interestingly enough, it was discovered during planning for conservation of this unique species that it DOES produce viable seeds like other conifers. Why it clones itself in the wild is unknown at this time.
MY RESPONSE:
If you have your information from New Scientist december 1997 than I have to dissapoint you. Coppicing was the initial thought of Peakall but according to Woodford's book (2000) it does not coppice, but sexually reproduces (see mailing #1).
3. The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.
MY RESPONSE:
That is true. Araucariacaea demonstrate very low variability and that is in accord with the hypothesis of a multiporpose genome. Low variablity due to extremely stable DNA guarded by hundreds of DNA repair enzymes. Observed variation is due to regulatory, rather than mutational phenomena. All in accord with the multipurpose genome.
This is bizarre, Peter - your own lengthy book quote completely refutes your hypothesis because the bloody plant is a clone of itself that's been isolated from all other populations for thousands of years! All you seem to be doing is rehashing yet another creationist coelocanth-is-a-living-fossil "argument from journalistic sensationlism".
MY RESPONSE:
For the sake of evolutionism I hope you are right, but you are not. The plant is not cloning itself (as mentioned before).
What do you mean by 'argument of journalistic sensationalism'? As far as I know nothing has been published on this tree for sensationalism. Please be specific in your statements.
O yes, I am also very interested in DNA studies on Coelecant, Horseshoe crab (they comprise two populations, an Atlantic and an East Asian: seperated for eons). But they haven't been carried out yet. Let's wait and see.
Best wishes,
Peter

This message is a reply to:
 Message 5 by Quetzal, posted 10-23-2002 4:09 AM Quetzal has replied

Replies to this message:
 Message 16 by Quetzal, posted 10-24-2002 3:20 AM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 14 of 317 (20664)
10-24-2002 1:04 AM
Reply to: Message 6 by Mammuthus
10-23-2002 5:08 AM


dear mammuthus,
Thanks for your lenghty response.
YOU WRITE:
PB:
As demonstrated on this site evolutionism can readily be falsified on the level of the genome and thus cannot be the right hypothesis to explain life on earth in all its variation.
M: You start with an unwarranted conclusion as you have yet to refute anything.
MY RESPONSE:
Even if you found a new organism in your garden tomorrow and found out in your lab that the DNA is completely invariable it wouldn't refute anything, would it? Your a faithful believer. (Nothing inherently wrong with that, although not very scientific)
YOU SAY:
PB:
Why? Evolutionism supposed to have its foundations in molecular biology and genetics, and when the theory can be falsified at this level it lacks a proper foundation and thus cannot be a good theory.
M: Evolution has its foundation in the study of morphology...Darwin and his predecessors had no knowledge of either molecular biology or genetics. You would do better to know the basis of evolution before you presume to refute it.
MY RESPONSE:
And that demonstrates that evolutionism is an outdated theory based on morphology. I think --and this will not be completely novel to you-- morphology is subject to DNA sequences and regulation of these sequences.
YOU SAY:
PB:
Therefore, I introduced the concept of the multipurpose genome.
The concept of a multi purpose genome is not entirely new since a similar concept has been introduced by P. Scheele in his book ‘Degeneration’ and by L. Spetner in his book ‘Not by Chance’.
In my opinion their hypotheses cannot explain all biological observations --like sequence similarities within related species-- and so it cannot be complete.
Therefore I also introduced and provided scientific evidence for non-random mutations. The non-random mutations should be conceived as non-random with respect to nucleotide and position. At present they should not be conceived as deliberately introduced as a response to environmental change, since that cannot be scientifically proven. In genetics non-random mutations are generally referred to as hot-spots. This type of mutations may have important implications for common descent (see my mailing # 184 in ‘molecular genetic evidence against random mutation’ and is still open for discussion). In conjunction with non-random mutation the idea of a multipurpose genome are able to explain all biological phenomena, including genetic redundancies and phylogenetics.
M: Your inability to understand what random means is the only astonishing content of this entire post Peter. When you have been called on your "non-random" mutation fallacy you invariably make minor protests and then cease to continue addressing the subject and then bring it up later in another context. Repeating this fallacy will not make it correct.
MY RESPONSE:
It should be clear now that I do not require deterministic mutations for this hypothesis. As demonstrated in this thread a major part of mutations are non-randomly introduced, i.e non-random with respect to nucleotide and position (see the 1G5 genes in Drosophila subpopulations, mtDNA in hominoids/human subpopulations).
YOU SAY:
Where in my HV1 or HV2 region exactly will I sustain the next mutation of my mtDNA? If you cannot tell me exactly then it is still a random process regardless of hotspots or not. C-T transitions are more likely to occur because of chemical constraints. But that does not mean you know which C-T will occur in any given lineage. Your non-randomness is falsified as mutations occur outside of hotspots as well. Here is a test for you. Get a bacterial clone and subject it to some kind of pressure for 1000 generations. You should be able to perfectly predict every single mutation in the genome before you start...see if it matches your prediction.
I SAY:
I concur that deterministic mutations have not (yet) been detected. I already predicted where your mutations most likely will be introduced in your mtDNA in a previous mail. And if you currently have a C on those positions they will likely be a T when it mutates. Thus, the non-randomness I speak off is with respect to nucleotide and position (not when), but may have important implications for molecular phylogenetics.
YOU SAY:
PB:
The concept 'multipurpose genome' holds that: 1) DNA sequences —although plastic-- are stable throughout time,
M: This is absolute nonsense. How can the DNA sequences be plastic yet not change throughout time? This is falsified as some organisms show extreme genetic diversity and others do not. DNA variation is itself variable among groups.
MY RESPONSE:
By plastic I mean that preexisting sequences can be duplicated and/or shuffled.
YOU SAY:
PB:
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,
M: This is not substantiated. Endogenous retroviruses are "selfish genes" not vital to the organism itself yet are selectively maintained as they themselves struggle to propagate within the host genome. Thus, they show selective constraint. Eye color genes are redundant and selectively constrained. rDNA genes i.e. 18S are highly repeated and show tremendous selective constraint. Point 2 is thus also falsified.
MY RESPONSE:
All according to the evolutionary paradigm. Actually the ribosomal RNAs are a nice example of stability that is maintained by the hypothetical idea of 'concerted evolution'. You should be aware that is but a hypothesis. In fact, evolutionism requires this hypothesis otherwise it cannot explain the high level of stability within the rRNA genes. However, I wonder whether this hypothesis is still tenable and probably it has to be replaced by purifying selction soon (as observed for the histon H3 and H4 genes. The one story is replaced by the other story. You are free to believe them, I don't). The hypothesis of multipurpose simply holds that these rRNA genes are guarded by highly specific DNA repair mechanism.
(By the way, did you mean the "selfish meme" )
YOU SAY:
PB:
3) adaptive phenotypes are due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes [=degeneration theory], and
M: This hardly seems to support a multipurpose genome. Actually a phenotype can only be adaptive if it provides some reproductive advantage to the organism. Most duplications or shuffling of genes cause severe disease or lethal mutations i.e Alu elements integrating in factor 8 gene etc. Also, minor changes in the timing and location of hox gene expression by point mutations in the promoters lead to the most phenotypic novelty. By making phenotypic change exclusively dependent on gene duplication and exon shuffling you have falsified point 3.
MY RESPONSE:
If all mechanisms that induce variations --due to shuffling of preexisting DNA elements-- are already present than it advocates a multipurpose genome and not evolutionism. Nothing evolved, only the order of the DNA elemenst is different.
YOU SAY:
PB:
4) the function of natural selection is to remove degenerate organisms.,
Nope, Wordswordsman is still around
Define degenerate. A single point mutation can result in spontaneous abortion...the entire organism was not degenerate.
MY RESPONSE:
If a single point muations leads to a big enough degeneration (for instance members of the Src-family), it will be lethal and selected against.
YOU SAY:
Natural selection sorts organisms by relative fitness not because of degeneracy. i.e. a species that better utilizes an environment better than another will replace the less adapted species. Niether species is degenerate.
I SAY:
The (sub)species that is not utilising an environment optimally is degenerate compared to the (sub)species that does. It will be selected against.
YOU SAY:
PB:
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).
M: What evidence is there for a morphogenetic field? This is a non-falsifiable hypothesis as it states that an unobservable (god/morphogenetic field) created all living things i.e. plane old creationism. And to top it off, it is an argument by you against abiogenesis as opposed to evolution i.e. you seem to not know what the difference is between the two.
MY RESPONSE:
The creatons and the morphogenetic field can be inferred from the fossil record. You infer evolution from the fossil record and fill in the gaps between the phyla with hypothetical transition forms, also a non-falsifibale hypothesis. So, what is the difference?
YOU SAY:
PB:
Predictions:
1) predicts that within species we do not see abundant variation with respect to genes, and usually such genetic alterations are neutral or degenerate (although distinct alleles can be expected through the principle of degeneration, which is in effect the action of entropy).
It also predicts that all organism --even the simplest-- have an elaborate and accurate mechanism to counteract mutations.
M: This absolutely does not follow from your statement that DNA is plastic and stable (polar opposites). Acutally nothing follows from premise 1. However, this is also falsified as some species do have abundant variation in some genes and others not. If your prediction is that all organisms have elaborate and accurate mechanisms to counteract mutation it does not fit with the observations that even related species have tremendous variation in genetic variability i.e. Homo sapiens and Pan troglodytes for example.
MY RESPONSE:
Expand on the example please. If you mean shuffling I don't see a problem. If you mean SNPs I also don't see a problem.
YOU SAY:
PB:
2) predicts that a considerable part of the genes of any organism can be knocked out without being lethal.
M: Knock out a hox gene and see what happens. As to lethality, that is immediate selection against the organism. But say you knock out a gene involved in sperm production. That specific organism has been just as effectively knocked out of the gene pool. Prediciton 2 is both wrong and overly simplistic.
I SAY:
I don't see a problem here. The organism that doesn't produce sperm will not produce offspring and is therefore degenerate. Its DNA will disappear from the genepool.
YOU SAY:
PB:
3) predicts that adaptive phenotypes of organism do never demonstrate new genes.
M: This sentence makes little sense but if I get your meaning the synsyctin gene (a captured endogenous retroviral envelope gene) which is critical for placental devleopment only in Old World Monkeys and hominids falsifies this prediction.
MY RESPONSE:
How do you know that it is a captured retrovirus gene? It can be the other way around. The retrovirus captured the protein and used it for its envelope. It happend a lot in the virus world that they capture genes from their hosts. I thought you used this method to explain the IL-1beta incongruence?
YOU SAY:
PB:
4) predicts that organism lacking vital DNA elements are selected against.
M: This actually falsifies your premise of a multipurpose genome as all organisms should have redundancies to compensate for the lack of a vital element in your argument.
MY RESPONSE:
No, it doesn't falsify anything (sounds familiar, in't it ). The multipurpose genome hypothesis hold that part of the genes is redundant, not all. In fact it holds that the part that is responsible for variations is redundant, and that are usually genes involved in regulation of gene expression. Hey, that is exactly what we see in biology: Redundant regulatory networks! In addition, there are also essential non-redundant genes.
YOU SAY:
PB:
5) predicts that there should be organisms that have not undergone genetic changes (yet).
M: This is not clear from your multipurpose idea either. Obviously to pre-compensate for the predicted envirnomental changes that the genome knows are coming it should be shuffling and duplicating all the time to have the proper genes for the predicted environment (Lamark thought this way to). Genetic homogeneity argues against your idea. And your lovely tree clone example is different from other species of pine thus it has undergone genetic change.
MY RESPONSE:
If an organism was created recently and doesn't yet have major defects (due to entropy acting on the genome) in DNA repair mechanisms, it is expected that the DNA does not change. That is what we see for the W. nobilis.
YOU SAY:
PB:
Falsification:
The concept will be falsified by the observation of the evolution of new genes unrelated to preexisting genes.
M: Actually, molecular biology and genetics and inconsistencies of your own falsify your idea. The morphogenetic field business is a non testable hypothesis and is a substitution for the words intelligent design or god.
MY RESPONSE:
Actually, molecular biology does not falsify this hypothesis. For instance, you showed me the '10.000 generations of bacteria reference' and it was demonstrated that SNPs were NOT abundant. Thus the sequences are stable and the phenotype-changes were merely due to shuffling/deletion/duplication of preexisting elements. All in accord with my hypothesis.
YOU SAY:
As to your truly funny tree example, please address Quetzal's comments regarding that subject.
I SAY:
See my reponse to Quetzal. However, in a previous letter you concurred that such organism would overturn evolutionism. Can you please expand a bit on this contradiction.
YOU SAY:
PB from the top...
...when the theory can be falsified at this level it lacks a proper foundation and thus cannot be a good theory.
M: Hence, the mutlipurpose genome/morphogenetic field/creaton idea cannot be a good theory
MY RESPONSE:
If so, than we have at present NO good theory. Certainly not a theory that can be presented as fact.
Best wishes,
Peter

This message is a reply to:
 Message 6 by Mammuthus, posted 10-23-2002 5:08 AM Mammuthus has replied

Replies to this message:
 Message 17 by Mammuthus, posted 10-24-2002 5:29 AM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 15 of 317 (20666)
10-24-2002 1:55 AM
Reply to: Message 13 by Itzpapalotl
10-23-2002 9:35 PM


Dear Itz,
You write:
As i understand it even recently duplicated genes (100% functionally redundant) are not freed from selection. This means there is no expectation of relaxed selection in genes with overlapping function and that even if the genes that masked the knokout penotype has exactly the same function they would not mutate faster. Also the poperty of genetic systems that allows component genes to be mutated and mask the phenotype seems to be interactions among unrelated genes that have their own unique role and so of course are not free to mutate.
Hughes, M.K. and Hughes, A.L. (1993) Evolution of duplicate genes in a tetraploid animal, Xenopus laevis. Mol. Biol. Evol. 10, 1360—1369.
Zhang, J. et al. (2002) Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey. Nat. Genet. 30, 411—415.
Wagner, A. Nature Genetics. Volume 24, Issue 4, April 2000, Pages 355-361. Robustness against mutations in genetic networks of yeast.
MY RESPONSE:
I know these interesting papers. Actually I tried to set up a communications with one of the authors on the redundant alpha actinin genes, since they falsify evolutionism, but never got a response.
And in response to your:
"Also the poperty of genetic systems that allows component genes to be mutated and mask the phenotype seems to be interactions among unrelated genes that have their own unique role and so of course are not free to mutate".
MY RESPONSE:
But how did they evolve than? In concert? Together as one? I know another nice example on this topic. The Src-familiy of transcription factors.
Anybody for a discussion on how this family of essential redundant (essential and redundant? Yes indeed. Essential redundant genes are genes that can be knocked out with minor/no problems but point mutations in these genes are lethal) falsifies evolutionism?
Best wishes,
Peter
[This message has been edited by peter borger, 10-24-2002]

This message is a reply to:
 Message 13 by Itzpapalotl, posted 10-23-2002 9:35 PM Itzpapalotl has replied

Replies to this message:
 Message 18 by Itzpapalotl, posted 10-24-2002 7:47 AM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 23 of 317 (20749)
10-24-2002 9:02 PM
Reply to: Message 19 by Mammuthus
10-24-2002 8:18 AM


Dear mammuthus,
You say:
M:
According to this premise, all organisms in close proximity to one another should be genetically identical. Thus, when you were concieved Peter, you should have been most genetically similar to your mother, father, and any bacteria, viruses, and fungi that would have been present. If anyone else was in close proximity, they would be equally closely related to you as their matter would also be in the morphogenetic field. Ultimately, there should be no genetic differences among any humans and there should also be no more than one sex since this is also a genetic difference.
My comments:
"You've watched too many movies" .
Will respond in more detail on your comments, but I can already reveal that the concept of a multipurpose genome --although it is a fact-- is not easy to understand.
I will elaborate on it soon.
Best wishes,
Peter

This message is a reply to:
 Message 19 by Mammuthus, posted 10-24-2002 8:18 AM Mammuthus has replied

Replies to this message:
 Message 31 by Mammuthus, posted 10-25-2002 9:24 AM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 24 of 317 (20755)
10-24-2002 11:03 PM
Reply to: Message 16 by Quetzal
10-24-2002 3:20 AM


Dear Quetzal,
First of all thanks for your scrutiny and your refernces. I missed them during my search, so I had to focus on Woodford's book, that is far from 'journalistic sensationalism' as you like to call it.
YOU WRITE:
--------------------------------------------------------------------------------
quote:
--------------------------------------------------------------------------------
Q: 1. The species is clonal. (I thought you said your magic organism wasn't a clone?) The miniscule population (39 individuals) represents the descendents of a single tree - the ultimate in population bottlenecks, hence refuting your #5 - the very point you thought it proved.
PB: If you know so much about this tree why don't you write a letter to Dr Peakall (University of Canberra), and explain to him how it all works. I think he will be pretty pleased, so he can publish his work --at last-- in a peer reviewed scientific journal.
--------------------------------------------------------------------------------
YOUR RESPONSE:
Actually, I did. Dr. Peakall was quite kind enough to forward to me two of his articles:
Hogbin PM, Peakall R, Sydes MA, 2000. Achieving practical outcomes from genetic studies of rare Australian plants, Aust. J. Bot. 48, 375—382
Peakall R. 1998. Exceptionally low genetic diversity in an ancient relic, the Wollemi pine: implications for conservation theory and practice. 45th Annual meeting of the Genetics Society of Australia. Abstracts 86.
From the latter:
quote:
--------------------------------------------------------------------------------
So far, within the Wollemi Pine no allozyme variability has been found at 13 allozyme loci. Furthermore, no variability has been detected at more than 800 loci, visualised by the AFLP method. While the absence of allozyme variability is know for other rare species, the lack of AFLP variation is unexpected, since this method normally reveals polymorphic loci, even when allozyme variation is absent. This suggests exceptionally low genetic diversity in the Wollemi Pine. Long term isolation, small population size and clonality may have contributed to this pattern.
--------------------------------------------------------------------------------
MY RESPONSE:
And if you paid attention to what you read you would have noticed that the title is a misrepresentaion of the content. They didn't find LOW varibility, they found NO variablity at all. In my opinion that is something completely different, and if it would have been LOW --instead of NO-- variability I wouldn't have shown it as an example!! You may think I am, but I'm not stupid!!
YOU SAY:
Ya see, Peter, I don't get my info from popular science books written by journalists. You ought to try it some time. BTW: Dr. Peakall also told me that a detailed genetics paper is now in preparation, and promised to forward a copy when it is submitted.
MY RESPONSE:
To judge from your intonation I hit a raw nerve. Well, at last you met somebody who checks all evo-claims and it may hurt a bit that I already overturned several claims. So, I can imagine that it not so funny. Sorry for that.
And apparently, you --like Dr Page-- seem to find it pleasing to be condescending. As soon as you are able to nitpick your so eager, it shows. I really feel sorry for that and if it demonstrates something: defence of your beliefs.
If you can send me a copy of the Peakall's articles as soon as you have them in, I would be very grateful.
Furthermore, as stated the tree doesn't demonstrate variation in the expected regions, so where exactly do my claims fail. I simply give it another interpretation. By the way, if I recall properly, it was you who claimed in a previous letter (on mtDNA) not to be a molecular biologist so you were not able to interpret the data on this topic. And now suddenly you are able to interpret these molecular data? Very confusing.
YOU SAY:
A point of correction: Dr. Peakall is with the Australian National University in Canberra, not the "university of Canberra".
I SAY:
Thanks for that, I knew he was in Canberra, but as usual I recalled by head (almost photographic memory, I presume). Nitpicking again. You just earned yourself 100 points.
YOU WRITE:
quote:
--------------------------------------------------------------------------------
Actually there are two populations of the tree, both were analysed and demonstrated exactly the same DNA (as mentioned in letter #1). Surviving populations with invariable DNA points in the direction of a stable multipurpose genome, not in the direction of evolution.
--------------------------------------------------------------------------------
Actually, there are THREE populations of the tree - which of course Woodford didn't know at the time he published his book.
MY RESPONSE:
Actually there are already SEVERAL populations of the tree. I've seen them in the Botanic Gardens in Sydney, the Botanic Gardens of St Thomas, the Zoo, etcetera.
YOU WRITE:
You really should look into some of the original sources rather than relying on a popular press book - no matter how good it might be. Would you let me get away with quoting Dawkins in a scientific argument? At least he's a scientist...
MY RESPONSE:
O yes since I am not in evolutionisms I am not a scientist. I almost laugh my pants off.
(By the way, Dawkins is a zoologist trying to get a bit of understanding of genes. I could educate him in this topic, and I wouldn't let you get away with qouting him, that's for sure).
YOU SAY:
"Surviving populations with invariable DNA" is a serious misstatement. Lack of genetic variability due to long-term isolation and/or severe genetic bottleneck is a relatively well-understood phenomenon. There are numerous examples, from cheetahs to elephant seals. It doesn't, however, imply that the DNA can't vary - simply that it hasn't for the reasons noted. Throw in clonality, and you'd almost expect it...
MY RESPONSE:
I notice that you are perfectly able to copy opinions of evolutionary biologists. I am not impressed by their opinions and you should know that by now. Did you ever ponder these evolutionary riddles youself? Do you have a personal opinion/explanation on these observations? I would really like to know about it.
Furthermore, if it is so well understood explain it to me.
And, it doesn't explain the invariable DNA between the two (or three, or more) stands in the wild.
Please explain to me why it is a misstatement. The trees survive wonderfully, and their DNA is unvariable. I don't see a misstatement here. How can their DNA be so stable? No somatic mutations? Ever thought about that?
YOU WRITE:
quote:
--------------------------------------------------------------------------------
Q: The species propagates by coppicing - roots grow out from the main tree, then send up shoots. IOW, it isn't a sexually reproducing organism in the wild. Interestingly enough, it was discovered during planning for conservation of this unique species that it DOES produce viable seeds like other conifers. Why it clones itself in the wild is unknown at this time.
PB: If you have your information from New Scientist december 1997 than I have to dissapoint you. Coppicing was the initial thought of Peakall but according to Woodford's book (2000) it does not coppice, but sexually reproduces (see mailing #1).
--------------------------------------------------------------------------------
Sorry to disappoint you, but I have my info from the person who actually studied the plant. You need to reread your book, as well as my post. The plant propagates by coppicing IN THE WILD. It was found during conservation planning, however, that it quite readily reproduces sexually ex situ - making it much easier to replicate the plant in collections in multiple facilities, and giving hope to the long-term conservation of the species. IOW, the species DOES produce viable seeds and pollen. The investigation into the reasons for this is on-going - and makes for quite fascinating research in its own right.
MY RESPONSE:
So it is able to copice and also to reproduce sexually. Sounds pretty redundant to me. Multipurpose genome?
YOU SAY:
Where you are correct is that there is no evidence yet that the three populations were connected by subterranean roots (digging up the ground between the stands could be hazardous to the trees). Given the physical separation between stands, Dr. Peakall considers it unlikely. That's why there's on-going study - to answer that question.
MY RESPONSE:
I was not only correct in this statement, all my claims on the tree's DNA are correct and you didn't show otherwise. Do you really think that I am presenting this site with disinformation? Of course not, I show all examples that violate evolutionism, including the Wollemia nobilis. I know the answer to their questions: multipurpose genome, no explanation in the evolutionary paradigm. And Peakall knows, since he talked about an ALL-PURPOSE genome regarding the W. nobilis.
YOU WRITE:
quote:
--------------------------------------------------------------------------------
Q: The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.
PB: That is true. Araucariacaea demonstrate very low variability and that is in accord with the hypothesis of a multiporpose genome. Low variablity due to extremely stable DNA guarded by hundreds of DNA repair enzymes. Observed variation is due to regulatory, rather than mutational phenomena. All in accord with the multipurpose genome.
--------------------------------------------------------------------------------
Nope, wrong again. The data indicates there are evolutionary constraints in action, not some mythical multipurpose genome.
MY RESPONSE:
Evolutionary constraints??? Come on Quetzal, don't fool yourself with these meaningless words. What are evolutinary constraints? That the 'DNA isn't plastic anymore', 'evolution ceased in this tree', 'Evolution slow-down' or other humbug.
Actually this all is exactly what the multipurpose genome predicts: "endstations of 'evolutinism'"
YOU WRITE:
See, for example, Setoguchi, H., Osawa, T.A., Pintaud, J.C., Jaffre, T. & Veillon, J.-M. 1998. Phylogenetic relationships within Araucariaceae based on rbcL gene sequences. Amer. J. Bot. 85: 1507-1516, or Hanson, L. 2001. Chromosome number, karyotype and DNA C-value of the Wollemi Pine (Wollemia nobilis, Araucariaceae). Bot. J. Linn. Soc. 135: 271-274.
In addition, the tree isn't all that similar to the Cretaceous Araucariaceae. See, for example: Chambers, T.C., Drinnan, A.N., McLoughlin, S. 1998. Some morphological features of Wollemi Pine (Wollemia nobilis, Araucariaceae) and their comparison to Cretaceous plant fossils. Internat. J. Plant Sci. 159: 160-171.
MY COMMENTS:
I've had a close-up look at all families of the Araucariacaea --the can all be found in Australia-- and I agree with you that I do not understand that Wollemia, Agathis and Araucaria are classified as Araucariacaea. They don't even resemble each other and are also highly distinct from fossilised Araucaria. (Never understood classifications beyond (sub)species anyway).
YOU WRITE:
quote:
--------------------------------------------------------------------------------
PB: What do you mean by 'argument of journalistic sensationalism'? As far as I know nothing has been published on this tree for sensationalism. Please be specific in your statements.
--------------------------------------------------------------------------------
Lol, almost everything published in the popular press on this tree, beginning with the first accounts of its discovery, have been sensational journalism in action. "Dinosaur tree", "living fossil", "green dinosaur", etc are all splashy, flashy journalistic bombast. Even the full title of Woodford's book which you like so much, "The Wollemi Pine. The Incredible Discovery of a Living Fossil from the Age of the Dinosaurs" lends proof to my contention. Nice try.
As to the horseshoe crab and coelocanth, please start a new thread if you want to drag out these old creationist chestnuts - more examples of "argument from journalistic sensationalism".
MY RESPONSE:
Dear Quetzal you really don't understand what I am trying to convey, is it? For your understanding: Between two isolated populations (like two or three isolated stands of trees) of 'living fossils' molecular evolutionism expects to find loads of variablity with respect to neutral positions, redundant genes, 'junk' DNA etcetera. If we don't find it, than I rest my case: multipurpose genome. We didn't observe it for the first organism analysed in this way, the W. nobilis. The other studies have not yet been carried out. I wait for them and I have a close eye on it, since I am almost certain that it will provide more falsification of evolutionism.
Best wishes,
Peter
[This message has been edited by peter borger, 10-24-2002]

This message is a reply to:
 Message 16 by Quetzal, posted 10-24-2002 3:20 AM Quetzal has replied

Replies to this message:
 Message 28 by Quetzal, posted 10-25-2002 6:57 AM peter borger has replied
 Message 29 by Quetzal, posted 10-25-2002 8:32 AM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 25 of 317 (20763)
10-25-2002 1:45 AM
Reply to: Message 17 by Mammuthus
10-24-2002 5:29 AM


Dear Mammuthus,
You write:
PB:
Even if you found a new organism in your garden tomorrow and found out in your lab that the DNA is completely invariable it wouldn't refute anything, would it? Your a faithful believer. (Nothing inherently wrong with that, although not very scientific)
M: If I found an unusual finding I would actually confirm it rigorously before running around pronouncing I had discovered something spectacular. It is not faith but the wish to do proper reproducible scienc. If I found a new organism that showed no or little genetic variation I would test for a genetic bottleneck or whether the organism is clonal and not claim woo hoo! genetics is dead. (that you do that is both inherently wrong and non scientific.)
MY RESPONSE:
What I understand from Quetzals mailing is that genetic variability hasn't been found between the trees in two (or three, now) seperated stands. That has been scientifically demonstrated in Peakall's lab. So, my claims on this tree are still standing. And, also my assertion that it violates molecular evolution still stands. Even the assertion that 'neither geneticist, paleontologist, dendrologist nor C14 expert would be able to disproof that the organism had been created a century ago' still stands.
PB:
And that demonstrates that evolutionism is an outdated theory based on morphology. I think --and this will not be completely novel to you-- morphology is subject to DNA sequences and regulation of these sequences.
M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.
MY RESPONSE:
Indeed, and how do you think this works?
PB:
It should be clear now that I do not require deterministic mutations for this hypothesis. As demonstrated in this thread a major part of mutations are non-randomly introduced, i.e non-random with respect to nucleotide and position (see the 1G5 genes in Drosophila subpopulations, mtDNA in hominoids/human subpopulations).
M: It should be clear that unless the system is deterministic your entire hypothesis falls apart. You claim that similarity between organisms is solely due to non-random mechansim making them seemingly similar not because of common ancestry.
I have asked without getting an answer before, do you believe you are related to your parents or was your DNA spontanously created and non-random giving the seeming appearance that you are related to them? In any case, as soon as you discover a mutation that occurs outside your "non-random" site your hypothesis is falsified and this has been observed in almost all instances.
MY RESPONSE:
I not only claimed that, but also provided scientific evidence for that. I already mentioned that there are two types of mutations: random and non-random. The latter is non-random with respect to nucleotide and position, and will give the illusion of common descent if one compares between species. I expect to find more evidence if we look within subpopulations instead of looking between distinct species.
PB:
I concur that deterministic mutations have not (yet) been detected. I already predicted where your mutations most likely will be introduced in your mtDNA in a previous mail. And if you currently have a C on those positions they will likely be a T when it mutates. Thus, the non-randomness I speak off is with respect to nucleotide and position (not when), but may have important implications for molecular phylogenetics.
M: This is not really a valid argument Peter. Sometimes you get C to G or C to A. Sometimes C to T. That C to T is more common is a purely chemical constraint. Which C to T mutates is random in a given generation. The only implication that it has for molecular phylogenetics is that the transition transversion ratio is taken into account as a variable.
MY RESPONSE:
That is what YOU expect. And I also expected to find this, untill I discovered that mutations can be non-random. As mentioned in the mtDNA example where subspecies are compared several observations can be made that are not in accord with molecular evolutionism. I already pointed it out in another thread and we could continue there if you like. (Observations: fast evolutionary clock, no common descent, non-random nucleotide substitutions)
PB:
By plastic I mean that preexisting sequences can be duplicated and/or shuffled.
M: So you don't believe there are point mutations, single base deletions, or complete changes in chromosomal content? You have some reading to do.
MY RESPONSE:
Of course, I acknowledge all these forms of mutations. They all have their place in the hypothesis of the multipurpose genome. Usually they are neutral or degenerate. Changes in chromosomal content I am not yet sure off. How? deletions? rearrangements? additions from other sources? However, I guess, they all fit the multipurpose genome. Will think about it if you elaborate on it.
M: The ZFX/ZFY paper also shows how point mutations accumulate in the ALU's...acutally when a HERV integrates the 5 and 3' LTRs diverge by point mutations and deletions etc etc etc.
MY RESPONSE:
Did the sequence divergence start after integration or did they already diverge before integration? How do you assess this?
PB: All according to the evolutionary paradigm. Actually the ribosomal RNAs are a nice example of stability that is maintained by the hypothetical idea of 'concerted evolution'. You should be aware that is but a hypothesis. In fact, evolutionism requires this hypothesis otherwise it cannot explain the high level of stability within the rRNA genes. However, I wonder whether this hypothesis is still tenable and probably it has to be replaced by purifying selction soon (as observed for the histon H3 and H4 genes. The one story is replaced by the other story. You are free to believe them, I don't). The hypothesis of multipurpose simply holds that these rRNA genes are guarded by highly specific DNA repair mechanism.
(By the way, did you mean the "selfish meme" )
M: Ever hear of gene conversion? There are a lot of basic (and observed) methods of DNA sequence homogenization of which you seem to be completely unaware. Selection on 18S is not on one copy and by the way, there can be very different 18S copies within a single genome. There can also be rDNA pseudogenes.
MY RESPONSE:
No, I know of these mechanisms. I only wondered where the other copies go? They seem to disappear from the genome without a trace since otherwise we would observe them as junk DNA and we would be able to track them back in time. In fact such mechanisms predict that a considerable amount of pseudogenes must exist that vary in sequence from 0-100 %. For histon H4 we don't find them. Why, I wonder?
PB:
If all mechanisms that induce variations --due to shuffling of preexisting DNA elements-- are already present than it advocates a multipurpose genome and not evolutionism. Nothing evolved, only the order of the DNA elemenst is different.
M: To bad that novelty and novel regulation does appear to refute this as the exclusive mechanism. Even for shuffled genes, the globin cluster of humans is exceptionally different from elephants....plenty of evolution occurring...
MY RESPONSE:
And who says that they derived through evolution? You see novelty and novel regulation and you say that evolution did it. It is but a plain statement. I do not negate that mutations occur. I negate that elephants and human have a common ancestor linked by a Darwinian mechanism.
PB:
If a single point muations leads to a big enough degeneration (for instance members of the Src-family), it will be lethal and selected against.
M: You sure about that one? Sickle cell anemia and cystic fibrosis are both extremely fitness reducing diseases yet both persist in the population...heterozygotes get an advantage from carrying the "bad copy" thus a big degeneration is maintained.
MY RESPONSE:
Apparently, the diploid genome allows this bit of degeneracy. However, it is loss of a diploid redundancy. So, I see no problem.
Talking about anemia. Did you know that the hemoglobin gene is an apparent "hot gene". I propose there is some kind of mechanism that prefers this gene above --say-- the ZFX gene. Over 250 mutations in the hemoglobin gene are known, while the ZFX gene is completely stable for 20.000.000 years [as discussed]. Directed mutations? Yes, I keep trying it!).
You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.
MY RESPONSE:
Nice example of redundancy. I see no problems here.
PB:
The (sub)species that is not utilising an environment optimally is degenerate compared to the (sub)species that does. It will be selected against.
M: Hey, welcome our new evolutionary biologist Peter Borger
Actually, that is not necessarily correct either. Both may diverge so that they do not overlap.
MY RESPONSE:
There is a big difference between selection against, and natural selection as driving force of evolutionism. You need the genes first and than you can select on these genes. So, the genes have to be derived from some other gene (duplication is the favourite, I guess) and than they have to evolve into another gene without selective constraint (the duplictated genes demonstrate redundancy after duplication) that gives selective advantage. Prediction: we should oberve redundancy correlated to duplication in any genome. Fact: we don't see it. Clear case.
PB:The creatons and the morphogenetic field can be inferred from the fossil record. You infer evolution from the fossil record and fill in the gaps between the phyla with hypothetical transition forms, also a non-falsifibale hypothesis. So, what is the difference?
M: If you find an animal fossil like say a mastodon that has many shared features with elephants but also pronounced differences, how is this evidence for creatons in a morphological field?
MY RESPONSE:
It isn't. However, if you find a manatee and an elephant and you claim (as evolutionism does) that the are linked by Darwinian principles, than I like to have evidence for that.
Otherwise, I claim that the genomes have been created through creaton-matter-interactions.
M:Why would there be gaps in a morphogenetic field? How do you quantifiy a creaton? All untestable and non falsifiable.
Maybe there ar gaps in the creatons. Maybe we pass through an interstellar creaton wave every 26.000.000 years or so. This vision would also nicely fit extinctions (anti-creatons?) and sudden appearance of species.
M: Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.
MY RESPONSE:
There have been books published on this topic. If I recall properly by Michael Cremo. Never read it though.
M: previous post M: This absolutely does not follow from your statement that DNA is plastic and stable (polar opposites). Acutally nothing follows from premise 1. However, this is also falsified as some species do have abundant variation in some genes and others not. If your prediction is that all organisms have elaborate and accurate mechanisms to counteract mutation it does not fit with the observations that even related species have tremendous variation in genetic variability i.e. Homo sapiens and Pan troglodytes for example.
PB: Expand on the example please. If you mean shuffling I don't see a problem. If you mean SNPs I also don't see a problem.
M: So you have no problem with data that falisifies your premise that there is only variation due to shuffling of genes and not point mutations etc?
MY RESPONSE:
I do not have objections to observations like point mutations. They have their place in the hypothesis of the multipurpose genome. Point mutations due to inefficient repair of DNA and this may be due to a degenerate loss of repair genes. Shared point mutations in related genomes may be due to non-random mechanism as previously explained.
PB: I don't see a problem here. The organism that doesn't produce sperm will not produce offspring and is therefore degenerate. Its DNA will disappear from the genepool.
M: But if it is a multipurpose genome obviously there should be a compensatory path for such mutation for such an important pathway. You are arguing from a strict selectionist point of view yet proposing a strictly Lamarkian pre-adaptation hypothesis...they are polar opposites.
MY RESPONSE:
As mentioned before the multipurpose genome also includes essential genes. Not only redundancies. The Lamarkian adaptation hypothesis coud be revisited, but has to be adapted to current understanding of (epi)genetics.
PB: How do you know that it is a captured retrovirus gene? It can be the other way around. The retrovirus captured the protein and used it for its envelope. It happend a lot in the virus world that they capture genes from their hosts. I thought you used this method to explain the IL-1beta incongruence?
M: Where did I say that about IL-1 beta? Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids.
MY RESPONSE:
In a previous letter. I was going to check out viral sequences in this region of chromoseme 2. Didn't find them yet. Where did the virus get his protein?
PB: No, it doesn't falsify anything (sounds familiar, in't it ). The multipurpose genome hypothesis hold that part of the genes is redundant, not all. In fact it holds that the part that is responsible for variations is redundant, and that are usually genes involved in regulation of gene expression. Hey, that is exactly what we see in biology: Redundant regulatory networks! In addition, there are also essential non-redundant genes.
M: This is totally inconsistent. You are constantly changing your terms and hypothesis around from selectionist to adaptationist and from here to partial redundant and multipurpose from only multipurpose. This is falsified by single copy genes involved in variation. If something is lacking in the genome your creatons should create it so that the organism can persist.
MY RESPONSE:
Do you think it a simple task to set up a new hypothesis that covers all biological phenomena? It takes a lot of effort, but luckily you and other biologists already provided some good comments.
Creatons are not omnipresent, so the phenomena we observe in the genome are usually the result of entropy, or preexisting mechanisms (shuffling, duplications, etc).
PB: If an organism was created recently and doesn't yet have major defects (due to entropy acting on the genome) in DNA repair mechanisms, it is expected that the DNA does not change. That is what we see for the W. nobilis.
M: To bad that is not what we see for muskoxen and bears where we see past diversity is much greater than that of today (i.e. ancient DNA). Quetzal also gave examples of organisms that have suffered genetic bottlenecks and were not created recently. Quetzal already pointed out your complete and total error regarding W. nobilis.
MY RESPONSE:
Apparently, these muskusoxes and bears have lost a lot of redundant gentic information that used to be present in their multipurpose genome. That happens a lot. It is predicted by the hypothesis.
PB: Actually, molecular biology does not falsify this hypothesis. For instance, you showed me the '10.000 generations of bacteria reference' and it was demonstrated that SNPs were NOT abundant. Thus the sequences are stable and the phenotype-changes were merely due to shuffling/deletion/duplication of preexisting elements. All in accord with my hypothesis.
M: Actually, they only measured gene rearrangments as it was easier...this was not a test of the increase in SNPs. There are plenty of examples of phenotypic change due to point mutations or have you missed 50 years of genetics?
MY RESPONSE:
Sometimes a point mutation in a PREEXISTING gene occurs and leads to phenotypic change. Either through inactivation of the gene (=degeneracy of the genome) or through a slight decrease of specificity. Spetner wrote a book on this topic. According to him none of the examples added information to the genome. Maybe you have such examples. I would be pleased to know about it.
PB: See my reponse to Quetzal. However, in a previous letter you concurred that such organism would overturn evolutionism. Can you please expand a bit on this contradiction.
M: The contradiction is as Quetzal pointed out, that you have not provided such an organism but have rather again shown a profound lack of population genetics knowledge.
As a suggestion you may want to get a copy of Danial Hartl and Andrew Clark's Population Genetics. It is a bit too mathematical at times but it is a fairly comprehensive book on the genetics of populations. That is not meant as an insult Peter but if you don't have a foundation in the subject matter then you will be far less prepared to object to it.
MY RESPONSE:
First of all, you are unable to insult me even if you wanted to. I'm always open for critique and completely stoic to insults.
However, I have provided such an organism. The three seperated populations of W. nobilis did not derive from cloning, still they were not able to demonstrate genetic differences. That's what I promissed and that is what you get. Maybe population genetics has something to do with it, since it says that low genetic variablity may be expected in small population (due to losses ). However, this example violates molecular evolution. You know that and I know that. Although the Wollemia nobilis may be an evolutionary riddle, it is not a riddle to me.
M: I look forward to your response to this post and to that of Quetzal's regarding W. nobilis.
MY RESPONSE:
Gleichfalls.
best wishes,
Peter
[This message has been edited by peter borger, 10-25-2002]

This message is a reply to:
 Message 17 by Mammuthus, posted 10-24-2002 5:29 AM Mammuthus has replied

Replies to this message:
 Message 26 by Mammuthus, posted 10-25-2002 5:06 AM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 32 of 317 (20840)
10-25-2002 8:32 PM
Reply to: Message 18 by Itzpapalotl
10-24-2002 7:47 AM


Dear Itz,
YOU SAY:
I don't know how resistance to mutation in genetic networks evolves or even if it has been selected for or is an accidental property of the organisation of genes, but that doesn't mean it can't have evolved. Before all the details of the interactions involved in the resistance to mutation of even one system is known speculating on weather it could or couldn't have evolved is futile.
MY RESPONSE:
If you have a close look at certain redundant genes --for instance the alpha actinin genes-- you can only explain them by 'neutral selection'. It has not been introduced in evolutionism for obvious reasons, although the meaningless term 'very weak purifying selection' has recently been introduced. It is so obvious that there is no explanation for these redundacies (another one is the src-kinase gene family coprised of 8 members) within evolutionism's paradigm. Why stick to evolutionism?
Best wishes,
Peter

This message is a reply to:
 Message 18 by Itzpapalotl, posted 10-24-2002 7:47 AM Itzpapalotl has replied

Replies to this message:
 Message 33 by Itzpapalotl, posted 10-25-2002 9:52 PM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 34 of 317 (20863)
10-25-2002 11:44 PM
Reply to: Message 26 by Mammuthus
10-25-2002 5:06 AM


Dear Mammuthus,
Thanks for your reply.
YOU WRITE:
PB:
What I understand from Quetzals mailing is that genetic variability hasn't been found between the trees in two (or three, now) seperated stands. That has been scientifically demonstrated in Peakall's lab. So, my claims on this tree are still standing. And, also my assertion that it violates molecular evolution still stands. Even the assertion that 'neither geneticist, paleontologist, dendrologist nor C14 expert would be able to disproof that the organism had been created a century ago' still stands.
M: First off, you can sequence the mtDNA of 3 cheetahs and find no genetic variation to. It is historically known that they went through a bottleneck (perhaps down to a single breeding pair) and they are still today extremely genetically uniform. All as predicted by population genetics much less evolution.
MY RESPONSE:
Population genetics is the field of multipurpose genome and allele frequency variation, not the field of evolution. Nothing evolved here, just variation with respect to preexisting alleles in the gene pool.
YOU SAY:
Same goes for the musk oxen. The entire population of musk oxen in Greenland were a transplant of a few from Alaska...thus, they are identical in the sequences thus far studied. Of 37 modern muskoxen only 8 very similar haplotypes were found...though I have some upcoming surprises about 15 thousand year old muskoxen
MY RESPONSE:
I am curious. Same genepool as contemporary muskoxen? It would fit 'multipurposism'.
YOU SAY:
Very few W. nobilis exist so it would have been a much greater surprise if the 3 stands demonstrated genetic variability as that would be inconsistent with a bottleneck. Bottlencks can be observed expreimentally and in the wild. Your concept of morphogenetic fields cannot so is thus unsupported.
MY RESPONSE:
There is no W. nobilis in the fossil record. So, your bottle neck is utterly hypothetical.
YOU SAY:
As to your arguement that no one could "prove" that W. nobilis was not created 100 years ago...(you don't prove in science which you obviously do not know)...Find the closest relative of W. nobilis and you can determine how long ago it separated from that relative..thus much evolution has occurred and had to occur before the trees present as the genome does not spontaneously change after the organism is present, except for a few loci
MY RESPONSE:
The closest relative of the pine is one of the Araucaria family. It is known that they have very low variablity. Maybe Quetzal can repond to this in more detail, since he has got the papers on the DNA work done on this topic.
YOU SAY:
M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.
PB:
Indeed, and how do you think this works?
M: Are you being serious or joking? Are you really unaware of why thalidomide is a mutagen? Before I go into this I need to know if you have any knowledge of developmental biology.
MY RESPONSE:
How does the environment have impact on gene regulation, I mean. Not the effect of thalidomide. I know how it works. It is a vascular growth inhibitor and now in use to treat certain solid tumors.
PB:
I not only claimed that, but also provided scientific evidence for that. I already mentioned that there are two types of mutations: random and non-random. The latter is non-random with respect to nucleotide and position, and will give the illusion of common descent if one compares between species. I expect to find more evidence if we look within subpopulations instead of looking between distinct species.
M: And again, you have not provided any evidence for non-random mutation except for your poor tactic of redefining random to suit your purpose though it is not correct. There are lots of papers on subpopulation variation and they don't show non-random mutation. You still cannot tell me for the hottest of hotspots if a mutation will occur there in the next generation or not.
MY RESPONSE:
Remember the 1G5 gene and ancient mtDNA? I also like to have a look on the paper that do not show this in subpopulations. Could you please provide me with the references.
PB:
That is what YOU expect. And I also expected to find this, untill I discovered that mutations can be non-random. As mentioned in the mtDNA example where subspecies are compared several observations can be made that are not in accord with molecular evolutionism. I already pointed it out in another thread and we could continue there if you like. (Observations: fast evolutionary clock, no common descent, non-random nucleotide substitutions)
M: We can continue as you like. Your repeating non-random mutation is not making it any more valid....so please continue but actually supply something substantive.
MY RESPONSE:
What evidence do you need to accept non-random mutations? I showed you the 1G5 gene and the ancient mtDNA already, what else do you need?
PB:
Of course, I acknowledge all these forms of mutations. They all have their place in the hypothesis of the multipurpose genome. Usually they are neutral or degenerate. Changes in chromosomal content I am not yet sure off. How? deletions? rearrangements? additions from other sources? However, I guess, they all fit the multipurpose genome. Will think about it if you elaborate on it.
M: Actually, you have previously denied other forms of mutation contribute to variation. However, you stated multipurpose genome was all about shuffling of existing sequences only with no acknowledgement of point mutations etc...do you wish to revise your premise?
MY RESPONSE:
Denial of mutations would be stupid. I probably refered to point mutations as not being relevant in generating novelties, and usually neutral or degenerate.
M: As to your questions, I think we may be talking past each other. I am not sure what you are asking me. I can give you examples of close species with different chromsomal content but I am not sure if that is what you are asking for.
MY RESPONSE:
Close species with different DNA content sounds multipurpose-like and differential losses of redundant genes. Yes, I am interested and could you please provide the references.
PB:
Did the sequence divergence start after integration or did they already diverge before integration? How do you assess this?
M: That is an easy one. Novel integration events have been observed including with HIV when the virus integrates into the genome of its host. The LTRs are identical..the divergence is post integration.
MY RESPONSE:
Sounds reasonable if the LTRs diverged. Can you refer to the paper.
PB: No, I know of these mechanisms. I only wondered where the other copies go? They seem to disappear from the genome without a trace since otherwise we would observe them as junk DNA and we would be able to track them back in time. In fact such mechanisms predict that a considerable amount of pseudogenes must exist that vary in sequence from 0-100 %. For histon H4 we don't find them. Why, I wonder?
M: Please read any basic chapter on recombination and you should be able in 2 seconds to see why the reciprocal recombinant is lost.
MY RESPONSE:
I wasn't referring to reciprocal recombinations. Is not how genes duplicated at the first place. I should be done by unequal crossing over. By any means, the identical copies of histon genes and the hundreds of copies of identical tRNA genes are by definition REDUNDANT. How can they be stable in the genome? Concerted evolution? I wanna see the evolutionary relics in the genome, diverging from 0-100% over time.
For histons the mechanism of concerted evolutionism has been abandoned recently for obvious reasons. It is now purifying selection.
PB:
And who says that they derived through evolution? You see novelty and novel regulation and you say that evolution did it. It is but a plain statement. I do not negate that mutations occur. I negate that elephants and human have a common ancestor linked by a Darwinian mechanism.
M: actually you deny that you are linked to your parents by common ancestry as well. It is not a plain statement but one supported by paleontology, morphology, biochemistry, and genetics....what have you got?
MY RESPONSE:
Inappropriate analogy. It has been observed that my parents are my ancestors. It is a biological observation.
You are wrong in your statement that it is supported by all these disciplines. It is inferred from the fossil record, although nobody ever demonstrated it beyond doubt (transitionforms). Morphology doesn’t say anything about evolution, and phylogenetics observations violate the rules wherever you look (IL-1beta, LDH, alpha-globin, maybe even cytochrome c) so you’re not on solid ground with your assertion. I do the same observations as you but I can explain them by inferring (anti)creaton-matter-interactions (for the appearance of new genera, extinctions, morphology). For the rest there is the multipurpose genome and non-random mutations (this is NOT deterministic mutations).
PB:
Apparently, the diploid genome allows this bit of degeneracy. However, it is loss of a diploid redundancy. So, I see no problem.
Talking about anemia. Did you know that the hemoglobin gene is an apparent "hot gene". I propose there is some kind of mechanism that prefers this gene above --say-- the ZFX gene. Over 250 mutations in the hemoglobin gene are known, while the ZFX gene is completely stable for 20.000.000 years [as discussed]. Directed mutations? Yes, I keep trying it!).
M: Ah, so now the mutlipurpose is now only semi-multipurpose on certain occasions? As to ZFX..you are not helping your case by posting this fallacy again (as discussed).
MY RESPONSE:
As mentioned the new theory is still in preparation/under construction. It took the neo-Darwinians almost a century to set up their non-falsifiable theory (untill I got involved ).
Fallacy? The ZFX gene doesn't change for 20 million years as demonstrated by biomolecular scientists and you call that a fallacy?
M:
You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.
PB:
Nice example of redundancy. I see no problems here.
M: Except that in almost all other organisms such a loss is lethal? Selective redundancy? Redundancies on Tuesdays but not Thursdays? I see big problems for your hypothesis with the redundancy argument.
MY RESPONSE:
No, all organisms have a tremendous amount of genetic redundancies. Why would al redundancies be the same? I don't see a reason for that. I already demonstrated redundancies for several organism including Arabidopsis and E coli. Leave out 10% of the genome and no problem for the organism. Apparently these genes --that do not demonstrate more change than essential genes-- are in the genome without selective constraints. It is a Darwinian paradox. Insoluble. Here, the multipurpose genome is far superior to Darwinism. You know that, but you are free to deny it.
PB:
There is a big difference between selection against, and natural selection as driving force of evolutionism. You need the genes first and than you can select on these genes. So, the genes have to be derived from some other gene (duplication is the favourite, I guess) and than they have to evolve into another gene without selective constraint (the duplictated genes demonstrate redundancy after duplication) that gives selective advantage. Prediction: we should oberve redundancy correlated to duplication in any genome. Fact: we don't see it. Clear case.
M: Clear to you but that is not a prediction of any evolutionary biologist. Some cases do operate as you have said. In other cases a gene involved in one function takes on a new function i.e. homoglobins in bacteria versus multicellular organisms. And you the need organism to be selected on by its environment at the phenotypic level, not the gene to be selected for to pre adapt the organism to something..get it?
MY RESPONSE:
All according to the FACT of evolutionism, isn’t it. I was objecting to evolutionism, since it is NOT a fact. As demonstrated --and denied-- over and over. Moreover, evolutionism also has to explain the origin of these novel genes.
PB:
It isn't. However, if you find a manatee and an elephant and you claim (as evolutionism does) that the are linked by Darwinian principles, than I like to have evidence for that.
Otherwise, I claim that the genomes have been created through creaton-matter-interactions.
M: There is a lot of evidence for a manatee-elephant association. you up for reading it?
MY RESPONSE:
There may be a lot of manatee-elephant associations. There is also a lot of bacterium-elephant association. Next thing you are going to say is since there is an association they have a common ancestor through a Darwinian mechanism. Well a red car and a red bike have also significant associations. Both consist of metal, have wheels, and even have the same colour. Am I to conclude that they are made in the same factory?
PB:
Maybe there ar gaps in the creatons. Maybe we pass through an interstellar creaton wave every 26.000.000 years or so. This vision would also nicely fit extinctions (anti-creatons?) and sudden appearance of species.
M: Except that it is a non-testable hypothesis just like plain old biblical creationism.
MY RESPONSE:
Actually extinctions are associated with an interval of roughly 26 million years. Case proven
How do you explain extinctions?
M: Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.
PB:
There have been books published on this topic. If I recall properly by Michael Cremo. Never read it though.
M: LOL!!!!!!!!!!!!!!!!!!!!
MY RESPONSE:
What’s the fun about? Is it a funny book? I didn’t read it yet, maybe I should?
PB:
I do not have objections to observations like point mutations. They have their place in the hypothesis of the multipurpose genome. Point mutations due to inefficient repair of DNA and this may be due to a degenerate loss of repair genes. Shared point mutations in related genomes may be due to non-random mechanism as previously explained.
M: Glad you don't object to point mutations as that would make for some very strange demonstrations in front of the White House
You have falsified your own hypothesis. Two humans have the same repair mechanism (as do chimps and humans)yet any two individuals have different amounts and locations of mutations so it cannot be due to loss of repair genes.
MY RESPONSE:
Your assumption is that these organisms have the same repair mechanism. However, the expression and interaction is differently regulated per individual. As mentioned several times now, there are 2 types of mutations non-random and random. The random mutations is all evolutionism requires, according to evolutionism. However, the non-random mutations line up if you compare (sub)species and give an illusion of common descent. In addition, they are alternated by random mutations. The latter are interpreted as being generated after the species split off from a common ancestor. In my opinion the two types of mutations work simultaneously. So, I don’t see a problem here.
PB:
As mentioned before the multipurpose genome also includes essential genes. Not only redundancies. The Lamarkian adaptation hypothesis coud be revisited, but has to be adapted to current understanding of (epi)genetics.
M: Go ahead an revisit Lamark and tell me what our current understanding is of epigenetics and how it relates to evolution and then how it relates to your hypothesis.
MY RESPONSE:
It is clear from my own field that some ‘adaptations’ occur that cannot have resulted from mutations in DNA alone, since the adaptations occurs suddenly and everywhere at the same moment. For instance, asthma. It is a desease affecting ‘solely’ Western societies, and its prevalence increased from around 1% 40 years ago to 10% now. That is within 1-2 generations. It suggests an effect of the environment/lifestyle on the development of the disease. It is my personal opinion that the disease is largely due to epigenetic modifications of chromatin and/or DNA structure that results in an alternative development of immune system and lungs (sometimes aggravated by genetic predisposition).
Similar observation have been done on rapid adaptations of human populations on high altitude. It is as if the info of adaptation is pre-existing.
PB:
In a previous letter. I was going to check out viral sequences in this region of chromoseme 2. Didn't find them yet. Where did the virus get its protein?
M: 8% of the human genome is composed of HERVs so there are plenty of options...you have a lot of work cut out to support your assumption
MY RESPONSE:
If the IL-1beta was carried by a virus and integrated adjacent to IL-1 alpha then I expect to find the remnants of the virus there too isn’t it?
PB:
Do you think it a simple task to set up a new hypothesis that covers all biological phenomena? It takes a lot of effort, but luckily you and other biologists already provided some good comments.
Creatons are not omnipresent, so the phenomena we observe in the genome are usually the result of entropy, or preexisting mechanisms (shuffling, duplications, etc).
M: You have claimed multiple times that it was easy to support your hypothesis and very easy to refute evolution based on your hypothesis. Suddenly it is hard? How do you know if creatons are omnipresent or not since you have never measured one or observed one? How will you go about identifying such a particle?
MY RESPONSE:
Not refute, I provide an alternative. And that will take a bit of time. Falsifications of evolutionism can readily be found by scrutiny of current literature on the topic. As demonstrated.
PB:
Apparently, these muskusoxes and bears have lost a lot of redundant gentic information that used to be present in their multipurpose genome. That happens a lot. It is predicted by the hypothesis.
M: Then the hypothesis is falsified as the ancient and modern muskoxen and bears have the same genetic content as modern representatives.
MY RESPONSE:
No, it is not. Apparently they didn’t loose their genetic content. It is not obligatory to loose genetic content, it is a possibility to get variation.
PB:
Sometimes a point mutation in a PREEXISTING gene occurs and leads to phenotypic change. Either through inactivation of the gene (=degeneracy of the genome) or through a slight decrease of specificity. Spetner wrote a book on this topic. According to him none of the examples added information to the genome. Maybe you have such examples. I would be pleased to know about it.
M: Syncytin for one.
MY RESPONSE:
Where does syncytin come from? I mean if it is a viral protein, the virus got it somewhere and integrated it into another genome. Where did the virus get it?
And you said in the previous letter: "Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids." Clear for the theory of evolutionism you mean. It can be envisagd that it was a unique old world monkey gene caputered by an endogenous retrovirus and later escaped from the genome. Where do you think viruses have their origin? In the genome of course.
PB:
First of all, you are unable to insult me even if you wanted to. I'm always open for critique and completely stoic to insults.
M: You often seem rather prickly these days. However, you did not deny your lack of knowledge of the fields you are criticizing and have not indicated a willingness to inform yourself. If you did so you might bolster your credibility and not make so many errors.
MY RESPONSE:
Yes, I have a cold. It affects the temper I guess. However, all I do is giving a different interpretation on scientific observations. Nothing wrong with that in my opinion. I learned a lot from this discussion and if a thesis is not tenable I give in. That’s the scientific way. It would be rather unscientific to claim that a hypothesis is a fact while it still can be falsified. But, I am working on that.
PB:
However, I have provided such an organism. The three seperated populations of W. nobilis did not derive from cloning, still they were not able to demonstrate genetic differences. That's what I promissed and that is what you get. Maybe population genetics has something to do with it, since it says that low genetic variablity may be expected in small population (due to losses ). However, this example violates molecular evolution. You know that and I know that. Although the Wollemia nobilis may be an evolutionary riddle, it is not a riddle to me.
M: On the one hand you say that population genetics predicts this and thus it falsifies evolution...evolution is population genetics...again Daniel Hartl and Andrew Clark Principles of Population Genetics..there is even a "Cliffs Notes" version with less of the mathematical derivations for some of the equations they present.
MY RESPONSE:
Since when is change in allele frequencies evolutionism? It is easy to explain by a multipurpose genome. If population genetics is evolutionism than I AM an evolutionist too. But, it is NO evolutionism, since it doesn't say anything about the generation of new organisms, novel genes, etc. You know --and every educated biologist should know-- that you cannot present population genetics as evolutionism.
Best wishes, And have a nice weekend
Peter
[This message has been edited by peter borger, 10-26-2002]

This message is a reply to:
 Message 26 by Mammuthus, posted 10-25-2002 5:06 AM Mammuthus has replied

Replies to this message:
 Message 35 by Mammuthus, posted 10-28-2002 4:23 AM peter borger has not replied
 Message 36 by Peter, posted 10-28-2002 5:33 AM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 40 of 317 (20971)
10-29-2002 12:05 AM
Reply to: Message 38 by derwood
10-28-2002 1:59 PM


dear SLPx,
You are purposely obtuse. You know what I mean and you know that I am right. Better try to find an evolutionary explanation for these observations. In addition, you still owe me an evo-explanation for the incongruence of the IL-1beta genes, and for the stability of the ZFX region studied by Kim et al. Next we can discuss --if you like-- the redundant alpha actinin genes, the redundant src-kinases and where they violate molecular evolution and how you try (?) to save evolutionism from falling.
And please stop trying to represent me as someone not knowing the difference between genes and exons. Maybe you can provide this site with a contemporary definition of a gene? That would be great. Thanks in advance.
best wishes,
Peter

This message is a reply to:
 Message 38 by derwood, posted 10-28-2002 1:59 PM derwood has replied

Replies to this message:
 Message 58 by derwood, posted 10-30-2002 12:24 PM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 41 of 317 (20972)
10-29-2002 12:07 AM
Reply to: Message 37 by derwood
10-28-2002 12:55 PM


Dear Dr page,
And, as demonstrated, I not only claimed it but I also demonstrated how to do it.
best wishes,
Peter

This message is a reply to:
 Message 37 by derwood, posted 10-28-2002 12:55 PM derwood has replied

Replies to this message:
 Message 59 by derwood, posted 10-30-2002 12:27 PM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 42 of 317 (20973)
10-29-2002 12:23 AM
Reply to: Message 33 by Itzpapalotl
10-25-2002 9:52 PM


dear Itz,
Thanks for your reply. About six months ago I encountered the redundant alpha actinin genes and I observed an evolutionary problem. Since Dr Wagner --the one you refer to-- seems to be the evolutionary expert in the field of genetic redundancy, I mailed him the letter below. Till now I didn't get a response. For obvious reasons.
"Dear Dr Wagner,
With interest I read your mini-review in Genome Biology. I am interested in the origin of genes and I recently found out about genetic redundancy. I am trying to understand it in the light of random evolution. Redundant genes usually demonstrate only moderate sequence homology. For instance the alpha-actinin genes. The a-actinins comprise a group of actin-binding proteins encoded by a multigene family. In skeletal muscle, they are a major structural component of the Z-lines that anchor the actin-containing thin filaments and maintain the spatial relationship between myofilaments. In humans, two genes (ACTN2 and ACTN3) encode the closely related a-actinin-2 and a-actinin-3 skeletal muscle isoforms. ACTN2 is expressed in all skeletal muscle fibres, whereas expression of ACTN3 is limited to a subset of type 2 (fast) fibres. A careful screening of muscle biopsies with dystrophic (118 specimens), myopathic (74), neurogenic (20) and normal (55) features demonstrated that all specimens contained normal a-actinin-2 expression. Deficiency of a-actinin-3 was identified in 51 of the 267 cases (19%), and was due to a common non-sense mutation that introduced a premature stop codon. So, the proper a-actinin-3 protein cannot be synthesised. Surprisingly, the deficiency was not associated with any particular histopathological or clinical phenotype [North et al, Nature Genet.1999, 21:353].
What troubles me is that I cannot think of any molecular mechanism that gave rise to such genes. As a biology student I always was taught that neo-darwianian evolution proceeds through the mechanism of random mutation and natural selection. According to theory, duplication gave rise to two alpha-actinin.
A close look at the redundant genes reveals that the differences are the result of point-mutations. Neutral evolution rate is about 10(exp)-9/nucleotide/year, and recent genome wide studies present evidence that purifying selection worked upon duplicated genes. The ACTN2 and ACTN3 genes are approximately 3000 bp, and share 85% sequence homology. Moreover, the ACTN3 gene is highly conserved within mammals, suggesting ancient duplication and rapid diversion.
I have a couple of questions regarding the evolutionary mechanisms involved in genetic redundancies. I was hoping that you can find the time to address them.
1) Do these data mean that approximately 450 bp changes occurred on neutral positions?
2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? Thus 150 million years for 450 neutral mutations?
3) Do these data mean that after each point-mutation there was neutral purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes?
3a) Is it independent from nearby genes? Independent from the rest of the genome?
3b) Does this type of selection take place on the level of the organism? How?
4) Are there identical (=very recently duplicated) genes in known genomes?
5) Is evolution a phenomenon driven by random mutation?
I hope you can help me out with my questions. I would be very grateful. Thanks in advance.
Sincerely,... "
These questions are still unanswered and maybe you are able to address them.
[Or maybe it is a nice challenge for Dr Page since he is the PhD-ed evolutionary biologist of this site and he knows how it works. I cannot answer these questions, since am only a "asthma research creationist guy".]
best wishes,
Peter

This message is a reply to:
 Message 33 by Itzpapalotl, posted 10-25-2002 9:52 PM Itzpapalotl has not replied

Replies to this message:
 Message 44 by Mammuthus, posted 10-29-2002 3:28 AM peter borger has replied
 Message 60 by derwood, posted 10-30-2002 12:32 PM peter borger has not replied

  
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