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Author Topic:   Endosymbiont theory wrong?
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 16 of 43 (17646)
09-18-2002 3:15 AM
Reply to: Message 12 by peter borger
09-11-2002 8:39 PM


quote:
Originally posted by peter borger:
Dear Peter,
Nobody understands the ToE at the molecular level, or any level. Why? Because evolution doesn't exist.

Not understanding how activity at the molecular level could
cause the effects seen at the species level does not mean
(necessarily) that evolution does not exist. It means that
there is a gap in understanding ... which considering the
relative youth of molecular biology I would expect.
quote:
Originally posted by peter borger:

Better name for the wat the ToE stands for would be Theory of Variation-induction (or something like that). Scientists are discovering that evolution as it was set up by the NDT-ers cannot work.

Is that in the same way that a bumble bee cannot fly?
quote:
Originally posted by peter borger:
In addition, why do you think that websites like these are around? If evolution was a fact --as claimed so often by proponents-- these sites wouldn't exist. Ever encountered a site for "flat-versus-round" earth-discussions? Of course not. There is scientific consensus about the earth. Not about evolution, since compelling evidence is lacking.

Someone else pointed out that there are those who suggest that
the world is flat.
quote:
Originally posted by peter borger:

I will always object to the nihilism underlying NDT. It's my main goal in life.

Please elaborate why NDT is nihilistic.
A general comment would be that you have still avoided my original
question.
If you know what NDT is described to be how can you use a
term like 'de-evolution'?
If that concept even exists within your consciousness in connection
with ToE, then you do not understand the proposal ... I have
asked nothing about your understanding of the facts, only of
the theory as currently presented.

This message is a reply to:
 Message 12 by peter borger, posted 09-11-2002 8:39 PM peter borger has not replied

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


Message 17 of 43 (18660)
09-30-2002 11:11 PM
Reply to: Message 5 by Itzpapalotl
09-09-2002 12:53 PM


Dear Itzpaplotl,
As mentioned before I had objections against the hypothesis of endosympbiosis. Although I have a lot, let me start by asking how do proponents of this hypothesis see the first step in endosymbiosis: the endocytosis of one prokaryote by another prokaryote. My first objection derives from the observation that prokaryotes do not have microtubuli (they are only found in eukaryota). Microtubuli are crucial in the process of endocytosis. No microtubuli, no endocytosis, and thus no uptake of the 'endosymbiont to be'. In my opinion the endosymbiontic hypothesis comes immediately to a grinding halt if you cannot solve this problem.
Best wishes,
Peter
--To know all is to understand all--
Evelin Waugh in 'Brideshead Revisited'
[This message has been edited by peter borger, 09-30-2002]

This message is a reply to:
 Message 5 by Itzpapalotl, posted 09-09-2002 12:53 PM Itzpapalotl has replied

Replies to this message:
 Message 18 by Itzpapalotl, posted 10-01-2002 5:23 AM peter borger has not replied

  
Itzpapalotl
Inactive Member


Message 18 of 43 (18693)
10-01-2002 5:23 AM
Reply to: Message 17 by peter borger
09-30-2002 11:11 PM


Hi Peter B,
Your objection is interesting but i have already answered it in a previous post:
"The fact that no bacteria were thought to live inside other bacteria was interpreted as evidence against endosymbiosis, but the discovery of secondary endosybitic bacteria within bacteria found inside mealybugs (Pseudococcidae) proves this not to be the case. These endosybionts were found to have a double membrane surrounding them like mitochondria do."
Bacteria live inside other bacteria, fact. So endocytosis must have happened, therefore your idea that microtublules are necessary for endocytosis just plain isn't true.
Reference:
Mealybug [beta]-proteobacterial endosymbionts contain [gamma]-proteobacterial
symbionts. von Dohlen, Carol D.; Kohler, Shawn*; Alsop, Skylar T.; McManus, William R.
Nature Volume 412(6845) 26 July 2001 pp 433-436.

This message is a reply to:
 Message 17 by peter borger, posted 09-30-2002 11:11 PM peter borger has not replied

Replies to this message:
 Message 19 by Itzpapalotl, posted 10-01-2002 10:45 AM Itzpapalotl has not replied

  
Itzpapalotl
Inactive Member


Message 19 of 43 (18716)
10-01-2002 10:45 AM
Reply to: Message 18 by Itzpapalotl
10-01-2002 5:23 AM


I did a bit of reading on the bacterial cytoskeleton and ended up finding out more interesting things about mitochondria. Bacteria do have a gene (FtsZ) that is similar to tubulin (the monomer that makes up microtubes) and so there was presumably a form of it in the universal common ancestor. This indicates that the eukaryotic ancestor could have had microtubules before endosymbiosis occured. The difference in much of the cellular machinery of mitochondria/bacteria and eukaryotes indicates they diverged substantially before endosymbiosis. Although this is just speculations since microtubules are irrelevant to endosymbiosis it doesn't really matter in this context.
The interesting thing about some mitochondria and all chloroplasts is that they use the products of bacterial FtsZ genes (most closely related to alpha-proteobacterial genes yet again) to divide. FtsZ has been lost in fungi animal and plant mitochondria in which division is mediated by dynamin a protein of eukaryotic origin but if FtsZ genes from mitochondria are put into organisms from which it has been lost the product interacts usefully with the mitochondria. Dynamin does seem to play a part in the division of intracellular parasitic bacteria such as Chlamydia that lack FtsZ.
Thanks peter B. without your post i wouldn't have looked into this area and found yet more compelling evidence in favour of endosymbiosis.

This message is a reply to:
 Message 18 by Itzpapalotl, posted 10-01-2002 5:23 AM Itzpapalotl has not replied

Replies to this message:
 Message 22 by peter borger, posted 10-01-2002 11:34 PM Itzpapalotl has replied

  
derwood
Member (Idle past 1876 days)
Posts: 1457
Joined: 12-27-2001


Message 20 of 43 (18736)
10-01-2002 1:58 PM
Reply to: Message 3 by peter borger
09-09-2002 3:59 AM


quote:
Originally posted by peter borger:
I say:
Of course it doesn't, because nothing can challenge --let alone falsify-- evolution theory. I think I will let you dream on"
...
By the way, there are no such thing as vestiges. That is 19th century blahblah.
And if you wanna discuss the "fairytale of the endosymbiont" you have just found your man.
Wow, the amount of pure creationist drivel oozing from "scientist" Peter B is astounding.
Gish and pals must be proud.
By the way,Peter, I am still waiting for your amazing 'disproof' of the vestigiality of the extensor coccygis and the auricularis muscles.
Beause, afterall, there is no such thing as vestigials, and science, according to you, will 'proof' this.
Proof away, creationist.

This message is a reply to:
 Message 3 by peter borger, posted 09-09-2002 3:59 AM peter borger has replied

Replies to this message:
 Message 21 by peter borger, posted 10-01-2002 8:07 PM derwood has replied

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


Message 21 of 43 (18762)
10-01-2002 8:07 PM
Reply to: Message 20 by derwood
10-01-2002 1:58 PM


Dear SLPx,
I can perfectly understand the loss of a trait that is not under selective constraint with a multipurpose genome. Actually, the hypothesis of (non-)random mutation in a multipurpose genome predicts that in distinct subpopulations distinct traits that are not crucial for reproduction will be lost. Your muscles are nice examples. Thanks for that. If you have more examples, don't hesitate to mail!
Best wishes,
Peter

This message is a reply to:
 Message 20 by derwood, posted 10-01-2002 1:58 PM derwood has replied

Replies to this message:
 Message 24 by derwood, posted 10-02-2002 9:58 AM peter borger has replied

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


Message 22 of 43 (18779)
10-01-2002 11:34 PM
Reply to: Message 19 by Itzpapalotl
10-01-2002 10:45 AM


Dear Itz,
Thanks for your detailed response.
you write:
I did a bit of reading on the bacterial cytoskeleton and ended up finding out more interesting things about mitochondria. Bacteria do have a gene (FtsZ) that is similar to tubulin (the monomer that makes up microtubes) and so there was presumably a form of it in the universal common ancestor. This indicates that the eukaryotic ancestor could have had microtubules before endosymbiosis occured. The difference in much of the cellular machinery of mitochondria/bacteria and eukaryotes indicates they diverged substantially before endosymbiosis.
I say:
Usually random evolution ceases as soon as the endosymbiont is engulfed. For instance, mitochondrial DNA is similar in all eukaryotes. For instance, the mitochondria of metazoa usually contain 37 genes, including the one constituting ATPase, cytochrome (oxidase), rRNA's, 4 subunits of NADH dehydrogenase, 2 rRNA's and 22 tRNA's. It is said that the genes moved to the nucleus, but than it is expected to be a random process. We always find the same protein and RNA genes in the mitochondria. I become rather suspicious if one invokes a random mechanism plus selection. I propose an non-random mechanism (plus selection).
You say:
Although this is just speculations since microtubules are irrelevant to endosymbiosis it doesn't really matter in this context.
I say:
No, to enter the cell you need endocytosis or a similar mechanism. Probably your Nature example does not cover the complete story. I can be reasoned that the secondary endosymbiont uses the hosts cellular equipment to get in the primary endosymbiont. The nature article has to be confirmed, and next the mechanism has to be elucidated. Furtehrmore, the figures in the article are not able to demonstrate the direction of uptake, since they are static images. Finally, in the Nature article it is tacitly assumed that the secondary endosymbiont has been present before the first endosymbiont was engulfed by the eukaryotic cell of the host (the mealybug). However, that cannot be concluded from the data. I like to see evidence of freeliving endosymbiontic prokaryota. That would be more cinvincing.
You say:
The interesting thing about some mitochondria and all chloroplasts is that they use the products of bacterial FtsZ genes (most closely related to alpha-proteobacterial genes yet again) to divide. FtsZ has been lost in fungi animal and plant mitochondria in which division is mediated by dynamin a protein of eukaryotic origin but if FtsZ genes from mitochondria are put into organisms from which it has been lost the product interacts usefully with the mitochondria. Dynamin does seem to play a part in the division of intracellular parasitic bacteria such as Chlamydia that lack FtsZ.
I say:
Loss of genes sounds familiar.
You say:
Thanks peter B. without your post i wouldn't have looked into this area and found yet more compelling evidence in favour of endosymbiosis.
I say:
Thanks Itz for your contribution. At least this is a discussion.
best wishes,
Peter

This message is a reply to:
 Message 19 by Itzpapalotl, posted 10-01-2002 10:45 AM Itzpapalotl has replied

Replies to this message:
 Message 23 by Itzpapalotl, posted 10-02-2002 9:41 AM peter borger has replied

  
Itzpapalotl
Inactive Member


Message 23 of 43 (18833)
10-02-2002 9:41 AM
Reply to: Message 22 by peter borger
10-01-2002 11:34 PM


Ok i am prepared to conceed that it might be impossible for a bacteria to be engulfed by another one outside of a eukaryotic host but until all the questions about the mechanisms of secondary endosymbiosis have been answered and hopefully more examples discovered will be found the possiblilty remains that i am wrong. But at the moment even though we don't know everything i would say it's evidence that is in favour of my point of view rather than your's peter B.
The point that the organism that evolutionists think engulfed the pre-mitochondrial bacteria was not a modern bacterium and therfore almost certainly had at least a proto cytoskeleton (the fact it is present in a similar form in all eukaryotes suggests this is true) is still valid. If Peter B. can provide evidence in favour of the hypothesis that ancient eukaryotic cells did not have a microtubule cytoskeleton then wheather or not bacteria can engulf on another IS irrelevant. If the ancestor of eukayotes at the proposed time of endosymbiosis had a rigid membrane like modern bacteria then the issue of bacterial endosybiosis would without question be relevant.
Although the gene complement of mitochondria is very similar amoungst metazoans its not necessarily a result of a non random mechanism. There are examples of genes such as FtsZ that have been lost in some lineages but retained in others (the fact that FtsZ product interacts with mitochondria that have lost it is highly suggestive that they once had it). To determine if the process of gene transfer is random or not it would be best to look at plastids where several different endosymbiotic events are thought to have taken place and see if the process has transfer has proceeded along different lines. Also the genes contained within mitochondria are the most essential for respiration and maintainance of the mitochondria so those are the genes you would expect to find due to natural selection. There are probably a limited number of solutions to the problem 'what is the minimal mitochondrial genome ?', therefore a limited number of possible outcomes. The hypothesis advanced by evolutionists is that the major genetic changes happened very rapidly and early in eukaryotic evolution and once a small and fairly stable genome had been formed there was no reason for it to change alot. Also research on Buchnera aphidicola, the obligate endosymbionts of aphids has revealed that once an organism has lost phages repeated elements and the RecA systems the genome becomes extremely stable at least with respect to rearrangements (not gene inactivation, loss and sequence evolution though). Even if it could be demonstrated that the genome of mitochondria is the result of directed non random change, how they got there in the first place would still be a mystery and enosymbiosis the most likely explanation.
Peter B. you say: "Loss of genes sounds familiar."
i am not sure what point you making but yes loss of genes has been demonstrated many times in intracellular, endosymbiotic and parasitic organisms, organisms in a similar situation to the ancestor of mitochondria. But it doesn't challenge the main point of the paragraph that mitochondrial FtsZ proteins are very similar to alpha-probacterial bacteria believed to be closely related to the ancestors of mitochondria and therefore common ancestory is the most likely explanation.
There are still many questions that havn't been answered by the critics of endosymbiosis which basically can be summarised as 'if mitochondria were not bacteria why are there so many similarities'. Also no theory (as far as i am aware) about the origins of mitochondria has been advanced by the critics of endosymbiosis to account for the features of miotchondria. If there is a choice between two clear theories the evidence can be used to distinguish between the two not liking a theory means its possible to criticise a theory without having to face the same critical examination.

This message is a reply to:
 Message 22 by peter borger, posted 10-01-2002 11:34 PM peter borger has replied

Replies to this message:
 Message 25 by peter borger, posted 10-02-2002 8:25 PM Itzpapalotl has replied

  
derwood
Member (Idle past 1876 days)
Posts: 1457
Joined: 12-27-2001


Message 24 of 43 (18834)
10-02-2002 9:58 AM
Reply to: Message 21 by peter borger
10-01-2002 8:07 PM


quote:
Originally posted by peter borger:
Dear SLPx,
I can perfectly understand the loss of a trait that is not under selective constraint with a multipurpose genome.
"Multipurpose genome"?
LOL!!!
You cretins never cease to amaze me....
Funny - it seems like your 'multipurpose genome' is the same thing that evolution postulates. Just like the 'baraminologists' clai that descent with modification via mutation and recombinations and such works, just like in evolution... They just put arbitrary limits on how far they will let this go...
quote:
Actually, the hypothesis of (non-)random mutation in a multipurpose genome predicts that in distinct subpopulations distinct traits that are not crucial for reproduction will be lost. Your muscles are nice examples. Thanks for that. If you have more examples, don't hesitate to mail!
Best wishes,
Peter
Oh, look! The creationmist is yet AGAIN taking evidence for evolution and claiming that it is REALLY evidence for his alternative!
Wow, you should hook up with another non-geneticist, non-biologist creationist Walter "Crazy Wally" ReMine. He does the same thing. And he, like you, refuses to actually tell anyone his 'testable' predictions...
Well, anyway, I will have to conclude that you simply cannot address the issue of vestigiality witrh anything other than the simpleminded creationist mantra about 'science disproofing vestiges' or whatever idiocy it is...

This message is a reply to:
 Message 21 by peter borger, posted 10-01-2002 8:07 PM peter borger has replied

Replies to this message:
 Message 27 by peter borger, posted 10-02-2002 10:19 PM derwood has not replied

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


Message 25 of 43 (18915)
10-02-2002 8:25 PM
Reply to: Message 23 by Itzpapalotl
10-02-2002 9:41 AM


dear Itz,
For convenience let's imagine that a prokaryote is engulfed by another prokaryote by the mechanism of endocytosis. The ATPases that translocate H+ ions will be orientated in such way that both endosymbiont and host are pumping them into the periplasmatic space (both organisms have a membrane, remember), that will induce a decrease in pH. The acididy will immediately kill the endosymbiont. How does proponenets of endosymbioses overcome this problem? Loss of genes?
best wishes,
Peter
[This message has been edited by peter borger, 10-02-2002]

This message is a reply to:
 Message 23 by Itzpapalotl, posted 10-02-2002 9:41 AM Itzpapalotl has replied

Replies to this message:
 Message 26 by Itzpapalotl, posted 10-02-2002 10:08 PM peter borger has not replied

  
Itzpapalotl
Inactive Member


Message 26 of 43 (18929)
10-02-2002 10:08 PM
Reply to: Message 25 by peter borger
10-02-2002 8:25 PM


Hi peter B.
Although your objection does provide an interesting theoretical block to endosymbiosis there are many observations that suggest that in practice there is not a problem. The previously mentioned secondary endosymbiotic bacteria have not been killed by low PH. A better model for mitochondrial and plastid endosymbiosis, rather than two prokaryotes is a eukaryote and a prokaryote especially intracellular parasites such as Rickettsia prowazekii which are thought to be the closest living relatives of mitochondria. These Rickettsia bacteria have also not been killed by low PH. In amoeba an endosymbiotic bacterium that can be a pathon has been found to have adapted perfectly happily to an intracellular lifestyle in some strains. In algae there are also examples of tertiary endosybiosis, that is they engulfed an organism that already contained mitochondria and plastids and made use of them. Also the relationship was not necessarily beneficial at first and could have been a form of parasitism in which case mechanisms to evade host toxicity would have evolved. So real life observations of intracellular bacteria and secondary endosymbiotic bacteria show no toxicity or immediated death.
As entertaining as defending the endosymbiosis theory is it would provide some variation if you could provide an explanation as to the origin of mitochondria and/or plastids and the evidence for it. I would also be curious as to the theoretical/philosophical basis of your objections to endosymbiosis.

This message is a reply to:
 Message 25 by peter borger, posted 10-02-2002 8:25 PM peter borger has not replied

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


Message 27 of 43 (18930)
10-02-2002 10:19 PM
Reply to: Message 24 by derwood
10-02-2002 9:58 AM


Dear SLPx,
You wrote:
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
Dear SLPx,
I can perfectly understand the loss of a trait that is not under selective constraint with a multipurpose genome.
--------------------------------------------------------------------------------
"Multipurpose genome"?
LOL!!!
I say:
Actually I can provide biological evidence for a multipurpose genome. I will do that, but not on this board (always save the best for later).
You cretins.....
I say:
Inhabitants of Crete?
...never cease to amaze me....
You:
Funny - it seems like your 'multipurpose genome' is the same thing that evolution postulates.
I say:
Exactly, it can explain what evolutionism explains and more. Yes, evolutionism has to postulate it to explain genetic robustness due to redundant networks. However, it cannot explain why these networks are stable in the genome. In fact they aren't stable in the genome, but over time they will be lost. Loss of genes is a prediction of the hypothesis of the multipurpose genome. Gain of redundant genes is a something I like to have an evolutionary explanation for, since there is no association between genetic redundancies and gene duplication (you also rather ignore this, although I have reiterated it several times in several threads).
You:
Just like the 'baraminologists' clai that descent with modification via mutation and recombinations and such works, just like in evolution... They just put arbitrary limits on how far they will let this go...
quote:
--------------------------------------------------------------------------------
Actually, the hypothesis of (non-)random mutation in a multipurpose genome predicts that in distinct subpopulations distinct traits that are not crucial for reproduction will be lost. Your muscles are nice examples. Thanks for that. If you have more examples, don't hesitate to mail!
Best wishes,
Peter
--------------------------------------------------------------------------------
Oh, look! The creationmist is yet AGAIN taking evidence for evolution and claiming that it is REALLY evidence for his alternative!
I say:
The hypothesis of non-random mutations in a multipurpose genome can explain all observations that evolutionism can explain. It also explains genetic redundancies. And don't pretend that evolutionism is able to explain genetic redundancies since it cannot. I gave you already the example of the alpha-actinins, and where they conflict NDT. I tried to discuss this topic with theoretical biologist Dr. Wagner, but he never responded to my mails. Better get used to the idea of a multipurpose genome.
You again with the familiar stuff:
Wow, you should hook up with another non-geneticist, non-biologist creationist Walter "Crazy Wally" ReMine. He does the same thing. And he, like you, refuses to actually tell anyone his 'testable' predictions...
I say:
I could do a testable prediction what is expected to be found in the human genome by applying molecular rules of evolutionism (it involves high abundance gene, think about it). If it is not found = QED.
You:
Well, anyway, I will have to conclude that you simply cannot address the issue of vestigiality witrh anything other than the simpleminded creationist mantra about 'science disproofing vestiges' or whatever idiocy it is...
I say:
I gave you a perfectly valid alternative explanation.
BTW, I thought you liked mantra's?
Best wishes,
Peter
[This message has been edited by peter borger, 10-02-2002]

This message is a reply to:
 Message 24 by derwood, posted 10-02-2002 9:58 AM derwood has not replied

Replies to this message:
 Message 28 by Quetzal, posted 10-03-2002 4:39 AM peter borger has replied

  
Quetzal
Member (Idle past 5872 days)
Posts: 3228
Joined: 01-09-2002


Message 28 of 43 (18964)
10-03-2002 4:39 AM
Reply to: Message 27 by peter borger
10-02-2002 10:19 PM


Only one little bit here, Peter:
quote:
Actually I can provide biological evidence for a multipurpose genome.
If you truly can provide solid evidence for a multipurpose genome, you would rock the world of biology to its foundation. However, simply asserting it doesn't make it so - even on a discussion board. What is your hesitation about providing at least a hint of your evidence? Afraid someone will steal your Nobel Prize? Science isn't a trial where the results might be biased by premature exposure. Perhaps you'd care to at least give us an idea of what kind of evidence your dealing with?
Also, it would significantly bolster your case here in the numerous threads in which you are involved. You continually use the "multipurpose genome" as evidence for your position, yet have thus far not provided any reason for anyone to take the idea seriously. Just a side comment.

This message is a reply to:
 Message 27 by peter borger, posted 10-02-2002 10:19 PM peter borger has replied

Replies to this message:
 Message 29 by peter borger, posted 10-08-2002 3:09 AM Quetzal has replied

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


Message 29 of 43 (19287)
10-08-2002 3:09 AM
Reply to: Message 28 by Quetzal
10-03-2002 4:39 AM


Dear Quetzal,
You say:
If you truly can provide solid evidence for a multipurpose genome, you would rock the world of biology to its foundation. However, simply asserting it doesn't make it so - even on a discussion board. What is your hesitation about providing at least a hint of your evidence? Afraid someone will steal your Nobel Prize? Science isn't a trial where the results might be biased by premature exposure. Perhaps you'd care to at least give us an idea of what kind of evidence your dealing with?
I say:
The first hint in the direction of a multipurpose genome is the presence of genetic redundancies. Up to >90% of the genes of organisms can be redundant. It is one of the big surprises of contemporary biology/genetics. Evolutionary biologists try to explain this by assuming very weak purifying selection. I don't believe in very weak purifying selection. And if you have a careful look at certain redundant genes one can only explain them by assuming neutral selection. It is nothing, so the evolution theory cannot explain this phenomenon. A multipurpose genome can, though. It could be evidence for creation, since the genes reside in the genome without selection. Moreover, how did redundant genes evolve without selection? How can it be that they are 'as stable as essential genes'? These phenomena do not advocate evolution theory. On the contrary.
In the meantime I accidentally found biological evidence for the existence of this multipurpose genome. It concerns a phenomenon that cannot be explained by evolutionism, only by the MPG. I will not present it here, but I will try to get it published. Here I presented only some examples OF NON-RANDOM mutation for the sake of dicussion.
You say:
Also, it would significantly bolster your case here in the numerous threads in which you are involved. You continually use the "multipurpose genome" as evidence for your position, yet have thus far not provided any reason for anyone to take the idea seriously. Just a side comment.
I say:
'All' my postings made perfect sense. Maybe you didn't see it. The NON-random mutations in a multipurpose genome explains ALL biological observations --including genetic redundancies-- although it does not address the origin. It can also not be addressed by evolutionism, so what is the difference? I already mentioned that the ideas concerning the origin cannot be addressed by science, since it is obscured by genetic uncertainty. In my opinion the search for the origin of genes is useless.
Best wishes
Peter

This message is a reply to:
 Message 28 by Quetzal, posted 10-03-2002 4:39 AM Quetzal has replied

Replies to this message:
 Message 30 by Mammuthus, posted 10-08-2002 4:35 AM peter borger has replied
 Message 31 by Mammuthus, posted 10-08-2002 4:35 AM peter borger has not replied
 Message 32 by Mammuthus, posted 10-08-2002 4:35 AM peter borger has not replied
 Message 33 by Mammuthus, posted 10-08-2002 4:35 AM peter borger has not replied
 Message 34 by Quetzal, posted 10-08-2002 5:40 AM peter borger has not replied

  
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 30 of 43 (19288)
10-08-2002 4:35 AM
Reply to: Message 29 by peter borger
10-08-2002 3:09 AM


quote:
Originally posted by peter borger:
Dear Quetzal,
You say:
If you truly can provide solid evidence for a multipurpose genome, you would rock the world of biology to its foundation. However, simply asserting it doesn't make it so - even on a discussion board. What is your hesitation about providing at least a hint of your evidence? Afraid someone will steal your Nobel Prize? Science isn't a trial where the results might be biased by premature exposure. Perhaps you'd care to at least give us an idea of what kind of evidence your dealing with?
I say:
The first hint in the direction of a multipurpose genome is the presence of genetic redundancies. Up to >90% of the genes of organisms can be redundant. It is one of the big surprises of contemporary biology/genetics. Evolutionary biologists try to explain this by assuming very weak purifying selection. I don't believe in very weak purifying selection. And if you have a careful look at certain redundant genes one can only explain them by assuming neutral selection. It is nothing, so the evolution theory cannot explain this phenomenon. A multipurpose genome can, though. It could be evidence for creation, since the genes reside in the genome without selection. Moreover, how did redundant genes evolve without selection? How can it be that they are 'as stable as essential genes'? These phenomena do not advocate evolution theory. On the contrary.
In the meantime I accidentally found biological evidence for the existence of this multipurpose genome. It concerns a phenomenon that cannot be explained by evolutionism, only by the MPG. I will not present it here, but I will try to get it published. Here I presented only some examples OF NON-RANDOM mutation for the sake of dicussion.
You say:
Also, it would significantly bolster your case here in the numerous threads in which you are involved. You continually use the "multipurpose genome" as evidence for your position, yet have thus far not provided any reason for anyone to take the idea seriously. Just a side comment.
I say:
'All' my postings made perfect sense. Maybe you didn't see it. The NON-random mutations in a multipurpose genome explains ALL biological observations --including genetic redundancies-- although it does not address the origin. It can also not be addressed by evolutionism, so what is the difference? I already mentioned that the ideas concerning the origin cannot be addressed by science, since it is obscured by genetic uncertainty. In my opinion the search for the origin of genes is useless.
Best wishes
Peter

*********************************
Hi Peter,
You never addressed my critiques of your proposition. However, please list for me one "purpose" of the genome outside of self replication. Your term multipurpose does not really suggest anything to me. Is my genome there to make a strong cup of coffee on Tuesdays and as another purpose to type on a keyboard? As for redundant genes, there are many examples of how recombination and transposable elements leads to gene duplications which can turn out to be extremely useful i.e. syncytin, or the genes for red and green color vision etc. I also find it disturbing that you claim that your ill defined hypothesis explains ALL biological principles and then claim you will not describe it here. It in no way explains why cytochrome b of mammoths is most similar to that of living elephants as opposed to marmosets. There are no predicitions you could make with your hypothesis either. You just say that redundant genes are evidnece that some mythical god waved his beard at DNA and created everthing a million years ago, 1 year ago, 5 minutes ago? If you actually DID some research you would find that redundant genes have been studied and known about for decades and is in no way a problem for evolution. Those that assume a novel function under a changed environment or even provide an advantage to the organism are fixed, some are fixed and maintained by drift, low mutation rate, and lack of recombination, others like many psuedogenes decay until they are barely recognizable as such. Your hypothesis would not even tolerate pseudogenes.
Most of us have been very forthcoming in our providing you with information, references, links, etc. and you claim that you will not reciprocate.
By the way, there are way more Paabo references regarding sub population genetic diversity. I chose the Kaessmann work because he focused on nuclear DNA. But just type Paabo S into medline and you will hit the relevant papers by scrolling through.
Cheers, M

This message is a reply to:
 Message 29 by peter borger, posted 10-08-2002 3:09 AM peter borger has replied

Replies to this message:
 Message 35 by peter borger, posted 10-10-2002 4:31 AM Mammuthus has replied

  
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