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Chromosome Fussion


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Poll: Is Chromosome fussion a myth of demonstrated mechanism in TOE? (6 member(s) have cast votes)

Is Chromosome fussion a myth of demonstrated mechanism in TOE?

  1. 1. It's a myth with no empirical basis. (4 votes [66.67%])

    Percentage of vote: 66.67%

  2. 2. It's a proven evoltutionary mechanism. (1 votes [16.67%])

    Percentage of vote: 16.67%

  3. 3. Other (explain) (1 votes [16.67%])

    Percentage of vote: 16.67%

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#21 Phaedrus

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Posted 29 August 2005 - 04:20 PM

I find several things wrong with this (and your paragraph on chimpanzees and humans).  You seem to be confusing form with content, the chromosomes being the 'form', and the genes the 'content'.  A lengthy novel may be published in multiple volumes, but regardless of the number of volumes, it's still the same story. The chromosomes are analogous to the volumes rather than to the story itself. There are a number of genetic disorders (thousands actually) that are caused by chromosomal abnormalities -- Down's syndrome being a well-known example -- but these are mostly analogous to 'volumes' being improperly distributed. The fact that individuals are able even to survive at all with these abnormalities suggests that there is more freedom for error than you appear to realize (Down's syndrome females have, though rarely, even been able to produce children).


Chromosome form:

How genes and chromosomes are built is what genetics is all about. From the early transcription of the DNA to the fully formed chromosome there are a number of checkpoints. Just before the cell completely splits during the anaphase is the spindle assembly checkpoint. Here the spindle must be built, the chromosomes must attached to the spindle and the chromosomes must aligned down the center. When the duplication process malforms it results in ASPM (abnormal spindle-like microcephaly associated) which results in a 70% reduction in brain size.

Gene function:

"The analysis of the most dramatic of these duplications, affecting 10% of human Chromosome 2, enabled a detailed reconstruction of the events leading to the appearance of a novel gene family. "

(Complex genomic rearrangements lead to novel primate gene function, linked below)

For this fusion (sorry about the typos earlier) to occur we are talking about no less the 22 gene duplications in a section covering 10% of Chromosome 2. You might be interested to know that Down's syndrome is due to the overexpression of genes. My point being that there are hazards to dramatic changes in the form and function of chromosomes. In order to put this into perspective lets try to grasp just what would have been effected and how:

"The eight members of this family originated from the highly conserved nucleoporin RanBP2 by several genetic rearrangements such as segmental duplications, inversions, translocations, exon loss, and domain accretion. "

Complex genomic rearrangements lead to novel primate gene function.

Ok, we have eight genes in a highly conserved region undergoing at least half a dozen genetic rearrangements. For a region to be considered highly conserved it must be very resistant to changes on this level and they seemed to have happened in a relativly short space of time. It seems to me that evolutionists would be in awe at the enormous changes that occured. As a creationist I am simply unconvinced that such changes are remotely possible without catastrophic conseqeunces like the ASPM gene and Down's syndrome.


And I'm not sure why you feel (if I correctly assess that as your implication) that such a splicing would necessarily take place at the centromere, or why it is 'damage to the spindle' that would be of primary concern; it seems to me that the spindle is much more likely to damage the chromosomes (that is, to botch their distribution) than to be damaged by them.


These changes were in close proximity to the centemere region. Bear in mind that these are just some of the more dramatic changes that would have had to occur, there are many others.In Chromosome 6 the centromere would have had to be moved not once but twice:

. "Contrary to this simple evolutionary scenario, however, the centromere was found to be located in three distinct regions, without any evidence of chromosomal rearrangement that would account for its movement. One of the two centromere repositioning events occurred in great apes ancestor."

Chromosome 6 Phylogeny in Primates and Centromere Repositioning

There is a reason that changes in and around the centromere can cause serious problems for the spindle alingment. If for whatever reason the centromere and the spindle don't line up properly the consequences can be devastating.

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And random chance (by definition) couldn't possibly care a fig about what 'you want' anyway; if it doesn't work, it simply gets selected out.


Random chance has nothing to do with how genes and chromosomes are duplicated. Now the recombination of genes are another matter and there is a natural process by which traits derived from favorable combinations get preserved while less favorable one simply don't survive. The genes are not changed much at all but how they are expressed changes greatly.

And (sorry, but this is really bugging me) it's: fusion.


Sorry about that, I really should edit my posts more carefully.

Well, I wouldn't -- but you might be surprised at how liberally some taxonomists have been willing to apply the species distinction. Using infertility as the sole criterion is the most conservative apporoach. For many biologists, any barrier to interbreeding may suffice, such as a behavioral or geological barrier.  For them, it doesn't matter so much why two groups aren't interbreeding as long as it is clear that they aren't interbreeding (neither fertility nor infertility can always be regarded with confidence as all-or-nothing propositions anyway). It's a judgement call.

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Actually, I would say it's like arranging the documents on your hard drive. You will organize then in such a way as to make them easier for you to use them. When Aristotle organized and classified animals in his own way that seemed fine untill the discovery of the New World. Then we had all of these different animals that had changed dramatically over time. I was reading a thing on the taxonomic classification of birds and it was interesting how simple or sophisiticated it could be. It all depends on what you are trying to organize into catagories. The more details you are organizing, the more complicated the taxonomic catagories will get. Taxonomic catagories are not objective, they are completly subjective. They are organized from the perspective of the observer and they are simply meant to make retrival easier.

In other words, taxonomy was made for man not man for taxonomy. :lol:

#22 Guest_Calipithecus_*

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Posted 29 August 2005 - 05:33 PM

It seems to me that evolutionists would be in awe at the enormous changes that occured.

I think creationists often have a tendency to underestimate the scientist's capacity for awe.

These changes were in close proximity to the centemere region.

Wait. Are you talking about chromosome 6, or are you still talking about chromosome 2? The article I linked indicates telomere-to-telomere fusion in chromosome 2. For some reason (looks like munged script, but it could be something local to my system) I am unable to retrieve the article, "Complex genomic rearrangements lead to novel primate gene function" from the link you provided.


If for whatever reason the centromere and the spindle don't line up properly the consequences can be devastating.

I agree. The process being as complex as it is, it doesn't come as a big surprise that it appears to happen all the time. But again, so what?


Random chance has nothing to do with how genes and chromosomes are duplicated.

Yet we observe that the duplication does not always proceed exactly the same way every time. How do you explain that?


Taxonomic catagories are not objective, they are completly subjective.

Yes, I agree. As if that weren't bad enough, just about any attempt to categorize anything perfectly -- so that every single bona-fide member is included while every non-member is excluded -- seems to ultimately suffer from the same weakness.


QUOTE: And (sorry, but this is really bugging me) it's: fusion.

Sorry about that, I really should edit my posts more carefully.

In this context, I cannot resist the temptation to point out that the word: fussion looks a lot like what you'd get if you took fission and fusion and, well, fused them (though I cannot imagine what the details would be regarding the sort of process that might produce such a mutant).

#23 Phaedrus

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Posted 29 August 2005 - 06:07 PM

I think creationists often have a tendency to underestimate the scientist's capacity for awe.


It is just that often when I encounter scientists in cyberspace they act like this is no big supprise which really puzzles me.

Wait. Are you talking about chromosome 6, or are you still talking about chromosome 2? The article I linked indicates telomere-to-telomere fusion in chromosome 2.  For some reason (looks like munged script, but it could be something local to my system) I am unable to retrieve the article, "Complex genomic rearrangements lead to novel primate gene function" from the link you provided.


Actually, I was talking about the centromere and it relationship to the spindle. I'm not really sure what the problem is with the link but its just an abstract. I found the article in full some time ago but it has been a while since I read it.


I agree.  The process being as complex as it is, it doesn't come as a big surprise that it appears to happen all the time.  But again, so what?


No it does not happen all of the time in highly conserved regions. What is more there would have had to be stabilizing selection to create the stasis that the human genome is now experiencing. Finally, either functional constraint or extraordinary positive selection would have had to have happened for changes like this to have occured. By the way, you completely bypassed the pitfalls of changes to the chromosome form and function.

Yet we observe that the duplication does not always proceed exactly the same way every time.  How do you explain that?


We are not really sure how gene duplication happens even though it has been observed on a micro level. The main obstacle is to keep the reading frame open as it was in the nylon bug that is thought to be such a great example of evolution. I'll buy an occasional nucleotide substitution having a beneficial effect from time to time but most often they are very marginal changes. The fact is that highly conserved regions don't undergo this kind of massive rearrangement, that is why they are highly conserved.

Yes, I agree.  As if that weren't bad enough, just about any attempt to categorize anything perfectly -- so that every single bona-fide member is included while every non-member is excluded -- seems to ultimately suffer from the same weakness.

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The nice thing about it is that you can organize it anyway that makes it easier to retrieve the information. Bear in mind that we are not just a different species from the chimpanzee we are a whole other genus. There are so many differences in the respective genomes that it must give evolutionary biologists fits trying to account for the differences. I think seperate lineages would make so much more sense that I am dumfounded that scientists have not explored this option. I mean seriously, it would not be all that hard to account for the differences between old and new world monkeys but apes to humans is a whole lot harder.

There is no genetic basis for these transitions and the problem is genome wide.

#24 Guest_Calipithecus_*

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Posted 29 August 2005 - 08:22 PM

No it does not happen all of the time in highly conserved regions. What is more there would have had to be stabilizing selection to create the stasis that the human genome is now experiencing. Finally, either functional constraint or extraordinary positive selection would have had to have happened for changes like this to have occured. By the way, you completely bypassed the pitfalls of changes to the chromosome form and function.

I don't think you grasped what I was saying there. What I'm saying is this:

Out of all of the eggs that become fertilized embryos, a large number will fail to develop, and a large number of those failures will be the result of chromosomal aberrations. Of those that do successfully complete the process of development, some number (a much smaller number) will also exhibit chromosomal aberrations. Of the individuals that manage to develop despite chromosomal aberrations, a large number will fail to to produce fertile offspring. None of these, up to this point, offers anything on which stabilizing selection might operate; the compromised 'form and function' resulting from their chromosomal aberrations will have rendered them evolutionary dead-ends. If any remain who are able to produce fertile offspring despite chromosomal aberrations, they will (I'm saying) fall into two categories: those whose chromosomal aberrations render them less productive as breeders, and those whose chromosomal aberrations have no effect on the number of offspring they produce (inversions, for example, are fairly common in many species, but usually do not compromise fertility).

Bear in mind that we are not just a different species from the chimpanzee we are a whole other genus.

I'm a little surprised to see you make a statement like that with so much apparent confidence so soon after we reached such a nice agreement that taxonomic categories are completely subjective. Attempts to empirically falsify the hypothesis that humans and chimps are separate species by the 'biological species' definition have yet to be reported on in scientific journals (finding willing human subjects for such experiments might be difficult, but I cannot imagine that would be entirely impossible, though interesting questions do arise as to the legal status of the results of any such experiments which succeed in falsifying the hypothesis, however).


There are so many differences in the respective genomes that it must give evolutionary biologists fits trying to account for the differences. I think seperate lineages would make so much more sense that I am dumfounded that scientists have not explored this option.

Well, that idea has been tried. But it is not merely the degree of similarity between (say) humans and chimps that leads to the conclusion that they share ancestry; it is the nature of some of the similarities that would be so hard to account for under a 'separate lineages' model. Genome wide, it is not only in the 'coding' regions that similarities are seen, but in the non-coding regions as well (in fact, similarities in non-coding regions are the most convincing, as they are invisible to selection). Similarities in chromosomal structure would also be difficult to explain under separate lineages. The example you began this thread with is an excellent one. The separate lineages model might reasonably be rejected solely on the basis of the evidence of the similarities we see between human and chimpanzee chromosome 2.

#25 John Paul

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Posted 29 August 2005 - 09:26 PM

Cal:
I chose to ignore it not only because I found its scope too broad, but because it was so transparently a diversionary tactic; a distraction from the questions I asked in the thread we already had going on the topic, questions which you went to such lengths to avoid.


Scope too broad? Just pick one area of evidence and focus on it.

Diversionary tactic? I started it to avoid the diversion you created with your fluff-n-stuff philosophical nonsense.

It all boils down to the evidence...

Cal:
You wanna talk about chromosomes, or what?


Actually I was doing just that until you took us down a tangent.

#26 Phaedrus

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Posted 30 August 2005 - 12:35 PM

I don't think you grasped what I was saying there.  What I'm saying is this:

Out of all of the eggs that become fertilized embryos, a large number will fail to develop, and a large number of those failures will be the result of chromosomal aberrations. Of those that do successfully complete the process of development, some number (a much smaller number) will also exhibit chromosomal aberrations. Of the individuals that manage to develop despite chromosomal aberrations, a large number will fail to to produce fertile offspring. None of these, up to this point, offers anything on which stabilizing selection might operate; the compromised 'form and function' resulting from their chromosomal aberrations will have rendered them evolutionary dead-ends. If any remain who are able to produce fertile offspring despite chromosomal aberrations, they will (I'm saying) fall into two categories: those whose chromosomal aberrations render them less productive as breeders, and those whose chromosomal aberrations have no effect on the number of offspring they produce (inversions, for example, are fairly common in many species, but usually do not compromise fertility).


These would have to be germline mutations that result in segmental duplications, inversions, translocations, exon loss, and domain accretion being fixed genome wide. We are not just talking about a viable embryo, there are checkpoints in the cell cycle that check for transcript errors in the DNA. The S phase is where the DNA is replicated in the cell cycle and there is a checkpoint that insures that the replication is without error. It’s like a quality control inspection in the G2 phase where the cell cycle is stopped. There is another one at the apoptosis checkpoint where if the enzyme survivin has not accumulated, cell death is automatic. There is the remote possiblity that it could happen during the cleavage stage but it is not without it's difficulties:

"Given the hierarchical, step-wise logic or "architecture" of animal development, early stages such as cleavage and gastrulation lay the groundwork for all that follows. Body plan structures in the adult, for example, trace their cellular lineage to these early stages. Thus, if macroevolution is going to occur, it must begin in early development. Yet it is precisely here, in early development, that organisms are least tolerant of mutations. Furthermore, the adult homologies shared by these vertebrates commence at remarkably different points (e.g., cleavage patterns). How then did these different starting points evolve from a common ancestor?" (see Cleavage Stage)

The point being that it would have to be a germline mutation that is screened through the cell cycle checkpoints.


I'm a little surprised to see you make a statement like that with so much apparent confidence so soon after we reached such a nice agreement that taxonomic categories are completely subjective.  Attempts to empirically falsify the hypothesis that humans and chimps are separate species by the 'biological species' definition have yet to be reported on in scientific journals (finding willing human subjects for such experiments might be difficult, but I cannot imagine that would be entirely impossible, though interesting questions do arise as to the legal status of the results of any such experiments which succeed in falsifying the hypothesis, however).


I still agree that taxonomic groups are subjective but the differences between Chimpanzees and humans is far greater then we have been led to believe. I certainly hope you are not suggesting the deliberatly creating germline mutations would further the cause of science. The experiments they do to explore the various hypothesis are done with BAC clones. I am not really sure what they are except that it is some kind of an annealing process.

Well, that idea has been tried.  But it is not merely the degree of similarity between (say) humans and chimps that leads to the conclusion that they share ancestry; it is the nature of some of the similarities that would be so hard to account for under a 'separate lineages' model.  Genome wide, it is not only in the 'coding' regions that similarities are seen, but in the non-coding regions as well (in fact, similarities in non-coding regions are the most convincing, as they are invisible to selection).  Similarities in chromosomal structure would also be difficult to explain under separate lineages.  The example you began this thread with is an excellent one. The separate lineages model might reasonably be rejected solely on the basis of the evidence of the similarities we see between human and chimpanzee chromosome 2.

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Actually, the seperate lineage model is rejected apriori under the single common ancestor model. Don't get me wrong I am well aware of the simularity in the comparison of the region that is believed to have merged. What is more, I realize that gene duplication has been observed and demonstrated just not on this level. What I am saying is that this would be an extraordinary development and there would be far more consequences then benefits for the populations.

Now as far as simularities (homology) in the chromosomes the closer you look at the comparative genomes the greater the differences. Again, there could only be two possible explanations for this overhaul of the genome for us to have a common lineage with the chimpanzee, monkeys and ulitmatly all mammals. One, relaxed functional constraint which allows changes in the functional genome to be altered. Two, intense positive selection that is providing such an advantage that results that it is fixed and stablized genome wide.

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Posted 30 August 2005 - 03:57 PM

there are checkpoints in the cell cycle that check for transcript errors in the DNA.

But that has nothing to do with chromosomal rearrangements.


I certainly hope you are not suggesting the deliberatly creating germline mutations would further the cause of science.

Actually, I was just making an attempt at a little light humor.


The experiments they do to explore the various hypothesis are done with BAC clones. I am not really sure what they are except that it is some kind of an annealing process.

It stands for: "Bacterial Artificial Chromosome". (The type of experiment I was referring to is, of course, of an entirely different nature).


Now as far as simularities (homology) in the chromosomes the closer you look at the comparative genomes the greater the differences

You're mixing form and content again. Homologies in chromosomal arrangements and homologies in genomes are two entirely different things.


Actually, the seperate lineage model is rejected apriori under the single common ancestor model.

And the single common ancestor model is rejected a priori under the separate lineage model. So what we do is, we look at the evidence and see which model it seems to support.




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