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Reproduction and Human evolution |
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| Feb19-12, 01:08 PM | #1 |
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Reproduction and Human evolution
Hey, I recently watched a video on YouTube by Kenneth Miller, The collapse of Intelligent Design.
One of the things he brought up in the lecture was a comparison between. Human and chimpanzee genome. What was specifically said was that we had 23 pairs of chromosomes while the chimp and all other apes had 24. What must have happened is that over the course of our evolution, two chromosomes in our common ancestors with the chimp must have fused. This was found to be the case, our chromosome #2 is this fused chromosome. What puzzles me is that before this mutation spread throughout the population that lead to us, it must have occurred in one individual to start. Now we get half our chromosomes from mum and half from dad. How did this Individual with 23 pairs reproduce given that everyone else in the population had 24? From what I remember from bio class, the chromosomes need to pair up. So how did this produce a viable offspring? What am I missing? Thanks. |
| Feb19-12, 01:23 PM | #2 |
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Evolution is change over time (and its thousands if not millions of years) occurring in a population or group of individuals in a particular environment. So changes occur in generations not in individuals. Of course I am not an expert in the field, maybe experts can comment on it. |
| Feb19-12, 01:44 PM | #3 |
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My problem was that you'd have a population with mostly 24 pairs of chromosomes with a handful (or one in the scenario i described in the OP) of individuals with 23. I'm have to assume that the 23's were breeding with the 24's so did all the offspring they had simply die? did the 23's get really lucky and keep finding each other? Basically, Am i wrong to think that our ancestors with 23 pairs cannot reproduce with those who had 24 pairs? |
| Feb19-12, 02:19 PM | #4 |
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Reproduction and Human evolution
Well Routaran, I too am no expert, and I’m sure the regular experts on this forum will respond eventually. But my understanding is that in its essentials, you are entirely right that any individual genetic mutation happens to an individual organism, but that organism has to have a sufficiently similar chromosomal layout to be able to breed with another member of the same species. This business of the fused chromosome two is something I have encountered before, and the particular issue you raise was not discussed when I encountered it. My strong speculation is that, where you are going wrong is in assuming that the fusion of chromosome two was itself a single mutation event. Exactly as thorium1010 suggested, significant evolutionary change is built up of many tiny incremental changes, and so too, would be my guess, was the fusion of chromosome two.
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| Feb19-12, 08:04 PM | #5 |
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| Feb19-12, 11:57 PM | #6 |
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This was originally posted bY bobze, so all credits go to him. |
| Feb20-12, 02:18 AM | #7 |
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I think that it has something to do with the fact that as long as all the genes are there in the correct proportions, then the organism will come out fine.
You can see in polyploidy that some organisms are haploid and have one set of chromosomes, some have 2 sets, some 3 and some 4. Generally the more sets they have the bigger they come out! But the point being, that if one gamete had 24 chromosomes and the other 23, as long as all the relevant genetic material was there in the correct proportions then the result is viable. |
| Feb20-12, 12:52 PM | #8 |
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Your assumption that two organisms with different chromosome counts cannot produce fertile offspring is incorrect. See the link below - there are at least two documented cases (one in sheep (Ref 7), one in horses (Ref 9)) where organisms with different chromosome counts produced fertile offspring.
http://www.gate.net/~rwms/hum_ape_chrom.html#5 |
| Feb20-12, 12:53 PM | #9 |
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"How did this Individual with 23 pairs reproduce given that everyone else in the population had 24?"
The following is from Monica Rodriguez of Stanford University: "As long as the information is all there, it mostly doesn't matter how it is packaged. The information that the ape has on the two 'split' chromosomes is the same as in our large chromosome 2. So even though we have one less chromosome, all of the information is still there. As I said before, this sort of chromosomal rearrangement actually happens in about 1 in every 1000 babies. It's called a Robertsonian translocation. A part of one chromosome joins together with another chromosome and just like with the ape chromosomes, no information is usually lost. So this person is completely normal despite having the translocation and one less chromosome. But this can be a problem when the person tries to have a baby. Half the time their children are fine. These kids are either normal or carry the translocation. Half of the time, though, a fertilized egg will inherit a missing or extra part of a chromosome. Most commonly, this results in a miscarriage." and "For example, wild horses have 33 pairs of chromosomes and domesticated ones have 32. This was a relatively recent change that happened because of the sort of translocation we are talking about. In fact, this happened recently enough that these animals can mate and have fertile horses. So there is plenty of evidence that this kind of thing (i.e., viable offspring from parents with different numbers of chromosomes due to translocation) happens. Read more and see some helpful diagrams from Dr. Barry Starr, also from Stanford, explaining how this works. |
| Feb21-12, 12:03 PM | #10 |
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Kenneth Miller, The collapse of Intelligent Design.
While I am not an advocate of Intelligent Design, neither am I swayed by Biological Evolution. The trokia of Biological Evolution is 1. Common descent 2. Random mutation 3. Natural selection Your conceptual experiment focuses on the weakest link of Biological Evolution - random mutation. How random can a mutation be if at a min a mating pair is required? This eludes to the same "random" mutation happening at least twice in a very short period of time. Obiter dictum - Biological Evolution works quite well when considering asexual reproduction. A lone "random" mutation can be perpetuated. However, with sexual reproduction a much great constraint is placed. |
| Feb21-12, 12:14 PM | #11 |
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| Feb21-12, 12:31 PM | #12 |
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(2) As I said above, this is simply not true. A single mutation can occur resulting in fusing two chromosomes to create 23 pairs, and this individual can then mate with another individual with 24 chromosome pairs and produce fertile offspring. See the references in my earlier post. |
| Feb21-12, 01:40 PM | #13 |
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Thoruim - I am not a biological wiz and perhaps I have it wrong.
With asexual reproduction - I actually mean perpetuation by cell division - a mutation happens and is moved forward without the requirement of a mating pair. This makes the perpetuation of a random mutation almost effortless. I am assuming, and perhaps this is wrong, that a mating pair is required to make a mutation viable. If my assumption is correct, and now I suspect it might not be, then a mating pair with the same "random" mutation" is needed to fit the same requirement. This is much more constraining. Not only is it much more constraining but most would not consider this event "random". |
| Feb21-12, 01:47 PM | #14 |
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Phyzguy - I am familiar with Robertsonian Translocation. Just because it occurs doesn't mean that in the case in question it happened but I am not debating that.
Again, I might be wrong, but I am assuming that for the mutation itself to be viable, it requires a mating pair with the same mutation. And yes you caught me out, it should be alludes, no thinking about it. |
| Feb21-12, 07:22 PM | #15 |
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A point mutation which changes an amino acid and alters the function of hemoglobin then, isn't going to inhibit mating by that "mutant" individual and another member of the population. |
| Feb21-12, 07:59 PM | #16 |
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Each chromosome has a centromere, which as a nucleation point for the kinetochore, who's job it is to aid in chromosome segregation during division. This centromere can be found in different places on the chromosome. ![]() In the case of acrocentric chromosomes they can fall in such a way that little, if any, necessary information lays on the short arm (if there even is one) of the chromosome. This can result then, in two acrocentric chromosomes fusing at the centromere with no loss of genetic material. ![]() Humans have a number of acrocentric chromosomes this could happen too; ![]() as did our ancestors (more on that later). For example, a fusion between chromosome 14 and 21 could occur; ![]() resulting in an offspring with karyotype on the right. While we consider this a "chromosomal abnormality", you'd never know it. The individual has all the necessary genetic information. If you met them on the street (and you very well could have as its estimated to occur in around 1.2% of births) you wouldn't know they were "chromosomally abnormal". What's important though again, is that the individual has all the necessary genetic information. And their offspring can potentially have it as well. How fused chromosomes arrange on the meiotic plate can get a little complex, so we'll leave that out for now. What's more important is the gametes that can be produced; ![]() I want you to focus on the second individual on the right there; with the gamete "t14/21". This gamete would produce an offspring who is a carrier also of the translocation, but like the parent remains unaffected by it (necessary genetic information again). Meaning the 45 chromosome parent can produce offspring with other members of the population ("normal individuals", or better "wild type") who also have 45 chromosomes. If any of these descendents happen to mate (two with 45 chromosomes) their offspring could possibly get the t14/21 from each parent, meaning the offspring will now have 44 chromosomes. Yet, still having all the necessary genetic information--Meaning they are "normal". Edit for an important note; You should also notice here that 2 of these individuals because of excessive genetic information (either the equivalent of 3 chromosome 21's or 14's) would be "non-viable" in some kind of historic world. Which means that if offspring were produced that would survive into adulthood then there was a 50% chance they were carriers or 50% chance they had the "normal" karyotype. How could this happen? Low population numbers with lots of inbreeding for one. If you had a small isolated population, it would be relatively easy for "chance" (better genetic drift) to fix this new chromosome number in the population. Populations go through these bottlenecks from time to time, humans possibly went through one about 80,000 years ago that reduced our population down to possibly around 10,000 individuals (some estimates put it as low as 1,000 individuals possibly). Does this really happen though? And the answer is yes. We know it happened once in our recent (geologically speaking) history with our second chromosome. When we look at human chromosome 2 and chimp 2p and 2q (note we've named them here in reference to our . Like Ken Miller (as others have referenced) is so eloquent at explaining, the "smoking gun" comes from genetics. Specifically the sequences. When we sequence our 2nd chromosome we find something peculiar. 4 telomeres and 2 centromeres! Normally there should be 2 and 1, respectively; ![]() At some point in our common ape ancestor past, we reduced the number of chromosomes from 48 (like all other greater apes) to 46 through a similar scenario as described above (though it is possible this new fused chromosome also entailed some kind of selective benefit, that is a discussion for another day). |
| Feb26-12, 12:37 PM | #17 |
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bobze, that was an amazing post! Thank you for sharing that, it helped tremendously.
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