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Author | Topic: Questions on "Random" Mutations | |||||||||||||||||||||||||||||||
Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
The answer is still the same one that Crash and I have both given you. The fact that there are less germ cells than somatic cells doesn't change the frequency of mutation events so there is no reason the odds should be any different. The odds of you having more somatic mutations than new germline mutations is high but only because you have so many more somatic cells. The odds of any particular cell being mutated need not be any different. There may be reasons why the odds could differ, such as mutagens which specifically target the germ cells, but the proportional number of somatic and germ cells is not a reason.
Given the number of novel mutations which are reported to be found in every newborn, and the reporeted mutation rates, I think the chances are pretty high that every gamete has some mutation, however small. TTFN, WK
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mick Member (Idle past 5008 days) Posts: 913 Joined: |
Wounded King writes: The odds of any particular cell being mutated need not be any different. There may be reasons why the odds could differ, such as mutagens which specifically target the germ cells, but the proportional number of somatic and germ cells is not a reason. Just a thought - I often hear the suggestion that up to 100 nucleotides differ between parents and their offspring. Presumably this means that each sperm differs from every other sperm (or each egg from every other egg) by around 50 nucleotides. Does that also imply that every cell in one's body also differs from every other cell by around 50 nucleotide substitutions (assuming that each cell has undergone the same number of cell divisions prior to its differentiation)? What do you think? Mick
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Doddy Member (Idle past 5931 days) Posts: 563 From: Brisbane, Australia Joined: |
taylor_31 writes:
Well, strictly speaking they are. As already mentioned, transitions (eg purine to purine) are more common than transversions (purine to pyrimidine).
But I thought that the probability rates of different mutations happening are different. taylor_31 writes:
Mostly just because there are so many nucleotides in any given gene. I mean, we could give a probability for every single nucleotide substitution, but then we also need to consider insertions, deletions, transposons etc...it just gets too complicated. If that's true, then why can't you predict which mutation would occur? In this way, it much like the toss of the coin or die that was mentioned. Strictly speaking, we could indeed predict which face/number will be up just by looking at the dice or coin as it falls - it is governed by well-understood physical laws (gravity, friction, inertia, elasticity etc). But, I don't know any computer (yet) that can analyse a falling dice and predict the result, even though it is predetermined by the hand that tossed it (there might be one that can for a coin...not sure). So, because we humans just can't compute all the data we have when we see a die or coin fall, it is considered random by those who operate casinos and so on. It's not intrinsically random, but we can't predict it with any accuracy either. It is much the same with a gene. It's just too much to consider. Contributors needed for the following articles: Pleiotropy, Metabolism, Promoter, Invertebrate, Meiosis, DNA, Transcription, Chromosome, Tetrapod, Phenotype, Messenger RNA, Mammals, Appendix , Variation, Selection, Gene, Gametogenesis, Homo erectus and others. Registration not needed, but if desired, register here!
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taylor_31 Member (Idle past 5945 days) Posts: 86 From: Oklahoma! Joined: |
Blastocyst stage, about 4-5 days post-fertilization. I read (on Wikipedia) that one distinguishing characteristic of stem cells from non-stem cells is the stem cells' "property of self-renewal." What exactly does that mean? I assumed that it meant that stem cells could make more of themselves. But can't every cell do that?
I guess I was unclear. I meant this as an example of it decreasing the odds of your existence, as defined by your genome - since chromosomal crossing increases the number of potentially different gametes. Damn it, I'm sorry, I meant the same thing that you wrote. I was confused as to why this "crossing over" would decrease the odds of our genome coming into existence. It was a trivial point, but I was slightly confused.
They don't chain up. They exist in a normal cell as 46 individual lengths of DNA, all tangled up with each other like a ball of spaghetti. That's surprising for some reason. I somehow expected DNA to be long and continuous and pretty. To clarify, this is how all the DNA of a cell organizes itself? This is not one super-long double-helix, but rather many separate strands of super-long helixes, right? And these separate strands give instructions for the rest of the cell, but only certain parts are "read" for any specific cell.
But that's just a convention that cytologists use, not a representation of biological reality. One of my biggest problems with biology is that I can't visualize the concepts behind it, and if I can't visualize them then it seems like nonsense to me. The picture you posted worked wonders for my imagination, because it made me realize that chromosomes are not colorful, neatly organized slots; rather, like you said, they seem like strands of thick spaghetti, or even worms.
Mutation is ultimately responsible for all variation between individuals. But can this mutation really account for the vast variety on Earth? I can see it causing differences between me and another human, but I have trouble seeing it explain the differences between me and, for extreme sake, a spider. I'm not sure how to quote an exterior source, so I'll just wing it:
CARM website writes writes: In order to create a new structure, however, the mutated genes must integrate or function in concert with one another. According to Professor Ambrose, the difficulties of obtaining non-harmful mutations of five related genes "fade into insignificance when we recognize that there must be a close integration of functions between the individual genes of the cluster, which must also be integrated into the development of the entire organism." I hate to admit this, but I don't see how mutations could form, say, an organ like the liver or the intestines. They just seem so specialized to me, and I can't see a mutation causing such organization.
You, yourself, carry about 300 germline mutations that are specific to you, plus who knows how many mutations from each of your parents Do all of those 300 mutations appear in each individual gamete? Or did you mean the total number of mutations for the entire gamete "population"?
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taylor_31 Member (Idle past 5945 days) Posts: 86 From: Oklahoma! Joined: |
I'm having writing difficulties.
I'm pretty sure that we agree. This:
The odds of you having more somatic mutations than new germline mutations is high but only because you have so many more somatic cells. is exactly what I was trying to say.
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Dr Adequate Member (Idle past 306 days) Posts: 16113 Joined: |
But I thought that the probability rates of different mutations happening are different. If that's true, then why can't you predict which mutation would occur? If the probability rates of all the mutations were the same, then it would be statistically random. Well, again, that's not what "random" means. The sum of two dice is random, but not all outcomes are equally likely; and this means that I can predict that 7 will come up a lot more than 12, on a statistical basis; but it still doesn't allow me to predict the outcome of a particular fall of dice.
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crashfrog Member (Idle past 1488 days) Posts: 19762 From: Silver Spring, MD Joined: |
I assumed that it meant that stem cells could make more of themselves. But can't every cell do that? Actually most cells in the body can't replicate themselves. As part of the differentiation process, they often lose unneeded organelles. For instance, red blood cells have no nucleus. Some cells in the body are constantly replicating - bone marrow cells, hair follicles, the outer layer of your skin, the inner layer of your gastrointestinal tract.
To clarify, this is how all the DNA of a cell organizes itself? This is not one super-long double-helix, but rather many separate strands of super-long helixes, right? Yeah, 46 such strands. Each chromosome is a seperate strand.
I can see it causing differences between me and another human, but I have trouble seeing it explain the differences between me and, for extreme sake, a spider. The only difference between you and the spider is the content and arrangement of your genetics. "Moby Dick" and "Pride and Prejudice" are two very different novels, but consider the fact that they're both written with the same 26 letters of the English language. The genetic alphabet is only four "letters" long. The most surprising discovery of the human genome project is that the entire human genome is only about 15,000 genes. What I'm saying is, it doesn't take a great deal of genetic information to represent the difference between you and the spider.
I hate to admit this, but I don't see how mutations could form, say, an organ like the liver or the intestines. Yeah, but we find livers in every single multicellular organism above the level of a sponge; the intestine is simply a tube. The basic roundworm has an intestine, and it just passed it on down. The basic cell already has functions for filtering and disposing of waste, as well as for storing energy. So the function of the liver doesn't seem like a big mutational stretch. If you're wondering what gene it takes to specify a liver, I don't know myself. That would be a question of evolutionary developmentology, I think.
Do all of those 300 mutations appear in each individual gamete? Or did you mean the total number of mutations for the entire gamete "population"? Every single one of your body's cells, including each of your gametes. Of course, your gametes have mutations of their own that could be potentially passed on as well. Mutations all over the place, that's what I'm trying to get across.
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Doddy Member (Idle past 5931 days) Posts: 563 From: Brisbane, Australia Joined: |
taylor_31 writes:
I don't see mutations causing that organisation either - at least not alone. Selection is needed to assist in that process - selection of those mutations that just happened to create something like an organ. After all, having a little pocket of your body that filters a bit of blood can make all the difference when toxins are present in the environment (which they usually are), and so selection will work to increase (or rather, keep the mutations that increase) that particular organ's function, and discard those that make a mess of things. I hate to admit this, but I don't see how mutations could form, say, an organ like the liver or the intestines. They just seem so specialized to me, and I can't see a mutation causing such organization. Contributors needed for the following articles: Pleiotropy, Metabolism, Promoter, Invertebrate, Meiosis, DNA, Transcription, Chromosome, Tetrapod, Phenotype, Messenger RNA, Mammals, Appendix , Variation, Selection, Gene, Gametogenesis, Homo erectus and others. Registration not needed, but if desired, register here!
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MartinV  Suspended Member (Idle past 5850 days) Posts: 502 From: Slovakia, Bratislava Joined: |
One of the most claimed and unproved darwinian statement is that behind evolution stands random mutation as the source of novelties. Both natural selection and drift (ultra selectionists vs neutral- driftists) depends on them.
In his latest article in NYT R. Dawkins (there is no free access anymore to it, but the link to it's transcription is on the bottom of my post) took for granted that random mutation is responsible for dog's diversity. Breeders would be surprised by such a statement. They only pick up desirable characteristics by combining of existing alleles. If those alleles arouse via random mutation is questionable. We cannot breed lizards or tigers - obviously desirable alleles are not present or those species do not mutate. Dawkins btw. ridiculed Behe using this argument:
quote: But this is obviously just a story:
quote: Not Found - The New York Times
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anglagard Member (Idle past 858 days) Posts: 2339 From: Socorro, New Mexico USA Joined: |
Astounding.
Your great argument against evolution has been reduced to the misrepresentation of St. Bernard's as portrayed in Bugs Bunny cartoons.
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MartinV  Suspended Member (Idle past 5850 days) Posts: 502 From: Slovakia, Bratislava Joined: |
Not at all. You haven't read the first part of my post. But I underestand you are ashamed reading Dawkins arguments.
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anglagard Member (Idle past 858 days) Posts: 2339 From: Socorro, New Mexico USA Joined: |
I read the first part of your post, but the idea that mutation does not exist, or that all mutation is somehow inherently negative for continued existence, is obviously false. Do I need to show you where mutations, including human mutations, proved to be positive? There are plenty of examples within and without this forum.
Edited by anglagard, : too much emotion
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MartinV  Suspended Member (Idle past 5850 days) Posts: 502 From: Slovakia, Bratislava Joined: |
I somehow didn't claim that mutations do not exist or are bad/positive. What I claimed is that mutation and natural selection/neutral drift do not lead to speciation. It would be observed if it were true. Artificial selection is used many thousands years. We have a lot of experience with it. Species do not change by random mutation and natural selection. There must be some other forces behind evolution.
It took a lot of time till 19 century that idea of natural selection as one of the sourcees of speciation appeared. Breeders of many generations and civilisation somehow didn't notice the simple fact. Dawkins mentioned only mutation in dogs. The other question is why we can't breed lizards or tigers. Either there are not alleles that can be used for domestication or these species do not mutate.
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
Could you point me to some reference for the thousand year breeding experiment to create new species, if there isn't one then absolutely none of what you say seems to have the slightest relevance. Its the same sort of nonsensical argument as the one by people claiming that decades of fly based mutational assays haven't produced new species, they are demanding a particular result from a process which was never intended or claimed to produce such a result.
Why would artificial breeders, whether in farming or hobbyists, be trying to breed for post-mating reproductive isolation or even setting up situations which would encourage its development? Do you have any evidence that they actually have done so?
The other question is why we can't breed lizards or tigers. Who says we can't? Other than you that is. Besides there are already hundreds of species of lizard, how many more do we really need? TTFN, WK
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anglagard Member (Idle past 858 days) Posts: 2339 From: Socorro, New Mexico USA Joined: |
MartinV writes: What I claimed is that mutation and natural selection/neutral drift do not lead to speciation. It would be observed if it were true. Fascinating, I guess you disagree with this Observed Instances of Speciation
Dawkins mentioned only mutation in dogs. The other question is why we can't breed lizards or tigers. Either there are not alleles that can be used for domestication or these species do not mutate. Perhaps the question is not so much can't but rather why. Why would our ancestors want to breed tigers, which are not communal hunters like dogs? After all, even the most nature-isolated person should be able to see that hunting dogs and humans are a serendipitous combination. Ever heard of a hunting lizard that puts food on a human plate?
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