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Author Topic:   molecular genetic evidence for a multipurpose genome
peter borger
Member (Idle past 6988 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

  
monkenstick
Inactive Member


Message 2 of 317 (20535)
10-23-2002 2:36 AM


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


Replies to this message:
 Message 3 by peter borger, posted 10-23-2002 3:21 AM monkenstick has not replied

  
peter borger
Member (Idle past 6988 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

  
monkenstick
Inactive Member


Message 4 of 317 (20539)
10-23-2002 4:02 AM


the fact that there are numerous genes which are lethal when knocked out falsifies point 2, and thus, your theory.

*dances on the grave of borger's theory*

(see how annoying it is borger?)


Replies to this message:
 Message 9 by Andya Primanda, posted 10-23-2002 12:23 PM monkenstick has not replied
 Message 10 by peter borger, posted 10-23-2002 8:24 PM monkenstick has not replied

  
Quetzal
Member (Idle past 5195 days)
Posts: 3228
Joined: 01-09-2002


Message 5 of 317 (20541)
10-23-2002 4:09 AM
Reply to: Message 1 by peter borger
10-23-2002 1:57 AM


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!

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.

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.

3. The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.

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".


This message is a reply to:
 Message 1 by peter borger, posted 10-23-2002 1:57 AM peter borger has replied

Replies to this message:
 Message 12 by peter borger, posted 10-23-2002 9:26 PM Quetzal has replied

  
Mammuthus
Member (Idle past 5798 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 6 of 317 (20545)
10-23-2002 5:08 AM
Reply to: Message 1 by peter borger
10-23-2002 1:57 AM


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.

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.

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.

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.

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.

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.

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.

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. 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.

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.

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.

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.

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.

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.

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.

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.

As to your truly funny tree example, please address Quetzal's comments regarding that subject.

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

cheers,
M


This message is a reply to:
 Message 1 by peter borger, posted 10-23-2002 1:57 AM peter borger has replied

Replies to this message:
 Message 14 by peter borger, posted 10-24-2002 1:04 AM Mammuthus has replied

  
Syamsu 
Suspended Member (Idle past 4913 days)
Posts: 1914
From: amsterdam
Joined: 05-19-2002


Message 7 of 317 (20546)
10-23-2002 5:13 AM
Reply to: Message 1 by peter borger
10-23-2002 1:57 AM


I've found a professional biologist talking about mulitpurpose genome on the groups.msn.com/talkorigins messageboard.

http://www.uvm.edu/~jdavison

There is his homepage.

As far as I can tell:
- He conjectures, in line with observation, that sexually reproducing creatures generally can't speciate.

- That sexually reproducing creatures have an ancestor that reproduced in another way that could speciate.

- That this can be proved by inhibiting the sexual reproduction mode of sexually reproducing creatures, so that they return to their pre-sexual "semi-meiotic" evolutionary mode where they are able to speciate

- That this ancestor had "preformed" information in it's multipurpose genome which through shuffling made new species.

- The source of the preformed information is a total mystery.

But again, this is all besides the point in my opinion, since he and you still describe organisms in terms of a possible future event of reproduction. Therefore yours and his theory fall within the scope of Natural Selection theory.

regards,
Mohammad Nor Syamsu


This message is a reply to:
 Message 1 by peter borger, posted 10-23-2002 1:57 AM peter borger has not replied

  
monkenstick
Inactive Member


Message 8 of 317 (20556)
10-23-2002 8:16 AM


the other problem with his theory is that speciation in sexually reproducing organisms has been observed.

  
Andya Primanda
Inactive Member


Message 9 of 317 (20580)
10-23-2002 12:23 PM
Reply to: Message 4 by monkenstick
10-23-2002 4:02 AM


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!

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 11 by peter borger, posted 10-23-2002 8:31 PM Andya Primanda has replied

  
peter borger
Member (Idle past 6988 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 6988 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 6988 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

  
Itzpapalotl
Inactive Member


Message 13 of 317 (20638)
10-23-2002 9:35 PM
Reply to: Message 10 by peter borger
10-23-2002 8:24 PM


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.


This message is a reply to:
 Message 10 by peter borger, posted 10-23-2002 8:24 PM peter borger has replied

Replies to this message:
 Message 15 by peter borger, posted 10-24-2002 1:55 AM Itzpapalotl has replied

  
peter borger
Member (Idle past 6988 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 6988 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

  
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