It is a very common occurence; it being correlated to speciation is, of course, much less common. It leading to speciation would be even less common. Of course, given hundreds of thousands to millions of years, the number of chromosomal abnormalities that happens in nearly 1 in 100 offspring really adds up.
There is one sort of chromosomal abnormality that frequently creates new species, and which we've observed several instances of. It mostly happens in plants, and I think maybe some fish and amphibians. Polyploidy, where the number of chromosomes is multiplied by some factor (typically two). Now, frequently polyploid individuals cannot interbreed with any other individuals, but sometimes polyploid individuals can interbreed with other polyploid individuals, but not with individuals of the parent species. And if its a plant species that can handle self-reproduction, that's all it takes for speciation (in one generation, no less). From that point on the new species can diverge from the parent species completely, because there's no interbreeding.
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Yeah, polyploidy is one of those wacky things that is simultaneously strange and amusing when you first learn about it.
One other thing that amuses me is endosymbiotic theory, the basic theory being that mitochondria and chloroplasts used to be separate organisms (proteobacteria and cyano bacteria) that were at one time "captured" and incorporated into cells, which ended up eventually leading to us (and plants, respectively).
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Over a thousand lethal defects in the human genome have been identified so far. They are fairly common. All of us have some. Most of the time they are recessive, and so are not expressed unless they happen to be doubled and matched in the genetic material from each parent. This is why people who are too similar genetically, such as siblings and first cousins, are legally forbidden to marry.
Of course spontaneous defects can occur, but they are suprisingly uncommon thanks to the sophisticated gene correction machinery we have in our genes.
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Uh, Ron, most of these chromosomal abnormalities (and I wouldn't call a good number of them defect) are not passed on. Chromosomal abnormalities are something we have been able to test for forever, and some of them have distinct phenotypical manifestations. They are much easier to spot than genetic abnormalities.
These occur all the freakin' time, anew. Neither parent has them, and the child does have them. That's pretty darn spontaneous.
Above and beyond, that 1 in 118 children is children who are born with chromosomal abnormalities. Chromosomal abnormalities that prevent fetal development (we know of several) are possibly even more common, just very hard to collect statistics on (the people don't even know they're pregnant, or have a miscarriage).
In fact, your whole mention of recessive indicates you have no idea what a chromosomal abnormality is. A chromosomal abnormality is not a gene. There is no recessive or dominant. It has to do with the structure of the chromosomes in cells. In a given cell, it either is or isn't.
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I agree that there are good mechanisms for avoiding errors, but they are by no means fool-proof: Cancer is an obvious proof that gene correction can fail.
And, since we're talking mostly about errors during the phase of sexual reproduction, the vast majority of the mechanisms you're probably thinking of have no bearing at all. They're mostly there to increase the fidelity of replication and/or gene expression (i.e., protein building).
An error that happens when the parental DNA complements join together is likely to be faithfully replicated in all the cells of that new individual BECAUSE of those error correction mechanisms you're talking about.
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I finally got around to watching this, I was very impressed. I am much more informed about the nitty gritty of both evolution and the ID movement now.
Just wanted to say thanks to Blayne for linking .
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"In humans, for example, it is estimated that each individual caries three to five recessive lethal genes. In humans, >40% of progeny born to full sib matings either die before reproductive age or suffer severe disabilities (May RM. When to be incestuous. Nature 1979;279:192-4;" Link: http://www.dorak.info/evolution/sreprod.html
Some other internet sources put the number as high as 8-9 lethal genes in each person. I remember reading an article a few months ago which said researchers had identified over a thousand lethal genetic defects commonly found in humans. Could not locate it in a brief internet search. But if there are 3-9 lethal genes present in each person's genes, then there could be a large number of lethal genes of various kinds spread throughout the human genome around the world.
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Lethal genes being carried have almost nothing to do with chromosomal abnormalities (that is, there are a very few exceptions). Chromosomal abnormalities are caused by problems during sexual reproduction and cell division. They arise spontaneously.
In other words, what is your point?
I notice you also still haven't addressed your nonsense about bringing up recessive genes in a discussion about chromosomal abnormalities.
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quote:Originally posted by Lisa: Okay, I have a question about this. Given the thing about 24 chromosome pairs merging into 23... what are the odds of that happening? And if it happened, as the evidence seems to show, how would the 23 chromosome pair critter reproduce? Wouldn't there have had to have been a whole bunch of 23 chromosome mutants all at once in a single generation?
I'm asking hoping for an answer, and not for a fight.
So I guess I'm not going to get an answer to this, right?
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quote:Originally posted by Lisa: Okay, I have a question about this. Given the thing about 24 chromosome pairs merging into 23... what are the odds of that happening?
It happens. There are plenty of humans waliking around today with an odd number of chromosomes, because they have a single fused one. The most common one is a Robertsonian translocation. According to this site, 1 in 900 people has one.
A person with, say a translocation between chromosomes 14 and 21, for instance, will have most of the normal chromosomes, one normal Chr 14, one normal Chr 21, and one fused chromosome with the DNA from both stuck together. They have all the right DNA in the right amount, so they are mostly fine.
quote: And if it happened, as the evidence seems to show, how would the 23 chromosome pair critter reproduce?
It's harder, because there are more ways to mess up meiosis. In meiosis, once the chromosome from your dad has doubled, it's supposed to line up next to the corresponding doubled chromosome from your mom. But since there are an odd number, that lining up can be tricky, and everything might not end up where its suppsoed to go.
Some of their gametes will get the normal one copy of each chromosome. Those gametes are fine. Some gametes get the single fused chromosome. Those gametes are also fine, and the offspring from that gamete will also have the translocation.
If a gamete ends up with the fused chromosome and a normal copy of, say, Chr 14, that's bad. Trisomies in the resulting offspring are usually lethal. If the gamete gets the fused chromosome and a copy of Chr 21, the offspring will have Down's. Likewise, if a gamete fails to get any copy of Chr 21 or 14, that's lethal for the offspring.
quote: Wouldn't there have had to have been a whole bunch of 23 chromosome mutants all at once in a single generation?
No. What you need is for that people carrying the fused chromosome to become a larger percentage of the group.
If a bottleneck happens, and the fused chromosome becomes more common in the population, then the people without one are at a reproductive disadvantage. It then become a pretty plausible mechanism of speciation.
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I'm still not buying the chromosomal abnormality angle. I know we had an extensive discussion about it on the other side.
My argument is that there have been enough generations of fruitflies and mice since folks have been paying attention to this to demonstrate a chromosome number shift.
I'll grant the tetraploid frogs are highly interesting, but I don't see that being a reliable mode of speciation.
Of course, it's part of a monkey-man sci fi series I want to write someday, crossover between humans and chimps by the fusion of the chromosome we have that is two pieces in them. IIRC, we have the same chromosome layout as some of the great apes that are considered more different from us than chimps.
Seems like you're trying to say on the one hand chromosome number shift can occur, but also saying it isn't necessary for speciation. It's not necessary for speciation, but I would contend that it is necessary for propogation. I'm working from the assumption that speciation is comprised of variation, competition and propogation of the fit/extinction of the unfit.
I just don't believe that 5 billion years is enough time to produce human beings if their change rate is anything like fruit flies.
Drawing "facts" from wikipedia, they put a fruitfly generation at 2 weeks, and a human generation at 40 years. The number of generations during which fruitflies have been studied (2 weeks into 100 years) comes out to 104,000 years, very near the time that fossils that satisfy the definition of homo sapiens date from. So we experienced speciation in the same number of generations during which fruit flies have remained the model genetic specimen.
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P.S. I'd also be interested to know if there are behavioral universals in animals governing inbreeding. It seems like I saw on Nova a bit about women sniffing T shirts and preferring the manstink of people more immunologically diverse from themselves.
From a natural selection standpoint, it benefits survival of most creatures to avoid close relatives and the effects of the inbreeding. (Which is necessary to the best case scenarios of the Darwinians) But I don't know, maybe when under extreme environmental stress these preferences reverse or something, on the chance your uncle's webbed toes could prove useful. Still, that's not going to improve the odds of going back 50,000 "speciation" cycles, if one wants to argue that's how it happened.
Of course, generation periods won't be the same as one goes backward in the family tree.
Let's go with some other numbers that have been thrown around in my biology training, which are probably bunk. If I'm 96% the same as a chimp, and 74% the same as a fruit fly... and what is the number for a banana? Like 38% or something? How do these figure in with the probability of evolution happening by accident?
(I'll be adding to this as I go, so I don't have a ton of replies by me)
quote: Full genome sequencing resulted in the conclusion that "after 6.5 million years of separate evolution, the differences between bonobo/chimpanzee and human are just 10 times greater than those between two unrelated people and 10 times less than those between rats and mice". In fact, 98.4% of the DNA sequence is identical between the two Pan species and human.
from wikipedia, homo sapiens
I see where people get the mistaken idea that it's enough to multiply 50,000 times 0.16 to get 8,000, well over 100%. But it brings us to a number of 1 in 80 in which we are saying something needs to happen. I'm not really sure what that something is, myself since I'm reasoning this through based on my initial statement that 5 billion years isn't long enough to evolve a human. 0.16% is the difference in genome between any two random members of the human species, and not the greatest possible difference. Of course, the greatest possible difference doesn't really matter because it's not as though some people are more like monkeys and others live on the crest of evolution, moving toward the next inevitable phase.
Ah, that's the thing. The closer two people are related, the more likely they are to propogate mutations, but then the diversity is less. Does that make any sense? Evolution happens not because of greater and greater genetic spread, but from zealous inbreeding.
Well, I'm still not sure what it means.
I have to say in general that I dislike the competition aspect of the theory of evolution as well.
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Lisa: take a look at the first post on this page by me. I don't know the specific probability of a merged chromosome out of all the different sorts of chromosomal abnormality, but we've seen it in quite a few living humans.
For instance, about 5% of people with Down's syndrom have it because of merged chromosomes. That's a huge number. There's a long list of other conditions caused by various degrees of merging (usually by a large chunk switching chromosomes, but there are other variants).
Ah, looks like swbarnes has address how incredibly common it is.
pooka: there are chromosome number shifts, all the time. But they're rarely advantageous. Look at the millions (tens of millions?) of humans who do not have the normal number of chromosomes. Those are certainly chromosome number shifts, but they're almost always disadvantageous. A significantly advantageous one, such as one that greatly increased problem-solving capability (and bred true) would quickly spread throughout a population, especially if parts of the population were fairly isolated at times.
However, fruit flies are kept in large numbers in hospitable situations, for the most part. They have chromosomal abnormalities, too, but for the most part they're just an annoyance interfering with
That our gene is a merging of two genes that came from a common ancestor with apes is pretty much settled, as we repeatedly find experimental confirmation. For instance, we thought we were likely to find signs of what was previously a telomere . . . and we did. They're not very mistakable signs, either -- the chromosome was two chromosomes at some point in our heritage. The only real question is when the merge occurred, and the parts of the larger chromosome coincidentally line up almost perfectly with those in ape relatives.
No, polyploidy isn't a 'reliable' mode of speciation, just a rapid and easily observable one. And as you note, it isn't the most common. I have no idea what you mean by 'necessary for propagation' -- that's certainly not a part of evolutionary theory.
And we might have observed it in flies, I'm not certain . . . but we observe it in mice all the time: http://www.genetics.org/cgi/content/abstract/136/3/1105 . Some species just have chromosome changes more often than others. We don't know why.
Ah yes, that addresses your last point. Rates of change are not constant in species, across time, or for many other values. For instance, however the first single-celled organisms arose, rates of change in single-celled organisms tend to be phenomenal. Rates of change in simple multi-celled organisms tend to be extemely high. Rates of change in simple plants tend to be very high. Rates of change in amphibians tend to be fairly high. Rates of change in insects tend to be fairly high. Et cetera.
And most of the time there isn't significant evolutionary pressure on a population, but when there is, rates of change can skyrocket.
Your understanding of evolution is also somewhat limited. There's a lot less distinction between the "fit" and the "unfit" and a lot more distinction between the "fit for a given niche" and the "fit for another niche"; also, populations as a whole can change very gradually over time from one species to another without there being any changeover point, because there's evolutionary pressure leading the successful adaptations to reproduce more and the unsuccessful to reproduce less. There's no big distinction between the fit and the unfit, or any noticeable die-off.
Oh, and regarding five billion years . . . We would need billions more of incredibly rapid laboratory breeding of fruit flies before we would achieve the number of offspring many a bacteria manages in a few dozen years (possibly less).
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Addressing the number of generations thing you added more specifically, I'd like to re-emphasize that fruit flies tend to be bred for consistency, not change. Of course, that's done too -- and it tends to work. There've been at least two or three pretty solid speciation events in fruit flies in labs, and we've caused there to be highly assortative mating between fruit fly populations dozens of times (which, depending on one's definition, is either just barely or nearly speciation).
That the speciation isn't due to chromosomal abnormality isn't relevant.
Fruit flies are considered highly adapted, btw. Some of the splits just in Drosophilia occurred somewhere around 18 million years ago, we think.
Evolution doesn't happen by accident, but neither does it happen by design. Accidents happen all the time (we've got good proof of that). Evolution describes how those accidents lead to change in genetics over time.
Those numbers aren't exactly bunk, btw, but there're several methods of counting, depending on exactly what we mean by the same as. I believe the similarity with chimpanzees is much higher in several methods. I'm not certain I understand your question, either. Evolutionary theory is all about genetics changing, and we find large numbers of changes in genetics (which, coincidentally, line up pretty well with what we'd anticipate given observed mutation rates and other data). We also find some areas of relative constancy, for fundamental parts of cellular metabolism (for instance), also as anticipated. Could you be more specific?
Regarding your question about mating practices, across animals (much less other species) as a whole there are no generalities. Name most of the bizarre variants you can imagine, and some animal will have something like it.
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quote:pooka: there are chromosome number shifts, all the time. But they're rarely advantageous.
Yes, this is the point I was alluding to in the many previous conversations about this.
How is propogation not important to evolution? Perhaps you should provide me with a more basic overview since the definitions from my college days are apparently obsolete?
Also, I thought fruit flies were observed because it was hoped that they would display variation because of their short life cycle. They were eventually found to be quite stable, and as I learned today, the males do not undergo meiosis. This is very confusing to me, since you'd think we would have noticed this in the experiments we did with red and green eyed flies in high school. The males somehow... make a genetic contribution, just not via meiosis?
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I also wonder if an ID advocate had posted a thread with typos in the title, if no one would have pointed them out. Maybe this is a kinder, gentler Hatrack than in my day.
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Propagation is necessary to evolution, what I don't get is how you're saying chromosomal number shifts are necessary to propagation. That's a completely different statement.
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Fruit flies were chosen because they're easily observable. They have short life cycles, they have few genes, and their chromosomes get really, really large (that's pretty unusual) at times.
We weren't looking for speciation when we started looking at fruit flies, but better understanding of basic genetics, which we got. Fruit flies are great for studying dominance and recession (et cetera).
Male fruit flies do contribute to their offspring's genetics in much the same way. They don't have meiotic recombination, which means that they send out what they took in, chromosomally. This also makes them a lot easier to study, though I don't think we knew that when we started.
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Male fruit flies do undergo meiosis- what they don't do is meiotic recombination ("crossing over").
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The people who started looking at fruit flies were hoping they would spit out some mutations in a controlled environment.
Isn't it a given that the rate of mutation is not going to be changed by fruit flies being in a relatively controlled environment? I mean, otherwise you have Lamarckian evolution.
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quote:IIRC, we have the same chromosome layout as some of the great apes that are considered more different from us than chimps.
We have the same number of chromosome as goldfish do too. Raw chromosome number is a lousy way of determinieng relatedness. The reason that chimps are "considered" to be more closely related is that there are a millions tests (protein similarity, DNA similarity, syntenty, etc), and we hypothesize that that if the chimps are more closely related, we will get a particular answer, and then we get that answer, every time.
Chimp and Macaque are there. You can see a lot of similarity between humans and macaque, but more between chimps and humans.
So, what primate has a better synteny than chimps? Just put up a link so we can all look at the synteny for ourselves, instead of having to take your word.
quote:Seems like you're trying to say on the one hand chromosome number shift can occur, but also saying it isn't necessary for speciation.
Pretty much
quote:It's not necessary for speciation, but I would contend that it is necessary for propogation.
Okay...contend away. I can contend that Jupiter is made of frosted flakes. That doesn't make my argument valid, or demonstrate that I'm worth listening to.
If you want to back up your assertion that chromosomal rearrangements are necessary for propagation with evidence, that would be nice too.
quote:I'm working from the assumption that speciation is comprised of variation, competition and propogation of the fit/extinction of the unfit.
That's nice. Your assumption is wrong.
Speciation, at least according to the classical definition used when talking about sexually reproducing organisms) is the process by which a population of organisms changes such that it could no longer breed with its progenitors.
So the reason that the population changes is because of variations building up, and natural selection can help with that, but it doesn't have to. You can have speciation based on the fact that two populations of closely related animals fail to recognize each others’ mating calls.
quote:I just don't believe that 5 billion years is enough time to produce human beings if their change rate is anything like fruit flies.
That's nice. Care to demonstrate that your belief is based on facts by showing us the evidence and the calculations for how much fruit flies "change", and how much "change" is required to get humans?
quote:Drawing "facts" from wikipedia, they put a fruitfly generation at 2 weeks, and a human generation at 40 years. The number of generations during which fruitflies have been studied (2 weeks into 100 years) comes out to 104,000 years, very near the time that fossils that satisfy the definition of homo sapiens date from. So we experienced speciation in the same number of generations during which fruit flies have remained the model genetic specimen. [/QB]
What exactly are you talking about? You can't be talking about chromosomal rearrangements, because obviously we haven't been studying those for 100 years...more like 50. And the chromosomal rearrangement in humans could have happened any time after the last common ancestor of humans and apes. That's at least a few million years, not just 100,000.
Of course, in the last 50 years of studying flies, we have seen speciation, just like you say we should. So I'm not sure what you think is missing, exactly.
And why are "facts" in quotes? Is is because you think that a good scientific discussion can take place using only contentions and assumptions, without any facts?
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Because they're from wikipedia, where someone could change what it says at any moment. And according to wikipedia, fruit flies have been observed for mutations since 1910.
Okay, it says here in my old fashioned paper book (Purves, Orians Life: The science of Biology) that Eukarotes evolve approximately 2.5 billion years ago, and the Cambrian period when most phyla emerge is 600 million years ago, mammals 245 mya, so that compresses the timeline I thought we were dealing with. If we want to treat the KT boundary as a major force in the expansion of mammals, that is 66 mya.
It uses the quite amusing calendar analogy to put the history of life on this planet into perspective. I find it amusing not because I'm not a young earthist, but because I've seen the 7 day creation mocked in children's videos about dinosaurs before. That is the kind of pseudo-scientific snobbery that causes me to resisted the accepted theories of evolution.
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If you google for Ken Miller, you'll find plenty of things by him. I'm not sure which points you're interested in.
The people who started looking at fruit flies?
We only barely understood genetics at that point; it had only really been rediscovered in 1900. They picked fruit flies because fruit flies are easy to breed repeatedly and observe. This turned out to be even more fortuitous than they knew. I'm not sure why you're so interested in why people chose to study fruit flies.
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Well, I'm not as much anymore with what I've learned today, but it was more because of the number of generations in which they have been closely observed. Though mice and rats also have been around since recorded history, having rather short generations (21 days?). Domesticated animals don't count, of course, and in a strange way, neither do humans because we have domesticated, as it were, ourselves. I wouldn't consider fruit flies domesticated because while we have controlled their environment, we have not selectively bred them in the same way we have c57 black mice.
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We haven't been able to observe speciation for most of recorded history, of course.
We have observed speciation in fruit flies (at least twice very solidly).
Mice (as I note previously) routinely have chromosome number variations that breed true. Mice in the wild, that is.
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quote:Originally posted by pooka: And according to wikipedia, fruit flies have been observed for mutations since 1910.
Okay, but that doesn't mean that every fly is checked for mutation, or that people were doing karyotypes in 1910.
People doing evolutionary studies will look for mutations, but people doing ordinary lab work will assume there are no mutations. If something strange comes up, they might try to figure it out, and lots of cool model strains arose because of a spontaneous mutation popping up in an ordinary strain of mice.
But if you are imagining that every fly for 100 years has been run through a magical mutation detection system, or that flies are routinely karyotyped so as to have examples of chromosomal rearrangments to wave in the faces of Creationists, think again.
quote: Okay, it says here in my old fashioned paper book (Purves, Orians Life: The science of Biology) that Eukarotes evolve approximately 2.5 billion years ago, and the Cambrian period when most phyla emerge is 600 million years ago, mammals 245 mya, so that compresses the timeline I thought we were dealing with. If we want to treat the KT boundary as a major force in the expansion of mammals, that is 66 mya.
Okay, treat the KT boundary however you want. However, since the evidence tells us that most of the major mammal orders were already in existance before the KT event, the rest of us will go with what the evidence says happened.
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There's no such thing as a "number of generations required for speciation." You could have a single lineage that, after its initial establishment, never again undergoes speciation, due to a number of possible factors. Perhaps the lineage simply goes extinct. Or perhaps it never gets divided into two non-breeding populations- by sheer luck of the draw, colonies of the species do not wander off, and no mutations happen to arise that induce divergence of a subpopulation within the species (such as the case of mating call recognition failure that swbarnes2 described).
Alternatively, you can get speciation after a single generation, such as in the case of polyploidization in certain plants, which result in fertile offspring incapable of reproducing with their immediate parents. In this case, because plants can self-fertilize, you can actually establish an entire population of the new species from the original polyploid individual.
There are many avenues to species divergence. All that's really required is that two populations of the species stop (or even just reduce) mating with each other, for whatever reason. The method generally mentioned in biology textbooks is adaptive radiation- the spread of one population to a new, isolated territory, such as an island. But that's hardly the only way. Again, you could have a small group that pitches its mating call slightly higher than others will recognize, or a group that simply goes into heat at a different part of the year than others of the species. These two groups are probably still biologically capable of mating for quite some time, but that doesn't matter, because they don't. Suddenly, the evolutionary tree begins to fork, and as each group begins to undergo genetic drift, it is quite likely that they will eventually reach the point of no return (when they are no longer capable of biological reproduction), after which the two lineages will never successfully interbreed again. Viola! Speciation has occurred.
This process can be drastically sped up by increased pressure from natural selection. If the resources in area are plentiful, even species in direct competition are under little adaptive pressure. However, if the resources suddenly start to dry up, differences in fitness that were previously minor suddenly start to mean a lot. Two semi-isolated populations of a species in this situation are placed under enormous pressure to produce adaptations that result in the survival and propagation of their closest relatives (i.e. the members of their subpopulation). Divergence is thus accelerated further.
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Fugu13, you do recognize that chromosomes are made up of genes, right? You could hardly have abnormalities in one without having abnormalities in the other.
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Okay, you don't understand how things work even more than I thought.
A gene abnormality has no effect on the structure of chromosomes (except in those very rare cases it interferes with chromosome replication). That would be like a pothole in the road having an effect on which roads intersect.
Chromosomal abnormalities happen all the time. They are frequently and repeatedly not 'corrected' because they are above the level our transcription checking 'routines' run at. In fact, the typical method of 'correction' in particularly bad abnormalities is for that cell to die. They are not (except in very rare circumstances) caused by genes.
If you are somehow arguing that chromosomal abnormalities are somehow 'carried' by recessive genes in people, you are wrong. That's the best guess I have to what you're trying to argue.
Perhaps you could clarify. Assume I'm dumb. Lay out every step of your argument, one by one.
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quote:Fugu13, you do recognize that chromosomes are made up of genes, right? You could hardly have abnormalities in one without having abnormalities in the other.
"Chromosomal abnormality" refers to defects in chromosomal structure and/or number, such as duplications or deletions of chromosomes, as well as chromosome fusions and breakage. You are, I guess, technically correct that an abnormality in a chromosome would affect the genes on that chromosome (and vice versa, albeit to a ridiculously minor degree), but that demonstrates a very simplistic understanding of how genetics works. Not everything operates at the level of individual genes. When we talk about "dominant" and "recessive" alleles, we are almost invariably talking about individual loci, because ultimately "dominance" is defined by the phenotypic effect of a particular allelic variant, and when you start dealing with multiple genes, the systems become far too complex to categorize as simply "dominant" or "recessive."
In addition, the gene correction machinery that you reference operates at the level of short DNA sequences. The two basic types of gene repair mechanisms are high-accuracy DNA polymerases, which detect mistakes in DNA replication as they occur and fix them, and DNA repair complexes that detect mutations induced by an outside mutagen such as UV light, and return the sequence to its original form. The latter gene repair system works by detecting mismatches in the DNA (like a G paired to a T, or an A paired to a C). Neither of these methods is 100% foolproof, which is why mutations inevitably sneak in anyway, and they both deal with relatively small errors- often single nucleotide substitutions. There exist other mechanisms to deal with somewhat larger types of DNA damage, but AFAIK none of these operate at a chromosomal level, especially since most chromosomal defects occur during meoisis and mitosis, and have nothing to do with DNA replication or sequence mismatch at all. That's why your argument about lethal alleles is irrelevant to a discussion about chromosomal abnormalities like the one that occurred between the human/chimpanzee divergence.
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quote:Originally posted by Ron Lambert: Fugu13, you do recognize that chromosomes are made up of genes, right? You could hardly have abnormalities in one without having abnormalities in the other.
Aboslutely wrong.
99% of DNA looks to be just filler. Sure, there are promotors and enhancers, and some Alu sequeces look to be important in chromosome binding and crossing over during meiosis, but there are big swaths that don't do anything.
A robertsonian translocation, like we've been talking about all day, could happen with the loss of genes. The acrocentric bits have almost no genes.
If you don't believe me, feel free to prove me wrong.
That's the mouse ensembl front page. All mouse chromosomes are acrocentric. Go right on ahead and show us the genes that would be lost when two mouse chromosomes fuse at their centromeres.
(Hint: unlike positions of human chromosomes, which are always specified as being on the p or q arm, mouse genetic loci are just measured by their distance to the centromere. Why do you think that no one in the mouse community needs to be told which arm their gene locations are?)
Or, if you don't like mice, you can get to the human page pretty quick.
Then you can get back to us on all the genes that would be lost if, say Chr 13 and Chr 22 had a Robertsoinal translocation, causing them to fuse such that they lost the short arms of the chromosomes.
Or you can say nothing, which will also be an answer.
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"Genes" are a concept from the pre-molecular study of inheritance. One can talk about eye-color or blood type as being the product of a gene, but it doesn't represent anything objective about the content of the chromosomes.
I'm still waiting for someone (well actually fugu, since swbarnes doesn't seem interested in dialogue) to provide a definition of evolution that is more accurate than mutuation/variation, competition, and propogation.
I'd also be more interested to hear about the speciation of fruit flies, if you'd like to provide links.
That's interesting about the mice and I'd like to see more on that as well, particularly as it relates to my monkey-men. Though it may be a case where like the fruit flies' meiotic recombination, their reproductive biology doesn't follow the rules that we previously assumed.
As I understand it, evolution is thought to encompass two processes. One is the "genetic drift" idea, where the variation within a population results in gradual adaptation to conditions. This pertains to phenomena such as ring species, and squirrels separated by canyons. Then there is punctuated equilibrium, wherein a mutation takes hold to produce a very different kind of animal like the first mammals with trilobdontic teeth or the giraffe.
What just doesn't gel for me is the idea that in less than a billion years either of these processes or the two of them working together could produce the differences in animals that exist.
Another thing that used to bother me was the rebuttals that were made to the old "Eve" controversy in the early ninetys, that there would be one human female from which everyone was descended. I don't really posess the sophistication to understand most of what they were saying, but it seemed to be that humans evolved in several places relatively simultaneously.
Evolutionary biology is an academic discipline in which argument between competing theories is ongoing.
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A billion years is a REALLY long time. Add the huge biomass of the earth, compared to the tiny samples in lab conditions. Add the absolute life or death imposed on all life: if you aren't adapted to conditions, your genes don't get passed on.
Also, fruit flies are used for genetic experiments specifically because they have a relatively small, well-understood genome. Consider how similar all fruit flies are, over numerous generations. Then look at the diversity among humans for a counter example. Greater diversity means greater chance that any particular genetic variation will appear, which might be quite beneficial in a specific environment.
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quote:Greater diversity means greater chance that any particular genetic variation will appear, which might be quite beneficial in a specific environment.
This is the principle I think I don't believe anymore. Variations become important when they are narrowly bred, or concentrated if you will. Now I'm seeing here that at gene pool is going to be like smoke in a room, and it will eddy and whorl as it pleases, and like a drying coffe stain, concentrations form, counterintuitively, along boundaries. But I'm still saying that I don't think there's enough time. I'll see if there's a map of homonid evolution on wiki, since I don't have my books with me.
P.S. So it puts the split between the Pan Genus and the Homo Genus at 5 mya, according to (and this is a new term to me, but basically what I'm talking about) a "molecular clock".
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quote:99% of DNA looks to be just filler. Sure, there are promotors and enhancers, and some Alu sequeces look to be important in chromosome binding and crossing over during meiosis, but there are big swaths that don't do anything.
quote:The new data indicate the genome contains very little unused sequences and, in fact, is a complex, interwoven network. In this network, genes are just one of many types of DNA sequences that have a functional impact. “Our perspective of transcription and genes may have to evolve,” the researchers state in their Nature paper, noting the network model of the genome “poses some interesting mechanistic questions” that have yet to be answered.
Other surprises in the ENCODE data have major implications for our understanding of the evolution of genomes, particularly mammalian genomes. Until recently, researchers had thought that most of the DNA sequences important for biological function would be in areas of the genome most subject to evolutionary constraint — that is, most likely to be conserved as species evolve. However, the ENCODE effort found about half of functional elements in the human genome do not appear to have been obviously constrained during evolution, at least when examined by current methods used by computational biologists.
According to ENCODE researchers, this lack of evolutionary constraint may indicate that many species’ genomes contain a pool of functional elements, including RNA transcripts, that provide no specific benefits in terms of survival or reproduction. As this pool turns over during evolutionary time, researchers speculate it may serve as a “warehouse for natural selection” by acting as a source of functional elements unique to each species and of elements that perform the similar functions among species despite having sequences that appear dissimilar.
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I think these three paragraphs help answer some of your questions
quote:Ah yes, that addresses your last point. Rates of change are not constant in species, across time, or for many other values. For instance, however the first single-celled organisms arose, rates of change in single-celled organisms tend to be phenomenal. Rates of change in simple multi-celled organisms tend to be extemely high. Rates of change in simple plants tend to be very high. Rates of change in amphibians tend to be fairly high. Rates of change in insects tend to be fairly high. Et cetera.
And most of the time there isn't significant evolutionary pressure on a population, but when there is, rates of change can skyrocket.
Your understanding of evolution is also somewhat limited. There's a lot less distinction between the "fit" and the "unfit" and a lot more distinction between the "fit for a given niche" and the "fit for another niche"; also, populations as a whole can change very gradually over time from one species to another without there being any changeover point, because there's evolutionary pressure leading the successful adaptations to reproduce more and the unsuccessful to reproduce less. There's no big distinction between the fit and the unfit, or any noticeable die-off.
Oh, and regarding five billion years . . . We would need billions more of incredibly rapid laboratory breeding of fruit flies before we would achieve the number of offspring many a bacteria manages in a few dozen years (possibly less).
The situation isn't a dichotomy between drifting and punctuation. There are evolutionary pressures, and when they increase, the rate of evolution increases. There isn't a switch.
We can see bacteria undergo huge genetic changes in a matter of weeks when periodically reduced to small populations and constrained in resources. We can see evidence of 'recent' (past million years) speciation all over the place (including evidence that speciation is often not obvious until some time after the fact; unsurprising given that the notion of species is an approximation).
And of course, there's that the records we have of life in the past line up as we'd expect by evolutionary theory (and evolutionary theory has successfully predicted the appearance of certain sorts of fossils). This strongly suggests that, whatever the time span in question (which is substantially backed up by things like atomic physics), things did evolve.
Evolutionary biology is definitely ongoing, but the overall picture has been substantiated by considerable evidence.
"mutuation/variation, competition, and propogation. " is a collection of words, not a definition of evolution. Evolution is the change in the inherited traits of a population from generation to generation (cribbed from wikipedia). Natural selection is generally considered the process by which this occurs, and involves some inherited traits (which are generally the result of mutation or other genetic change) leading to higher reproduction than other inherited traits, meaning that they are 'selected for', changing the makeup of traits in a population in their favor.
I don't think you have a very good grasp of what a billion years is like. Most species on this planet are simpler than the fruit fly. If they speciate at the (relatively slow) observed rate of the fruit fly, which we'll take as conservatively once every hundred years (remember, we think we've observed two or more instances in the last 50), then starting with one species a billion years ago and speciating in that rate could result in 2 to the 10 millionth species on the planet . . . of course, it doesn't work like that, and 2 to the 10 millionth is rather more than the number of atoms in the universe (we think). But even if over 1 billion years each species only became two species slightly under every 4 million years (and all the species stuck around), there'd still be 115,792,089,237,316,195,423,570,985,008,687,907,853,269,984,665,640,564,039,457,584,007,913,129,639,936 species on the planet. There aren't quite that many. Guesstimates put the number of species at 100 million or less; lets imagine there are over 4 billion, though. To reach that number (again, just assuming all species stay around and they split after a certain interval), each species only needs to split every 31 million years. I assume you're willing to consider that a new species arising every 31 million years isn't much of a stretch?
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MightyCow: fruit flies aren't as similar as you think, they just all look the same to us . For instance, a population of fruit flies can have truly astounding weight/size changes over time, far greater than the variation in human weights/sizes.
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quote:Originally posted by pooka: "Genes" are a concept from the pre-molecular study of inheritance. One can talk about eye-color or blood type as being the product of a gene, but it doesn't represent anything objective about the content of the chromosomes.
Not true. "Gene" is a technical term defined as a sequence of DNA capable of being transcribed and translated into a protein. It was originally used to describe individual Mendelian traits, true, but that vague definition has been pinned down quite specifically in the past 50 years.
quote:I'm still waiting for someone (well actually fugu, since swbarnes doesn't seem interested in dialogue) to provide a definition of evolution that is more accurate than mutuation/variation, competition, and propogation.
While competition and propagation frequently occur over the course of evolution, they aren't strictly necessary. As fugu said, change in inherited traits between generations is how evolution is defined; stuff like competition and propagation are methods through which natural selection can work. But they aren't the only ones.
quote:What just doesn't gel for me is the idea that in less than a billion years either of these processes or the two of them working together could produce the differences in animals that exist.
Massive changes in physiology can occur from relatively simple changes in genotype, due to the way that development works. Keep in mind that what we as humans think of as a major difference between two individuals is often highly biased by our own point of view. Changes in structure, size, and color are more obvious to us than, say, differences in iron metabolism machinery, and we often make the mistake of assuming that the genetic basis of these "big" differences is similarly greater, when this is often untrue. You can get extra limbs simply by expressing a single master regulatory gene at the wrong place at the wrong time. You can massively alter size by simply increasing production of growth hormones.
The master body plan is governed by a surprisingly limited set of genes, each of which is expressed differentially in gradients. The interaction between these master regulators induces the expression of more specific regulatory genes, each of which often activates and deactivates a further set of regulatory genes, and so on and so forth. You often have to dig through many layers of gene regulators to get to the genes that actually do something directly structural (such as the genes encoding myosins and actins in muscle). This means that a mutation in a regulatory sequence earlier on in the pathway can have incredibly complex effects on the resultant phenotype.
Here's an example in fruit flies. In this case, the mutation of a single master regulatory gene (part of the "homeotic gene" complex responsible for body patterning along the anterior/posterior axis), and the subsequent deactivation of that gene, caused the duplication of one of the thoracic segments, which happens to include the wings, and the erasure of the segment that is supposed to be there. This is a pretty severe phenotypic alteration, and all it took was a single mutation.
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I'm finding the reading on Alfred Russel Wallace quite entertaining. I guess Darwin saw competition as a much larger factor in natural selection, where Wallace saw environment as more significant. It's part of why he opposed Social Darwinism (which I was suprised to find was being discussed contemporaneously) because for him natural selection was something that united a species and not something that divided it. It's an important distinction, one I hadn't really grasped.
I had a sense of it from a presentation we had in college where we heard a quote from him about the aborigines of Malay, and he saw in them not the missing link that some might have looked for, but intelligent members of his own species.
Along with this is his idea that evolution provides not only the impetus for change, but the ability to remain the same as we see in crocodiles, sharks and coelacanths. Coelacanths only look like 450 million year old organisms from the outside, their internal structures are most likely different.
P.S. That's a wacky fly alright. Though... I thought the haltier was more like a vestigial wing. Weird. But it's kind of like having an extra finger or not, isn't it?
Thanks for the clarification on genes. My biology education began some 25 years ago, though it extended up through the mid-90s, and I watch a lot of Nova.
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Oh, their internal structures could be substantially the same (though I don't know in that particular case). A well adapted population can remain the same for quite some time.
Luckily, there are plenty of things that prevent populations from being/staying well adapted, resulting in lots of evolution.
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But Wallace said that evolution is occuring when organism remain the same.
Let's see if it's still in my clipboard:
quote:Others have noted that another difference was that Wallace appeared to have envisioned natural selection as a kind of feedback mechanism keeping species and varieties adapted to their environment.[69] They point to a largely overlooked passage of Wallace's famous 1858 paper:
The action of this principle is exactly like that of the centrifugal governor of the steam engine, which checks and corrects any irregularities almost before they become evident; and in like manner no unbalanced deficiency in the animal kingdom can ever reach any conspicuous magnitude, because it would make itself felt at the very first step, by rendering existence difficult and extinction almost sure soon to follow.[58]
When I bring up a coelacanth, I'm talking about a lifeform that has persisted for pretty much half the history of life on earth.
Fruit fly speciation from Fugu's link above:
quote:5.3.1 Drosophila paulistorum Dobzhansky and Pavlovsky (1971) reported a speciation event that occurred in a laboratory culture of Drosophila paulistorum sometime between 1958 and 1963. The culture was descended from a single inseminated female that was captured in the Llanos of Colombia. In 1958 this strain produced fertile hybrids when crossed with conspecifics of different strains from Orinocan. From 1963 onward crosses with Orinocan strains produced only sterile males. Initially no assortative mating or behavioral isolation was seen between the Llanos strain and the Orinocan strains. Later on Dobzhansky produced assortative mating (Dobzhansky 1972).
5.3.2 Disruptive Selection on Drosophila melanogaster Thoday and Gibson (1962) established a population of Drosophila melanogaster from four gravid females. They applied selection on this population for flies with the highest and lowest numbers of sternoplural chaetae (hairs). In each generation, eight flies with high numbers of chaetae were allowed to interbreed and eight flies with low numbers of chaetae were allowed to interbreed. Periodically they performed mate choice experiments on the two lines. They found that they had produced a high degree of positive assortative mating between the two groups. In the decade or so following this, eighteen labs attempted unsuccessfully to reproduce these results. References are given in Thoday and Gibson 1970.
So we've got some mules and selective breeding which was unable to be reproduced.
But it was fun to feel scared that I might be deeply wrong for that short period of time.
You know what was cool? Those domesticated foxes they bred in Russia. Though it makes me sad to consider for some reason, breeding out everything that would allow a fox to survive in the wild.
quote:Originally posted by pooka: [QB] I'm finding the reading on Alfred Russel Wallace quite entertaining. I guess Darwin saw competition as a much larger factor in natural selection, where Wallace saw environment as more significant. It's part of why he opposed Social Darwinism (which I was suprised to find was being discussed contemporaneously) because for him natural selection was something that united a species and not something that divided it. It's an important distinction, one I hadn't really grasped.
I'm not sure they're really that distinct. Environment is often crucial in promoting competition- limit the available resources, and competition (whether between or within species) goes up. And the vice versa can be true as well- it does little long-term good for your species if your evolutionary arms race with your direct competitor ends up denuding the entire savana of grass.
quote:I had a sense of it from a presentation we had in college where we heard a quote from him about the aborigines of Malay, and he saw in them not the missing link that some might have looked for, but intelligent members of his own species.
Along with this is his idea that evolution provides not only the impetus for change, but the ability to remain the same as we see in crocodiles, sharks and coelacanths. Coelacanths only look like 450 million year old organisms from the outside, their internal structures are most likely different.
Their internal structures are actually probably fairly similar as well, especially in the case of sharks, in which we have found numerous lineages that branched apart quite a long time ago, but which still share a number of shark-specific internal features. What has undoubtedly changed, whether alterations in bauplan have occurred or not, though, is the genetic sequences of such species. Genetic drift will have occurred in the intervening time between speciation and today, minor and silent mutations will have accumulated, and transposable elements will have found their way into the genome any number of times. This is why we can use sequence homology to estimate the evolutionary history of organisms.
quote:P.S. That's a wacky fly alright. Though... I thought the haltier was more like a vestigial wing. Weird. But it's kind of like having an extra finger or not, isn't it?
Yes, the haltere is a vestigial form of the second set of wings observed in non-fly insects. However, in this particular case, the segment containing the haltere is being completely replaced by a copy of the preceding thoracic segment. This isn't a case of the vestigial haltere being "de-vestigialized"; rather, one entire segment is just plain gone, and another grown in its place.
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Is it a case that one part of the genome calls for this many segments in the thorax, but there is only detailed plans for one less than that, so it reduplicates the last available set of plans?
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quote:Luckily, there are plenty of things that prevent populations from being/staying well adapted, resulting in lots of evolution.
Oh, yeah, Wallace had some insight related to Malthus and the population bomb, as we would call it today. Darwin saw organisms competing for resources so they could gain a greater foothold. Wallace saw them outstripping their resources. Well, in one way that seems to be the opposite of what I said about their positions a few posts back. I wonder if it had to do with Darwin being very socially secure, while Wallace was-- I don't want to say a hanger-on, because he's one of my heroes, but basically that.
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quote:Originally posted by pooka: Is it a case that one part of the genome calls for this many segments in the thorax, but there is only detailed plans for one less than that, so it reduplicates the last available set of plans?
Not in this case, although that's certainly a scenario that I could imagine being true somewhere. Like all bilateral animals, fruit fly development is governed by a set of genes that are expressed in gradients down each major axis. The homeotic genes are expressed linearly along the anterior/posterior (front-to-back) axis, like so, in simplified form:
Keep in mind that homeotic gene expression isn't discrete- each of the "locations" I gave above is actually the peak of a gradient of expression of that gene. Each of the homeotic genes in turn activates and suppresses a host of other genes. Because gene expression can be controlled not only by discrete "on/off" action of a higher regulator, but also by measuring local concentrations of higher regulators, the gradients mentioned above allow for the further segmentation of each major body segment. So in the thorax, for example, you might get the following:
I hope the formatting works. Anyway, the end result is that you get finer and finer definition along the axis. Combined with a similar set of regulatory genes governing the dorsal/ventral and left/right axes, you effectively establish a Cartesian coordinate system capable of controlling what happens at each point with incredible precision, and all stemming from a simple basic set of master regulators.
In the haltere example, the mutation caused the suppression of "Gene 2" (at least, in my simplified model- the reality is somewhat more complex, but the principle is the same). Thus, rather than having a low Gene 2 area followed by a peak, you have low Gene 2 throughout. Thus, the segment that would normally become thoracic segment 2 experiences gene expression roughly akin to thoracic segment 1, and is ultimately patterened identically to thoracic segment 1.
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Many of those that don't develop normally die, so they're not obviously present in the sample.
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