Also is there any other instance of a more "advanced" life form "losing" chromosomes?
How come we have 46 chromosomes and other primates have 48?
- Thread starter nietzschefan
- Start date
distantcube
Registered Member
I don't think the chromosomes were 'lost'. From memory, they fused together into a single chromosome.
Edit: htt p://w ww.evolutionpages.com/chromosome_2.htm
ht tp://w ww.gate.net/~rwms/hum_ape_chrom.html
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Just a random mutation?
From your second site:
We are perhaps a "domesticated human"?
From your second site:
We are perhaps a "domesticated human"?
I don't know exactly how chromosomal numbers change, but it obviously isn't unusual.
Take Down's syndrome, for example, which involves an additional chromosome.
Then there are sex-related chromosomal variations, such as people who have XXY or XYY, with an additional chromosome. There are also cases where a chromosome is missing, so a person might have just a single X chromosome.
Take Down's syndrome, for example, which involves an additional chromosome.
Then there are sex-related chromosomal variations, such as people who have XXY or XYY, with an additional chromosome. There are also cases where a chromosome is missing, so a person might have just a single X chromosome.
Well mosts primates don't have philosophers. Philosophers will cost you two chromosones. 
All natural mutations are random. From what I understand we have a lot of junk in our chromosones. But I am not an expert in this arena.
All natural mutations are random. From what I understand we have a lot of junk in our chromosones. But I am not an expert in this arena.
It was a chromosome fusion, http://godbegone.blogspot.com/2007/09/how-chimp-chromosome-2-proves-evolution.html
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That didn't explain "chromosome fusion" at all. How does this happen?
Centromeres are, as their name suggests, towards the center of a chromosome, and telomeres are at the two ends [kind of like an engine/caboose combo]. The centromeres are used by the spindle apparatus, and thin threads attach to them to help pull apart the replicating chromosome [which is incredibly long] to keep them from getting mixed up with other chromosomes that are also duplicating. The telomeres are to signal the end of the chromosome, and to keep it from sticking to another chromosome.
DNA is quite 'sticky', which is why the two halves stick together [review your chemistry for the Hydrogen bonding].
By accident, all kinds of mistakes can happen during the replication process, which are usually lethal to that particular cell.
One of the mistakes is that two chromosomes could become attached to each other, end to end, at the telomeres, which would stick together. Normally, that would prove to be a fatal mistake.
For a reason not yet understood, two primate chromosomes in the human ancestral lineage stuck together at the telomeres, but that mistake did not prove fatal, and instead appeared to present a slight advantage [positive mutation]. What that advantage was is not presently known. However, that individual which now had two chromosomes fused into one passed that mutation to his/her offspring, and it proliferated in the community of its clan due to the advantage it conferred, eventually being present in the entire clan and its descendants [likely an early Homo or Austrolopithecus genus].
It would be interesting if we could ever extract DNA from preserved Homo bones [like we've done from some T-Rex bones] to determine if they had that mutation. When exactly it occurred is not presently known, though there will likely be some effort at genetic-clock analysis to determine that dating.
What is quite interesting is that the DNA from the two combined chromosomes matches almost exactly with the two separate chromosomes in the other primates.
The retrovirus-markers, which are present in the primates showing infected DNA passed to offspring and eventually existing in the entire community/species are also present in the human lineage in the same locations. Since they provide no net benefit or detriment, they are part of the 'junk' DNA that we share in common with the primates, showing our common linkage in our ancient ancestors.
Creationists, of course, have to account for this evidence [as they do for all other evidence of evolution] by asserting that the 'Creator' deceptively made these changes to make it appear as if evolution had occurred, when it had not, as a test of our faith. Either way, it is interesting to keep looking and finding these evidences of evolution.
DNA is quite 'sticky', which is why the two halves stick together [review your chemistry for the Hydrogen bonding].
By accident, all kinds of mistakes can happen during the replication process, which are usually lethal to that particular cell.
One of the mistakes is that two chromosomes could become attached to each other, end to end, at the telomeres, which would stick together. Normally, that would prove to be a fatal mistake.
For a reason not yet understood, two primate chromosomes in the human ancestral lineage stuck together at the telomeres, but that mistake did not prove fatal, and instead appeared to present a slight advantage [positive mutation]. What that advantage was is not presently known. However, that individual which now had two chromosomes fused into one passed that mutation to his/her offspring, and it proliferated in the community of its clan due to the advantage it conferred, eventually being present in the entire clan and its descendants [likely an early Homo or Austrolopithecus genus].
It would be interesting if we could ever extract DNA from preserved Homo bones [like we've done from some T-Rex bones] to determine if they had that mutation. When exactly it occurred is not presently known, though there will likely be some effort at genetic-clock analysis to determine that dating.
What is quite interesting is that the DNA from the two combined chromosomes matches almost exactly with the two separate chromosomes in the other primates.
The retrovirus-markers, which are present in the primates showing infected DNA passed to offspring and eventually existing in the entire community/species are also present in the human lineage in the same locations. Since they provide no net benefit or detriment, they are part of the 'junk' DNA that we share in common with the primates, showing our common linkage in our ancient ancestors.
Creationists, of course, have to account for this evidence [as they do for all other evidence of evolution] by asserting that the 'Creator' deceptively made these changes to make it appear as if evolution had occurred, when it had not, as a test of our faith. Either way, it is interesting to keep looking and finding these evidences of evolution.
Thanks Walter.
I'm not really interested in a creationist viewpoint on this, frankly it seems to make controversy where there is none.
Does anyone know the kinds of things that chromosome-2(the fused one?) controls? Like headshape? Voicebox? Losing the opposable toe?
I'm not really interested in a creationist viewpoint on this, frankly it seems to make controversy where there is none.
Does anyone know the kinds of things that chromosome-2(the fused one?) controls? Like headshape? Voicebox? Losing the opposable toe?
Fraggle Rocker
Staff member
Horses and donkeys have different numbers of chromosomes and they are not only species within the same order (perissodactyls, analogous to primates) but they are in the same genus Equus, analogous to Homo. It's as if Neanderthals and modern humans had different numbers.
I think I read somewhere Neanderthals had 46 also, so whatever happened, probably happened to Homo Erectus or before that. They only have fossils of Home Erectus so far.
It is also possible that the mutation of two chromosomes becoming joined into one provided no net benefit, but that through a process called 'genetic drift', in essence by happenstance, it became the genotype for the entire species. It would be interesting to determine whether the joining of the two chromosomes might have served to inactivate a gene or genes, providing a benefit.
Have they analyzed the chromosomes to see which two were joined? Or did one chromosome split into two? That would require an entirely new centromere, which seems far less plausible, though not necessarily impossible.
This would be interesting as an example to try to isolate whether the joining provided a benefit, and if so, what that is.
Our chromosome 2 lines up almost exactly with the ape/chimp chromosomes known as "2p" and "2q", except for one large-ish sequence inversion, which must have happened sometime after chromosome fusion. Since the other great apes all have 2p and 2q, the join logically represents a join of those two in our lineage, not a split in all of theirs.
Incidentally, chromosomes splitting in two isn't that uncommon, Walter L. Wagner. There is a maximum stable length for a chromosome; if a chromosome becomes too large because of insertion/duplication mutations, then it almost inevitably breaks. And although centromeres are extremely useful for ensuring proper chromosome duplication/splitting during cell replication, they are NOT actually crucial -- so the chromosome has a decent chance of "surviving" until it acquires a centromeric sequence.
Incidentally, chromosomes splitting in two isn't that uncommon, Walter L. Wagner. There is a maximum stable length for a chromosome; if a chromosome becomes too large because of insertion/duplication mutations, then it almost inevitably breaks. And although centromeres are extremely useful for ensuring proper chromosome duplication/splitting during cell replication, they are NOT actually crucial -- so the chromosome has a decent chance of "surviving" until it acquires a centromeric sequence.
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Witness Intelligent Design.
Do you have any examples? How would a chromosome go about acquiring a centromeric sequence? I presume that as chromosomes lengthen over time, they would tend to 'break' and increase chromosome number, but I'm not certain how that occurs. Are all of the centromeres the same in chromosomes, or are there various different 'types'?
Likewise, are there various types of telomeres, or are they all alike?
Sorry, not ignoring questions, just hella busy right now. I'll give you the nutshell version first.
Telomeric sequences are pretty consistent from one species to the next -- the basic telomeric sequence is TTAGGG, repeated N number of times, where N can equal anything between 60 and 6000. This exact base sequence is shared with at least 100 other vertebrate species, and while other eukaryotes show some variation, it tends to be very similar and heavy on the guanine. Only the number of repeats really varies hugely between species.
And telomeres are built up by a ribonucleoprotien (a mixed structure of a protein and RNA) called telomerase, at the ends of chromosomes. The only reason we start losing bits off the telomeres as we age is that telomerase only tends to be active in germ cells -- the cells that become sperm & eggs, or spores, or whatever method that species uses to reproduce (in some species telomerase is active in other situations, but that is considerably more rare). So new chromosomes in the germline cells automatically get "capped off" with telomeres when a suitably scraggy end of a chromosome presents itself.
Centromeres are more complicated. There is no such thing as "a" centromeric sequence -- the only criteria are that the centromeric sequences be reasonably short, and multiply repetitive, and have sequences of a rough composition that cen proteins can attach to. (And yes, sometimes telomeres can act as centromeres, too -- they do in mouse chromosomes!) These can spontaneously appear as insertion and duplication mutations, from several different (very common) sources -- I'm perfectly willing to go into this if you're interested, just when I've got a little extra time.
Centromeres vary in humans from one chromosome to the next because the repetivite sequences come from different elements to start with -- and in fact, 19 of our chromosomes have several extra, nonfunctional "neocentromeres" -- which are generally kept inactivated by a couple of defense mechanisms that cells ahve developed, because having two active centromeres is another way that chromosomes break apart. Generally, if one of those neocentromeres becomes active and induces a chromosome breakage, it just results in a genetic disorder. However, on rare occasions, such a breakage leaves two perfectly functional smaller chromosomes and the person can continue on as normal -- with the standard small odds of passing that on to offspring, too.
I do have have to run, I have so much to do, but if I've just confused the issue more or failed to explain adequately, say something and I'll try to have a better go at it. Same if you want more info on anything.
Telomeric sequences are pretty consistent from one species to the next -- the basic telomeric sequence is TTAGGG, repeated N number of times, where N can equal anything between 60 and 6000. This exact base sequence is shared with at least 100 other vertebrate species, and while other eukaryotes show some variation, it tends to be very similar and heavy on the guanine. Only the number of repeats really varies hugely between species.
And telomeres are built up by a ribonucleoprotien (a mixed structure of a protein and RNA) called telomerase, at the ends of chromosomes. The only reason we start losing bits off the telomeres as we age is that telomerase only tends to be active in germ cells -- the cells that become sperm & eggs, or spores, or whatever method that species uses to reproduce (in some species telomerase is active in other situations, but that is considerably more rare). So new chromosomes in the germline cells automatically get "capped off" with telomeres when a suitably scraggy end of a chromosome presents itself.
Centromeres are more complicated. There is no such thing as "a" centromeric sequence -- the only criteria are that the centromeric sequences be reasonably short, and multiply repetitive, and have sequences of a rough composition that cen proteins can attach to. (And yes, sometimes telomeres can act as centromeres, too -- they do in mouse chromosomes!) These can spontaneously appear as insertion and duplication mutations, from several different (very common) sources -- I'm perfectly willing to go into this if you're interested, just when I've got a little extra time.
Centromeres vary in humans from one chromosome to the next because the repetivite sequences come from different elements to start with -- and in fact, 19 of our chromosomes have several extra, nonfunctional "neocentromeres" -- which are generally kept inactivated by a couple of defense mechanisms that cells ahve developed, because having two active centromeres is another way that chromosomes break apart. Generally, if one of those neocentromeres becomes active and induces a chromosome breakage, it just results in a genetic disorder. However, on rare occasions, such a breakage leaves two perfectly functional smaller chromosomes and the person can continue on as normal -- with the standard small odds of passing that on to offspring, too.
I do have have to run, I have so much to do, but if I've just confused the issue more or failed to explain adequately, say something and I'll try to have a better go at it. Same if you want more info on anything.