Endosymbiont theory wrong?

dear I,You say:
"This paper really doesn't challenge endosybiosis at all..I say:
Of course it doesn't, because nothing can challenge --let alone falsify-- evolution theory. I think I will let you dream on"And you say:
"..it says that these parasites did't diverge from other eukaryotes before the gain of mitochondria. In fact it makes sense that a parasite that gets all of its energy from its host would have smaller or vestigial mitochondria."I say:
It makes sense indeed, but it cannot be used to support evolution. If it demonstrates anything it is de-evolution.
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.Best wishes,
Peter

dear I,
Thanks for the references.
I will have a close look at them.
Best wishes.
Peter

Dear Peter,How can somebody understand something that isn't?Best wishes.
Peter

Dear Peter,Nobody understands the ToE at the molecular level, or any level. Why? Because evolution doesn't exist. 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.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.I will always object to the nihilism underlying NDT. It's my main goal in life.best wishes,
Peter

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]

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

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

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]

Dear SLPx,You wrote:quote:
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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:
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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]

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

Dear mammuthus,You say:
You never addressed my critiques of your proposition.I say:
Still thinking about them.You say:
However, please list for me one "purpose" of the genome outside of self replication.I say:
Rapid adaptation to changing environment.Yos say:
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 say;
This hypotheis has been tested and falsified. There is no relationship whatsoever between genetic redundancies and duplications. Evolutionisms' biggest frustration: redundant genes unrelated to duplications. In addition, redundant genes do not change more rapidly than essential genes. How did redundant genes evolve into different genes, while there is no selective constraint on the genes? Answers not to be found within the evolutionary paradigm.You say:
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.I say:
All information an organism needs to adapt to an environment is already present in the genome. It only has to be activated. This can be in response to external stimuli. The activation may lead to gene shuffling (as recently observed in some bacteria), or maybe even to non-random mutations in promoters. The SNP we see in genes throughout the genome may be generated in a similar way due to a degenerate mechanism of gene shuffling, non-random mutation etc.You say:
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.I say:
First prediction:
The major part of the genome is not used (redundant). As a matter of fact that is wat we see.
Second prediction:
Mutations are introduced at the same spots within related species. As a matter of fact that is what we see, too.
Third prediction:
Mutations are the same with respect to nucleotide. That is also what we observe.You say:
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?I say:
There are species that demonstrate no variation at all with respect to DNA sequences (without being a clone), and one could interpret this phenomenon as created last year, last century. Whatever.You say:
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.I say:
Not tolerate pseudogenes? I do not deny the observed well established genetic phenomena. They are all included in the hypothesis. Duplication of genes, and the subsequent inactivation of genes to generate pseudogenes. I have no problems with that in my hype.You say:
Most of us have been very forthcoming in our providing you with information, references, links, etc. and you claim that you will not reciprocate.I say:
I was also very forthcoming in providing my vision, and backed it up with references. I am still thinking about it, and I let the ideas vintage. Of course, the new hype has to be polished.You say:
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.I say:
I know a great deal of Paabo's interesting work .Best wishes,
Peter