Natural selection is a simple theory because it can be understood by anybody; to misunderstand it requires special training.
Graham Bell, The Masterpiece of Nature
Interest has been expressed in a thread on selection and drift, so I thought I’d start one, and offer my own 2-cent summary of the concepts.
Evolution, as commonly understood in biology, simply involves change in a lineage. Through mechanisms of change – principally, mutation and the insertion of ‘foreign’ DNA sequence – offspring frequently contain DNA sequences that do not derive by simple copying from their parent(s). This change is inevitable and, iterated, inexorable. There is no memory, no externally-stored blueprint for organisms; the specification of a species ‘floats on the breath of the population’, as Doctor Johnson wrote of the unwritten Gaelic language. Unless there is some kind of boundary blocking all possible avenues, a continuing source of variation is sufficient to keep a lineage exploring never-before-seen genetic space ad infinitum.
Among close ecological competitors (among, for example, the genetically similar members of a species), at a given locus in a finite world one individual ancestor’s genetic sequence is headed towards being the ancestor of every instance of that locus in a future population, and all the others with which it shared a population are heading for extinction. This derives from two facts: samples are more likely to deviate from the frequencies in the wider group than match them, and the probability of fixation of an allele is equal to its current frequency. The distortions on generational sampling tend to reinforce, through to extinction of all but one variant. This same tendency underlies the ecological principle of competitive exclusion between non-interbreeding competing species.
If a particular locus is invariant in a population, fixation has already happened. An original mutation, occurring in a single ancestor, has been passed to every member of the current population. Looking forwards, the mechanism of this concentration continues to operate, and so one particular individual from the present population will become the ancestor at that locus of all members of a future population. From any given starting point, a population of N diploid individuals will take a mean 4N generations to achieve fixation of one ancestor’s copy, and the probability for any diploid locus of being that copy is 1 in 2N. This doesn’t mean that large populations cannot fix neutral alleles, however – the number of mutations occurring scales with population size, so mutations will be fixed at the same rate they are generated, completely irrespective of population size. Doubling the population gives twice as many mutations taking twice as long to fix – the result is the same number of mutations being fixed per generation.
At the point of fixation, all instances of that locus descend from the same ancestor – they coalesce upon that ancestor. The case described – where there is no variation at all at the locus, ie there is just one allele – is the baseline process, the neutral case. If there is no variation, there is nothing for Natural Selection to ‘see’. The only process in operation is random genetic Drift – even though in this instance, it effects no evolutionary change because there are no variant alleles. The change occurred with the original mutation. This latter fact leads me to prefer the view of ‘descent with modification’ over the population geneticist’s ‘change in allele frequency’. It is true that allele frequency change is also evolution, the only part over which selection and drift have a role, but as far as each lineage is concerned, the change occured at the moment of mutation. The lineage changed at that point; the population changed somewhat later, when this mutation became the norm.
Suppose we could uniquely label the locus for every member of the population, in a heritable manner. Now, we have essentially created 2N alleles. If we allow them to operate neutrally, just as when there was no variation, evolution will now occur because allele frequencies must change in the population. Because our labelling has had no effect on the neutral ancestry-fixation process, the label itself will surf to fixation on this process, while all others become extinct.
If, instead of labelling every instance, we simply labelled one, we would find that it still had the same 1 in 2N chance of becoming fixed. And this is the situation for any neutral mutation: 1 in 2N neutral mutations will become fixed; the neutral mutation simply functions as a label.
So now, having laboured the neutral case, where all is Drift, we can look to introduce a differential between alleles. If a new allele consistently performs better or worse than the existing one – meaning that it enhances or hinders the survival and/or reproduction of its bearers – then Natural Selection has come into play. It is a simple and obvious and non-tautological!) truth that a consistent increase in survival/reproduction – in fitness – will tend to favour such alleles over the purely neutral case, and render fixation more likely and speedy, while a reduction will increase the likelihood and speed of elimination.
Unlike the purely neutral case, in which population size is cancelled out, the behaviour of selectable alleles is affected by population size. In smaller populations, random factors have a greater influence than in larger ones, and hence alleles may behave as effectively neutral despite possessing an advantage which would see them selected in a larger population.
Drift does not simply disappear when you start to turn up the selective ‘heat’. Drift essentially derives from random sampling, the tendency of subsets to deviate from the distribution of the complete set, and such sampling is in effect almost all the way along the continuum of selective advantage (apart from alleles that are so strongly detrimental that they never gain a foothold). Even a favourable allele can disappear through Drift, likewise a deleterious allele can become fixed through the same mechanism. But more often, progress will go with the expectation, not against it. The large-number tendency is for genomes to become enriched in advantageous alleles and impoverished in detrimental ones. Because this process is environmentally conditioned, it allows populations to adapt to their circumstances, by purging the traits that do worst in the recent environment.
There continues to be a debate about the relative importance of Selection and Drift in evolution generally, and in driving speciation among sexual forms. Only selection can be adaptive, because it is the only component that is responsive to the environment. But they both have significant contributions to make, and cannot readily be teased apart. Both tend to reduce the variation in a population, which variation is only restored by mutation, recombination or immigration.
Actually, in my recent numerical example I did not declare either allele to be deleterious, nor did I declare either allele to be advantageous. I also did not invoke the phrase “survival of the fittest”.
phoodoo failed to notice this.
I just gave a case with three genotypes, the ones formed by two alleles. I gave their fitnesses and the population size. Then I asked phoodoo to.predict what would be the probability of fixation.
If the theory of natural selection is vacuous, and if I have failed to see this important logical point, then phoodoo should be able to tell us the outcome. Asking phoodoo should become our main method. This would avoid the difficulty of solving equations or numerical integration.
phoodoo can henceforth be an oracle who tells us what will happen, since phodoo has had the brilliant insight that we all missed all these years.
Provided, of course, that phoodoo can make the prediction.
Alan Fox,
What does that have to do with proposing a theory which says advantageous mutations should spread through a population at a specific rate, and then defining advantageous mutations as those which spread at the rate which your theory just proposed they would?
There is no way for such a theory to be wrong.
Joe Felsenstein,
Joe, by your little theory, I don’t have to decide which is advantageous and which is deleterious beforehand, because after I see the alleles spread through the population, I can then decide if it is advantageous or deleterious.
There is no meaning to the terms, other then how much they spread through the population. If you get it wrong, you just change the designation for the allele.
Are peacock feathers advantageous? Of course, because they have spread throughout the population.
http://en.wikipedia.org/wiki/Mutation#By_effect_on_fitness
A deleterious mutation decreases fitness. That it spread through the population more than what was expected does not mean it increases fitness.
By the way, it should be noted (by you, phoodoo), that we are talking about two different concepts of fitness.
Allan is talking about the modern conception of (biological) fitness (the ability to both survive and reproduce, equal to the average contribution to the gene pool of the next generation that is made by an average individual of the specified genotype or phenotype).
That’s not the concept of fitness involved in the phrase “survival of the fittest” (which would be just the ability to survive and reproduce, i.e. having adventageous characteristics).
Natural selection alone is not a theory, it’s a component of one. It’s an observed process, being used as a mechanism of a theory. It’s not he only mechanism.
The theory is that populations of organisms change and adapt to their environment through natural selection of arising changes, over generations. This can easily be falsified, if you could show that beneficial adaptive changes do not arise at all, or that they are not heritable. They observationally do, not definitionally. For example, we could theoretically observe that all mutational change is deleterious. Or we could observe that when an adaptive change arises, this cannot be passed on to the offspring (like a somatic mutation). Both of these would falsify the hypothesis that adaptive changes happen and contribute to evolution by being fixed in populations over generations.
Of course, this is not what we observe, so the theory has survived this attempt at falsification. As explained earlier, we can also use this to predict the average propensity for certain mutational changes to become dominant in the population, when and if they arise.
Again with the same bullshit?
Adventageous mutations can be identified because they spread through the population, they are not defined as mutations that spread through a population.
Spreading through the population is the RESULT of peacock’s feathers being adventageous, NOT THE CAUSE.
The concept behind “survival of the fittest” is that THERE IS A CAUSE to peacock’s feathers being adventageous, that is related to its ecology. There must be some instance in the peacock’s life when having those feathers is better than not having them. That’s the meaning of BEING ADVENTAGEOUS.
Haha Guillermoe, you are funny. How do you know peacock feathers are advantageous?
Because they have spread through the population of course!. Hohoho.
phoodoo,
If carriers produce fewer offspring than non-carriers, then it continues to be deleterious. Because deleteriousness is not defined by whether it spreads or not, but by its effect on the mean offspring numbers of carriers vs non-carriers, which you can measure independently of allele spread. If the probability of fixation is non-zero, then some of the time it must fix, surely?
As noted, and repeated, and I’ll repeat it again: by its influence on the mean offspring numbers of carriers vs non-carriers. Which can actually be tricky to measure, but that’s not really the issue here. Given a particular differential, there will be a distribution of frequencies of fixation and loss for hypothetical repeat runs of alleles with that differential. Pick any differential you like, including none, and there will be a probability distribution of fixations/losses associated with it.
Whereas of course the alternative ID “explanation” is that the designer wanted it that way. Or do you have something that explains the observed fact of the tail better then that?
Yet at least it exists! So you can stop with that claim, or be dishonest, as you prefer.
phoodoo:
Now, can you prove this wrong? You can’t . Its undeniable. Its totally unfalsifiable because the definition of someone who is a Good hitter, is someone who hits it 60% to right field, because I decided this is what the definition of a good hitter is. Its not batting average, or home runs, or anything else you might THINK it is, it is what I defined.
No one can prove that is not your definition, but everyone else’s rule will be to ignore your metric unless you can show a basis for it.
Again, you’re confusing how one knows something with what it is that someone knows.
That’s a good point. If noting that fitness increases survival propensity were tautologous, noting that ANYTHING produced survival propensity would have to be equally tautologous–including whatever ID proposed.
So, e.g., suppose the reason there are humans is that God, in HIS infinite wisdom wanted to create something a little bit like HIM (i.e., in HIS image). Our knowledge that HE did this would have to be inferred from the current existence of humans. All explanations would be tautologous.
Of course, this has been explained to you about 85 times now.
Allan,
when you say, “Because deleteriousness is not defined by whether it spreads or not, but by its effect on the mean offspring numbers of carriers vs non-carriers.”
So it is already a “given” that deleterious mutations will have a certain effect on the mean number of offspring in a population. So when you have a theory that tries to answer whether or not deleterious mutations will have that effect on the mean offspring number of carriers vs. carriers, and then define deleterious as those which have the results you are testing to find…guess what you are going to find???
That deleterious mutations exactly match the definition that you have just given for it, because if it didn’t match, it wouldn’t be considered deleterious. And seventh graders could understand that circular reasoning.
You are so dumb. Listen to this dumb example: if you shout Guillermo when you are close to me, I will answer. So, you can KNOW, DETECT, that my name is Guillermo because when you call that name I answer.
Now, the reason I am called Guillermo is that when you call that name I answer OR IS IT THAT MY FATHERS CHOSE THAT NAME FOR ME.
I can KNOW that peacocks’ feathers must be adventageous because they spread through the population.
But the REASON peacocks’ feather ARE ADVENTAGEOUS is that females prefer males with large feathers.
The concept is that adventageous features have a high tendency TO SPREAD IN THE POPULATION.
Adventageous features are adventageous because the are helpful and THE RESULT (NOT THE CAUSE) is that the spread through th population.
Basically, you are distorting semantics to sustain your stupid view. You are confusing how we know something is a certain way with WHY IT IS that way.
phoodoo,
They could equally see the emptiness of your attempt to argue away the concept.
If an allele reduces fitness (reproductive output), it is deleterious. If it didn’t reduce fitness, it would not be considered deleterious. And? This is, after all, the definition, so it would be peculiar if it were any other way. Reduce this to a general case. If an X has characteristic Y, it is X’. If it does not have characteristic Y, it cannot be X’. Super. So everything is devoid of explanatory power, now?
The losers are the team scoring the fewest goals. So, to paraphrase …
It’s sex, phoodoo. Peacock sex! Part of the niche.
What phoodoo is kindly trying to get the focus away from is the fundamental idea that deleterious and advantageous features are not deleteroius or adventageous PER SE, but there is a connection between the feature and the ecology of the population considered.
A deleterious mutation decreases fitness, but it’s not deleterious and decreases fitness just because it’s deleterious and decreases fitness, as phoodoo sustains.
If we study the life cycle of the organism considered, we can detect exactly how that feature is becoming a disadvantage to the individual carrying it. And it’s because of that, because that feature in a certain moment of the life cycle of this organism becomes a disadvantage, that, on average, it reduces fitness.
There is connection between the feature, the life cycle and the average reproductive rate. That’s what survival of the fittest means, and it’s no tautology, because that connection might have not existed.
phoodoo,
It is a given that the fitness differential s between two alleles will have some value (even if zero). One can calculate the expected fate of alleles with any value from that continuum. One can try and measure s. No-one is trying to find out whether a mutation that reduces fitness reduces fitness.
Or how we identify a trait with the reason it is a trait.
We identify advantageous traits by differential reproductive success. Why they are advantageous is another question. It may or may not be obvious.
One trait may ride on the back of another.
This, exactly this. Phoodoo seems to think he’s hit some kind of deep homerun by showing how that which corresponds to the definition, definitionally corresponds thereto.
Holy shit, stop the press! I’m still waiting for the punchline. Actually I’m not, I know there isn’t one. Phoodoo has confused himself into thinking this statement about tautologies means natural selection is an invalid concept.
That’s not what the theory is trying to answer.
The theory is trying to answer how it is that extant biodiversity came to exist and be so well adapted to it’s environment. In order to do that, it draws on an observed mechanism: Natural selection. Natural selection is not the theory itself, it is one of the mechanisms of the theory.
Natural selection is not what the theory is trying to explain, it is but one of the components responsible for the change the theory is using to explain extant biodiversity and it’s adaptedness to the environment.
Please, please get this.
But in my numerical example, I did not use the terms “advantageous” or “deleterious”. Nor did I use the phrase “survival of the fittest”.
And we’re still waiting for your prediction of which allele will spread.
It would be trivial to falsify the mechanism of natural selection as a substantial contribution to evolutionary change: Either you could show that adaptive changes never arise (if all mutations without exception were deleterious), or that if they arise, they aren’t heritable.
Phoodoo, here’s why you should stop posting: You’re wrong at a trivial and embarrassing level.
Allan,
First one needs to find out whether or not it is true that deleterious mutations actually spread through the population in the way you predict, and if advantageous mutations also spread through the population in the way the theory predicts.
But of course if you alter the definition of advantageous to mean that which spreads through the population as you theorize it might, well, bingo! You theory is proven before you even have to confirm it.
So do advantageous mutations REALLY spread through the population the way Joe says they do?
Yes, in the same way that good hitters hit to right field 60% of the time, if the definition for being a good hitter is hitting to right field 60% of the time.
(Actually we don’t know if that is true or not, but the theory is rigged to assume the outcome before we even have shown that it is true-circle, get it…..No of course you don’t. So go join Guillermoe, he is equally unable to penetrate this deep thought.)?
You know Allan, it is actually possible that advantageous mutations spread through the population at a much much lower frequency that what you are assuming, but since you have tied you definition to the result, you can never get a wrong outcome. Gee, what a tough concept to grasp. Holy Cow.
But Alan knows it is true, that is why he hopes you ignore it, because it is becoming painfully obvious.
What he is missing is the full picture of this concept. As has been said, we detect advantageous traits because of their higher fitness, i.e. reproductive rate.
But the reason they are advantageous is not that higher reproductive rate, but the way it affects the life of the individual carrying it. And this is the part phoodoo is refusing to see. That trait PLAYS a role in the life of this organism.
The concept of survival of the fittest is that according to that effect being positive, neutral or negative, that trait will spread more or less in the population. THERE IS NO TAUTOLOGY. Just omission of part of the concept.
Rumraket,
Or that getting the luckiest gene mutation isn’t the biggest factor for determining what provides the statistical advantage for survival. It could well be that deleterious mutations spread through the population just as easily as advantageous ones, but if you theory assumes the answer, then the conclusion is also the question.
Whats the best mutation, one for speed, one for slow, one for fat, one for skinny, one for big teeth, one for no teeth, one for poison venom, one for no venom, one for good eyesight, one for bad eyesight, one for slow metabolism, one for fast metabolism…You can’t answer any of these. The only way you can answer is by saying that which spreads the way you assume it will is always the best one. And they all do.
Why is a mouse grey? Because it is advantageous.
How do you know. Because it spreads though out the population with the highest frequency. And so you circle is united!
phoodoo,
Oh, knob off! I’ve already given you the definition of advantageous in terms of mean fitness of carriers, which can be considered as independent of any particular run of the allele through to fixation or loss. I haven’t altered it to mean that which spreads through the population. You keep doing that. By mathematical analysis (and common sense), fitter alleles must be frequently lost, particularly at low frequency, so that would be a silly definition. No-one uses it; you are tilting at straw windmills.
“(Actually we don’t know if that is true or not, but the theory is rigged to assume the outcome before we even have shown that it is true-circle, get it…..No of course you don’t. So go join Guillermoe, he is equally unable to penetrate this deep thought.)”
This is a strawman. Your dumb example about hitters has nothing to do with survival of the fittest.
I already asked you to show how survival of the fittest is always true with a real biological example: field crickets.
I think that you are the one trying to stop us from penetrating your bubble of fantasy by denying to analyze a real case.
That’s not the theory for fucks sake. Natural selection is not the theory, is is a mechanism of a theory. The theory of evolution by (among others) natural selection.
The question isn’t “what is advantageous”? Or if that really is your question, then yes – the answer is “that which does better on average”. But then your question is without meaning or consequence to the theory of evolution as a whole, all it does is capture what the definition of a beneficial mutation is. Define X such that if it does Y, it isX. All definitions are like this.
But really, the question is “how did extant biodiversity come to exist and be so well adapted to the environment”? One part of the answer is that mutations that alter the something about the organism arise, and that subsequently they are subject to negative or positive selection.
Not in blanket fashion like that, no. It would require extensive knowledge of the environment where the mutation is introduced. So the answer is it depends.
No, all I can say is that if it arises and spreads, then it beneficial by definition. That doesn’t mean I know it is the best one.
Clearly not, there are plenty of mutations going to extinction all the time.
Without context you can’t actually say that. All you can say is that either it inherited it’s colour from it’s parents, or it arose by mutation with conception of the mouse
Congratulations, you’ve explained how the concept of a beneficial mutation corresponds to the definition. That’s how definitions work.
You are really fucking things up. Nobody said that advantageous traits are those that spread and deleterious are those that don’t.
Advantageous traits increase fitness (wether they spread or not) and deleterious traits decrease fitness (wether they spred or not). The prediction is that advantageous traits TEND to spread.
How stupid is this. The purpose of this theory IS NOT TO CLASSIFY traits as good or bad per se.
A trait being advantageous or not DEPENDS ON THE ORGANISM CONSIDERED AND ITS ENVIRONMENT.
What the concept states is that when a trait spreads through a population it is because IT REPRESENTED AN ADVANTAGE. So we can study the population and determine how it was advantageous.
Again: field crickets. Being silent is not good or bad. Singing is not good or bad. Both traits are advantageous and disadvantageous somehow. What we can conclude of this example is that escaping enemies is more significant in this case than finding mates. That males can overcome their silent condition more effectively than they escape the wasp when they sing.
So, the population did not turn silent for no reason. It did not turn silent because god decided so. It did not turn silent because the intelligent designer changed its mind. It turned silent because the environment changed and being silent became a significant advantage.
Before you make a stupid comment, pay attention to this: the main claim here is not that being silent is advantageous. The main claim is that silence being advantageous IS THE REASON for population change.
It’s not a tautology BECAUSE THAT CHANGE COULD BE OWED TO OTHER REASONS.
Allan Miller,
Allan, You seem to think that if you add in the caveat that over the long run, the numbers will work out as predicted, as if that somehow nullifies the definition being the same as the result. It doesn’t.
The point is much simpler than that. How do you have ANY basis for saying how often advantageous mutations will spread through a population (its Joe who is making this claim by the way)? How do you know that advantageous mutations don’t spread through a population with the same frequency as neutral ones? Or deleterious ones?
The initial theory the question looks to answer is how easily do advantageous mutations spread through a population? Joe gave the formula. Now how do we know that formula is correct? Because if it weren’t correct, we wouldn’t call them advantageous? THE FORMULA IS THE SAME AS THE DEFINED RESULTS!
How do you know Joe’s formula (Kimuras) is correct?? Are you able to answer this? You can only answer it by going back to your circle.
When you say this Allan:
” Seed a succession of populations with individual beneficial, neutral and detrimental alleles in single copy and track progress, and the beneficial ones will fix more often than the neutral or detrimental ones, over large numbers of trials”
That’s an unsupported statement. You have already decided beforehand what the definition is for beneficial and deleterious, so you can’t falsify the conclusion, because if you did, you would have to rearrange what you call beneficial and what you call deleterious.
Ask Alan, he finally realized you were losing hours ago.
And Allan, HOW can you know, before you run your test, which are the advantageous ones, which are the neutral ones, and which are the deleterious ones, in order to know which ones you seed the population with.
By going backwards and seeing which ones were beneficial or deleterious based on the exact same definition previously. And then every time the mutations don’t match the predicted outcome, all you do is change the classification of the mutation.
phoodoo, The question “Why is a mouse grey?” could mean, “what particular genetic structure produces that particular color fur?” Or it could mean “what reproductive history has resulted in this species of mouse having that color? Presumably, you are interested in the second question. And you say (rant, really), “According to the (non-existent) theory of evolution, the mouse is grey because greyness is survival-enhancing and grey mice (not purple ones) have survived! Thus, this ‘theory’ explains nothing; it only takes credit for claims that could not be false.”
That, I take it, is the sum and substance of your criticism. Let us start by agreeing about that. Once that is accomplished we can then let one of the evolutionary biologists here respond specifically to this claim either by saying, “Oh shit! you’re right!! I’ve just been assuming that grey must be survival-enhancing because I see that all the mice around are grey, and if my pet theory is correct, mice have to be grey just in case they ARE grey. My life has been a waste of time–there really IS NO Theory of Evolution. It is all based on a confusion.”
Or, alternatively, the supporters of evolution can (once more) explain to to you that no one but IDists claim that mice HAVE to be grey because it follows deductively from axioms of their theory that if some animal IS grey, it must be fitter than a non-grey version of that animal.
Anyhow, it’s quite clear that no one is getting anywhere here on the convincing front, so I propose we start right at the beginning, by first getting a clear statement of your objection and agreement from all parties regarding precisely what it is and claims. I have tried to do that above. Please correct me, if I’ve gotten it wrong. Thanks.
Observations in the real world!!! Validation with real organisms!!!!
“Now how do we know that formula is correct? Because if it weren’t correct, we wouldn’t call them advantageous? THE FORMULA IS THE SAME AS THE DEFINED RESULTS!”
How stupid are you? We already told you that if a trait doesn’t spread but it increases averagae fitness IT IS STILL ADVENTAGEOUS. The result of the formula DOES NOT AFFECT the definition.
“How do you know Joe’s formula (Kimuras) is correct??”
Observations in the real world!!! Validation with real organisms!!!!
“That’s an unsupported statement. You have already decided beforehand what the definition is for beneficial and deleterious”
No he hasn’t and he has already clariffied that being advantageous or deleterious depends on average offspring number and NOT ON SPREAD THROUGH THE POPULATION. Don’t you ever read comments you respond to?
walto,
Yes Walto, all evolution starts with the assumption that traits that exist today, do so because they provided some evolutionary advantage. Or at least were neutral and didn’t cause a big enough disadvantage to destroy the reproduction of that allele. That is the assumption from the beginning.
So then we go back in time, and try to make up a story for WHY that particular trait was advantageous (because we are already sure that it is advantageous). Why do we create art? Well, because it must have been advantageous to show what a great mind you have to discerning females.
Why don’t we have fur like other animals. Because it was advantageous. Now let’s try to create a story as to why.
Any feature you can think of, with just a tiny bit of imagination, you can come up with a story to say why it is advantageous, because the assumption that it was advantageous simply can’t be wrong by definition.
Why do we have thumbs? Its advantageous? Why do horses have hooves instead of thumbs? Advantageous of course. Why do we have hair on our balls. Just create a story, it will always be right.
phoodoo,
I am waiting for you to “penetrate” on the example of the field crickets and show us how survival of the fittest is a tautology.
Guillermoe,
“We already told you that if a trait doesn’t spread but it increases averagae fitness IT IS STILL ADVENTAGEOUS.”
Really? You are a genius Guillermoe.
Why the whales have lungs?
My answer, from evolution, is “their ancestors where terrestrial; they needed lungs”.
I don’t know what you are talking about when you say that our answer is just “it was adventageous”.
And, if this story is made up, it won’t be difficult for you to come with a better explanation. I would really like to hear it.
And you are an idiot who needs to be told one simple thing ten times to finally being able to realize THAT HE WAS TOLD!!!
Now, let’s se if you understand it.
Please, an explanation to change in field crickets population not based on survival of the fittest, a demonstration of how singing male crickets are fitter, and an explanation to whales having lungs that is not a made up story like the one of the terrestrial ancestors.
I notice you have a HUGE difficulty in sustaining your views when facing real examples.
The funniest thing about this is when phoodoo says he’s “winning”. Irony doesn’t get better than this.
Thanks for giving a clear statement of your objection.
Let me pare it down a bit–and again, if you think any cuts I make result in a misrepresentation anywhere, please speak up!
You write:
[E]volution starts with the assumption that traits that exist today, do so because they provided some evolutionary advantage.Or at least were neutral and didn’t cause a big enough disadvantage to destroy the reproduction of that allele.
Ok, first, it seems to me that “providing an evolutionary advantage” and “not providing a big enough disadvantage to destroy the reproduction of some allele” are not the same thing. That is, on that view a trait may actually be contrary to survival-enhancement, and nevertheless continue because it does not provide a big enough disadvantage to countervail some other traits (or dumb luck). So, right off the bat, you seem to be conceding that the existence of a trait does not necessarily entail that that trait is survival-enhancing.
Second, any non-evolutionary explanatory theory will also have to begin by looking at currently surviving species and traits and, if possible, comparing them with species or traits that are no longer around. Surely, it can’t be a criticism of an empirical science that it observes nature.
Then you go into the “making up of stories” to explain why this or that species or trait has continued. Theory construction is, in a sense, always a matter of “making up stories” and testing them. So, e.g., you mention creation of art. Is it a trait human beings current exemplify? [Check] According to the theory was it not sufficiently “unenhancing” to have disappeared [Check]. Can we infer that it, itself is survival enhancing? I wouldn’t think so. Not from its continuing existence alone, anyhow. Someone might suggest that it is, but any such claim would require empirical confirmation or it is just idle speculation.
Do people sometimes speculate idly in that fashion? Sure. Is this the theory’s fault? Or better, Can we infer from the existence of such idle talk that the theory is no good? I don’t see why. But I can imagine tests that might be performed to see if there’s any sense to the claim, which, surely, is not tautological.
phoo is “winning” because he’s playing a different game. It’s not a game that will impress the neutral “onlookers” here but it impresses the crowd at UD.
STOP FEEDING THE TROLL (but I’m just as bad…)
Guillermoe,
Why did the crickets sing in the first place Guillermoe?
Ah, can’t worry about that kind of thing. Better I think to emulate Trollope’s Septimus Harding, and not be so anxious to prove oneself right, as to actually be so.
ETA: A friend tells me, though, that group selection favors groups that are fanatical and care only about winning. SWTHDIK?
It’s Calvinball.
Why are you changing the question? Can’t you answer it? Ashamed to recognize it?
Are you trying to get us out of a known, observed case, with known mechanisms and known explanations, to hypothetical cases where everything is possible and yuo can argue whatever you want?
Is that how your arguments work? They are fine when imagining things but if we talk of something concrete, of real cases, they fail?
For some discussion of why I requested this thread, we have the latest essay by Jerry Coyne.
http://whyevolutionistrue.wordpress.com/2014/11/07/the-group-selection-dustup-continues-e-o-wilson-calls-richard-dawkins-a-journalist/
It’s Dawkins vs Wilson, not selection vs drift, but it illustrates that the topic of selection still stirs up controversy among biologists.
phoodoo,
Wrong. In principle at least, you can know which ones you are seeding the population with by measuring their selective advantage, in the currency of offspring, before you let a copy loose in the population. Those single-copy mutations must have some value for selective (dis)advantage. Given this, you can determine for all values of s what the fixation probabilities are. You can cover the whole continuum, and be sure you have a result for every possible ‘real’ allele. And you can verify that those falling in the ‘beneficial’ part of the continuum (those producing a net gain of offspring) fix much more readily than those in the ‘deleterious’ part. If you had a magic box that calculated things you could run trials and confirm that simulations followed the math. The physical experiment is more tricky, given the vast resources and time required. And that appears to be your feeble hope, that somehow reality doesn’t follow the math, and nothing is ever fixed or lost without the say-so from Above.
It is NOT a retrospective determination from a single fixation/loss run. Paste that in your hat. You can’t determine selective advantage from the behaviour on a single trial, because any one trial can result in either fixation or loss, for most values of s in finite populations. That’s why people don’t do what you keep saying they do do, and crown the survivor ‘advantageous’. This is how you ‘win’, by failing to grasp this simplest of points.