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Evolution Can Occur Much Faster Than Previously Thought (ox.ac.uk)
An anonymous reader writes: An Oxford study on chickens discovered that evolution can make significant changes to a genome in as little as 15 years. "For a long time scientists have believed that the rate of change in the mitochondrial genome was never faster than about 2% per million years. The identification of these mutations shows that the rate of evolution in this pedigree is in fact 15 times faster." Professor Greger Larson, senior author on the study, said, "Our observations reveal that evolution is always moving quickly but we tend not to see it because we typically measure it over longer time periods."
See the Earth is only 4,000yrs old :)
Well considering that for the longest time, fossils were our main source of viewing evolution through time, of course it would seem to be slow. Who knows how many speciation events happen and die off before being able to leave a mark in the fossil record.
Those who do not learn from commit history are doomed to regress it.
Nobody has thought for decades that evolution is a slow continuous process. Rather that it has periods where nothing much happens, then there's a spurt of changes, then another period of calm.
Pick the right time interval and duration and you can see either one or the other, as you want. Great way to make data fit your favorite theory :-)
"Transparent" is a shit show that trades on every stereotype going. A man in drag is NOT a transsexual.
The chickens with mutations were kept for further study and their genes live on.
The other chickens are thrown away.
There appears to be a survival advantage.
Domesticated animals have changed significantly in the past few few decades let alone the past few thousand years. Modern broilers (meat chickens) can't even self procreate due to the changes but also grow from chicks to food in a couple months. Dairy cattle are another example, Today 9.3 Million dairy cattle produce 59% more milk than 25.6 Million cattle produced in the 40s. This isn't limited to animals, grain producing plants have significantly changed since the 30s, corn specifically has went from around 25 bushels per acre in the 30s to over 140 bushels per acre today. Anyone with even a passing knowledge of farming could have told you this. It should be noted though that while these plants/animals work well for modern farming, most would almost certainly go extinct after a few years without human care due to their extreme specialization (grain production, milk production, meat production, egg production etc).
We've never observed evolution yet
Wrong
some scientists only assume it from observed differences in the fossil record.
Not "assume", "infer", and anyway decades of molecular biology, genetics, and genomics have proven at least as useful as fossils. My favorite example here.
If you ate the same chili I did, they won't be in your gut for long.
You are welcome on my lawn.
There's a common misconception that fear can cause your hair to turn white. It's wrong, but true. What happens is that your hair us going white. It's 10% white, and nobody notices. 30% white and people can see it clearly, but don't point it out. But when you are at 30% white and have a strong fear event, you can have some hair fall out. The hair that falls out is disproportionately non-white. So it gives the appearance of a sudden whitening of your hair, caused by fear.
And my first thought on this was the same thing. Random mutation is long-term. But when a selection event happens, the "hidden" trait isn't created, but selected for. There is no "evolution", but a selection pressure that reveals the previous mutation as a preferential trait, making it appear to happen suddenly and revealed by the "cause" but not actually caused by the "cause".
Learn to love Alaska
Who is "we," kimosabe? Because the repeated emergence of antibiotic resistance, for example, is observed evolution. Then, if you're going to hang your hat on supposed horizontal gene transfer for antibiotic resistance, there's that niggling problem of emerging resistance to antimalarial drugs...
You-we may never have observed evolution, but medical-we certainly has.
"it's not random and undirected, a requirement for evolution."
Counterpoint, by J. B. S. Haldane:
"Teleology is like a mistress to a biologist: he cannot live without her but he's unwilling to be seen with her in public."
The paper is here but it is probably paywalled. (I have institutional access, so I'm not sure what that link will do to people who don't.)
This is part of an ongoing debate about rates of evolution. To a large extent it was kicked off by a 2005 paper by Simon Ho et al. (Ho is second author on this paper.) They observed that estimates of mutation rates derived from studies over short time periods are much higher than mutation rates derived from studies over long time periods. Short time periods are up to a few thousand years, e.g. comparing populations that have been separated by for a few thousand years, or ancient DNA compared to modern DNA in the same species, or multigenerational studies over a few years or decades such as this one. Long time periods are from comparing species whose common ancestor is typically millions of years ago.
This apparent acceleration in mutation rates is controversial.
I'm going to read the paper now, so I may have more to say later.
Quattuor res in hoc mundo sanctae sunt: libri, liberi, libertas et liberalitas.
We have better than 2 dozen scientifically confirmed speciation events fully documented and available in the literature in the less than 200 years we've been watching.
Evolution is a fact. There are entire branches of biological sciences based on it that would not be viable sciences without the existence of evolution. Those branches of science have a direct effect on you several times a year and one day they might cure your cancer. To deny evolution denies the reality around us every day.
There are two issues here. One is that a single DNA site could mutate several times. If we only see the end points, it looks like only one mutation has occurred (or even zero, if it mutates back to where it started.) This is pretty easy to correct for. E.g. if you compare two sequences and they differ in 10% of sites, it is reasonable to think that 1% of sites have actually mutated twice. (That is a little oversimplified, but not by much.)
The other issue is that a DNA mutation can spread through part of the population, but then go extinct. If you measure over short time periods, you see these mutations, but over long time periods you don't. There are mathematical reasons to think this does not affect your measured mutation rates if the mutations are neutral (neither helpful nor harmful.) Look up "neutral theory of molecular evolution" for details. However, if they mutations are slightly deleterious, this can be an issue, but there are limits to what you can achieve with this mechanism. (I wrote a paper on that once.)
Quattuor res in hoc mundo sanctae sunt: libri, liberi, libertas et liberalitas.
Viruses meet all the requirements needed for evolution to apply to them.
Quattuor res in hoc mundo sanctae sunt: libri, liberi, libertas et liberalitas.
Let me see if I understand. By measuring over a long period, we're measuring the long term rate of mutation survival after applying selection pressure, and that could be noticeably different than the raw rate of mutation. Is that a correct summary?
Please go slowly with me. I'm an engineer, not a biologist, and I admit biology is not my strongest subject. I am actually curious, though.
I remember hearing that there are large sections of DNA in many living things that are effectively "junk DNA," or at least we think are junk DNA. By junk DNA, I mean DNA that doesn't code for any useful proteins or other molecules, and generally seems to take up space. (I'm skeptical that there is much that is really "junk," but bear with me.) If there really are large stretches of non-useful baggage, it would stand to reason that these sections would not be subject to selection pressure, and so mutations to these sections aren't directly subject to selection pressure, because they don't affect the fitness of the organism.
Is there a way to measure the mutation rates for different sites in the overall genome of a given organism, so that: (a) we can determine if some regions are actually junk because mutations to them do not affect organism fitness, and (b) can distinguish between the rate of mutation and the rate of mutation survival? (This question more or less assumes my understanding in the first paragraph is accurate.)
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Let me see if I understand. By measuring over a long period, we're measuring the long term rate of mutation survival after applying selection pressure, and that could be noticeably different than the raw rate of mutation. Is that a correct summary?
Yes, that is correct. The technical term for 'mutation survival' is 'fixation'. A mutation is 'fixed' once the entire population carries it. It is 'extinct' (unsurprisingly) when it no longer exists in the population. When it exists in part of the population it is 'segregating'.
There are huge amounts of DNA that have no known purpose and appear to be junk. This is over 98% in humans, but varies a lot between organisms. The junkness of this is under debate. My feeling is that much of it really is junk, but some of it has a function we don't yet understand. (Also, sometimes the function is simply "we need a certain amount of space between these two bits of non-junk". This has a clear purpose, but is 'junk' in that the DNA letters don't matter.)
This particular experiment is about mitochondrial DNA which has very little 'junk', and that which it does have probably at minimum has something like 'need this amount of space' function.
Yes, scientists do like using 'junk' DNA for phylogeny (making family trees of organisms) because it is (we think) not subject to selection. On the other hand, you need to find the corresponding junk regions in all your critters and sequence them. It is easier to identify corresponding genes, and often someone else (who cared about the genes themselves) has done the sequencing work for you. Often the choice is doing phylogeny on genes using only a computer, when phylogeny on junk DNA requires samples and a molecular biology lab. Another issue is time scale: the junk DNA mutates faster, so it is good for closely related species (e.g. 'apes') but for distantly related species (e.g. 'vertebrates') you need highly conserved sequences (genes). The junk DNA will have mutated so much that it is all noise, no signal.
Is there a way to measure the mutation rates for different sites in the overall genome of a given organism, so that: (a) we can determine if some regions are actually junk because mutations to them do not affect organism fitness
Yes, if we have diverse organisms and a good alignment of their DNA, we can look for 'junk' regions by how much mutation occurs where. (Actually it tends to be the other way around - we see islands of conserved sequence, and deduce therefore that they have a function. This isn't how genes are detected, as there are more sensitive gene-specific ways of doing this.)
and (b) can distinguish between the rate of mutation and the rate of mutation survival?
Only I think by comparing mutation rates over pedigree time scales (a few generations) with mutation rates over long time scales - which is what this paper addresses.
Quattuor res in hoc mundo sanctae sunt: libri, liberi, libertas et liberalitas.
https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment
E. coli evolved to eat a new chemical (citrate). It developed a new enzyme to do it. E. coli was previously defined as not being able to eat citrate. By the former definition, it has evolved into a new species.
How is antibiotic resistance a loss of function? Troll better, please.
Several of them are listed here: http://www.talkorigins.org/faq...
What I don't understand, is if it takes so many generations for a mutation that may or may not do anything, how do you explain complex functions that require thousands of beneficial mutations before the new functionality actually causes a survival benefit. I can't see how it would ever happen.
It's like throwing match sticks on a floor hoping one day it makes a sentence. You may after billions of attempts get a letter, but you will never achieve a whole sentence when those partial non beneficial mutations that are yet to form a beneficial structure are mutated back out again.
46137
Selective breeding is not evolution. First, it's not random and undirected, a requirement for evolution. Second, it creates no new traits. Selective breeding can only select among traits already existing in the genome.
Evolution isn't random and undirected. Random mutation paired with non-random selection results in evolution in the way it is conventionally thought of. Selective breeding changes the populations being selected, so does result in evolution.
Thank you for the thoughtful and detailed response. I think I have a better understanding. (But, I'll always stay mindful of the Dunning-Krueger effect... ;-) )
BTW, this statement captures something I was trying to express more clearly than I stated it:
What I was trying to get at was that if a section of DNA performs some useful function, even if we don't know what it is, it'll tend to be preserved because selection pressure will tend to preserve it by "selecting out" individuals whose mutations tampered with it. The observed long-term mutation rate for any given point should in some sense be inversely related to that point's significance. (More significant => fewer mutations, likely by a function much more stark than just "1/x", where "x" is significance. Key proteins should have a really strong bias to remain unmodified in viable offspring, for example.)
I now have a slightly different question: You mentioned the rate of repeated mutations, where the same piece of DNA was mutated twice or more, sometimes back to its original state. Suppose the environment shifts, such that selection pressure would favor a certain set of mutations to adapt a species to that new environment, and then the environment shifts back. I'm thinking fairly long term, cyclic shifts such as ice ages and the like.
Would such cyclic shifts meaningfully affect the assumptions underlying the multiple mutation rate? You gave this example: "if you compare two sequences and they differ in 10% of sites, it is reasonable to think that 1% of sites have actually mutated twice." I realize you mentioned it was oversimplified. It jibes with a basic knowledge of statistics and statistically independent random variables. I guess what I'm getting at is that cyclic shifts that affect which mutations improve, decrease or are neutral with respect to fitness would imply at least some of the variables aren't independent.
I guess it comes down to what fraction of the mutations actually affect fitness with respect to these cyclic forces. I imagine it's a fairly small proportion relative to the total set of mutations whose fitness effects are completely orthogonal to those long-term cyclic changes. If that's the case, am I correct thinking the effect wouldn't be large?
I guess in general, if the total delta between two samples is still relatively small (10% in your example), any second order effect such as this could only affect that approx 1%, and so that already bounds the potential error from simplifying assumptions anyway.
Again, thank you for your helpful (to my understanding, at least) response.
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What I was trying to get at was that if a section of DNA performs some useful function, even if we don't know what it is, it'll tend to be preserved...
Yes.
Would such cyclic shifts meaningfully affect the assumptions underlying the multiple mutation rate?
I'd expect it to be a very minor effect. I'm not aware of anyone getting worried about this. It is a matter of statistics: if you're comparing 100,000 DNA sites, you don't care much if 50 of them behave weirdly in some fashion. If you successfully target 'junk' DNA for the comparison, it is not an issue.
A related effect is convergent evolution. Say two species of bacteria each colonize high temperature environment. Then certain mutations which are favoured in high temperature will likely occur in both of them. When we compare their DNA, this can make it look like they are more closely related than they really are. This is more of an issue in morphology (Darwin's finches, for example, or cormorants, which look very similar all around the world but turn out often not to be closely related) but it can happen at the DNA level too.
Quattuor res in hoc mundo sanctae sunt: libri, liberi, libertas et liberalitas.
Got it. With everything else you've explained, that makes sense.
Ah, that also makes sense.
I thank you again for the informative responses. You've expertly escorted me up to (or possibly even well past) the edge of my competency. :-) I've certainly enjoyed the trip.
It's truly a fascinating topic, but for me to really get much more out of it, I think I need to do some homework to learn more about what's already known. There's only so much a generically analytic mind can do w/out learning what's already known in the field.
Thanks again.
Program Intellivision!
Humans and chickens are in a symbiotic relationship. We use them for food, they use us for getting more chicks. So chickens will evolve to be more tasty (because we select them that way), while we evolve to digest chickens more effectively and become less sensitive to the diseases they carry (because they select us this way). That we perceive to be in charge and are doing this "consciously" (whatever that means) is irrelevant from an evolutionary perspective.
I could have spent the effort debating the creationists. This was much more fun.
Quattuor res in hoc mundo sanctae sunt: libri, liberi, libertas et liberalitas.
What I don't understand, is if it takes so many generations for a mutation that may or may not do anything, how do you explain complex functions that require thousands of beneficial mutations before the new functionality actually causes a survival benefit. I can't see how it would ever happen. It's like throwing match sticks on a floor hoping one day it makes a sentence. You may after billions of attempts get a letter, but you will never achieve a whole sentence when those partial non beneficial mutations that are yet to form a beneficial structure are mutated back out again.
You understand correctly. It is extremely rare if non-existent for even small non functional changes. All changes have some intermediate functional state. You can have horizontal transfer in some cases, but this does not imply you get a free lunch, nor does an inactive or 'junk' sequence acquiring an advantage.
It's also beneficial to note that with organisms like bacteria, over long periods of time, it's not billions of attempts, not trillions, not quadrillions. It surpasses quintillions of attempts for a single species and all it takes is one success to fix it in a population. It's a massively parallel process and just because humans often are extremely poor at conceptualizing it, that does not invalidate reality.