Somehow you have gotten in your mind that adding selection pressures will speed up this process.
Where "somehow" involves (a) a mathematical proof (b) common sense (c) a computer simulation (d) empirical evidence.
So if you have some math, involving "nested binomial probability problems" or otherwise, that shows different, now would be a great time to present it.
You think starvation is a soft selection pressure?
That depends crucially on whether it's hard or soft.
Do you think the intensity of selection in the Lenski experiment is hard or soft?
quote:
All adaption by rmns requires lineages to address nested binomial probability problems.
Well, perhaps you could show us some math.
Again? That would make Percy unhappy.
quote:
And why do you keep ignoring my question whether the intensity of selection alters the evolutionary trajectory to adaptation?
Where did you ask me that?
The answer is obviously yes.
Now I would like to see some empirical evidence of that, you obviously have that. If that were true, why would sequencing HIV be of any value to identify drug-resistant variants?
quote:
If the same selection pressure is applied at low intensity, does it require different mutations for adaptation than if the selection pressure occurs at high intensity?
So do you think the amplification time (starvation alone=>about 1000 generations per beneficial mutation) would speed up if a small thermal stress was added to his populations or would the number of generations per beneficial mutation increase?
As I already said
quote:If the experiments were MORE lethal, then they couldn't be easily compared, we'd need to know population size per generation before being able to estimate
Basically I don't know because you haven't provided any numbers. Intuitively, if the conditions result in a low maximum population size it is likely to take more generations to find solutions.
However, as I said, if you reduce the starvation as you increase the thermal stress to retain an equilibrium in population size such that it remains comparable in both experiments, then we might expect it would simply take twice as long, counted in generations. This is a simplification, of course, to point out we don't need to worry about the multiplication problem here. With other considerations we might find it takes less.
Large numbers of low intensity selection pressures do not cause rmns to work, you get drift under these conditions.
Again, that depends on HOW LOW. There is a middle ground that exists between TOO LOW and TOO HIGH, we predict that species that are undergoing adaptation exist here. It is useless then to use examples where the selection pressure is obviously too high or too low. The selection pressures acting in combating viruses and bacteria, especially with regard to combination therapy are specifically designed to be to TOO HIGH.
You have to determine the magnitude of the selection pressures facing the dinosaurs to determine whether it was too high for feathers to evolve. You have just examined the conditions of HIV under certain therapies and concluded that HIV's evolution in inhibited in that case. You have tried to say that this demonstrates that multiple selection pressures always inhibit evolution, but you have not addressed the issue of magnitude which invalidates your argument. That's the bit you need to address.
Do you think the intensity of selection in the Lenski experiment is hard or soft?
Lenski takes a random sample of 1% of the population every day to start a new colony and discards the rest. Insofar as it's meaningful to ask under such circumstances whether the environmental pressures are hard or soft, they're soft.
Again?
Well, so far all you've shown us could have been knocked off in five minutes by a bright middle-schooler and comes nowhere close to proving your point, so yeah, some more math would be nice.
Now I would like to see some empirical evidence of that, you obviously have that.
Try considering the case where the intensity is 0.
Why might that happen?
Adaptive evolution is often a tradeoff. If there is more of an upside associated with making a change, then it's more likely to outweigh the potential downside.
As for the Citrate metabolizer (e coli has alway been able to metabolize Citrate because it has a Krebs cycle), appeared at about generation 31500, not at 100 generations.
I said "change the circumstances". I know the Lenski experiment took over 30,000 generations for Cit+. The multi-mutation adaptation can happen in less than 100 generations in other circumstances.
That, ironically, is a paper by creationists who didn't like the idea that the occurrence of Cit+ in Lenski is special, and set out to show that it could happen easily. It can.
Interesting paper. So do you agree with them when they said, "We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
quote:So, where are your calculations? Surely they're not based on the view that an adaptation involving 5 or more mutations in sequence would take ~31,000 generations in a culture of bacteria in any or all environments? How are environments factored in?
You still seem to be assuming that organisms have to be threatened with extinction in order to evolve, as suggested before. They don't. Flying squirrels evolve alongside the non-flying versions they descend from, and both thrive. It's just better to be able to glide in certain environments. Same with dinosaurs. The fliers existed alongside the non-fliers for tens of millions of years. They just fill different niches
I disagree with you. I think combination selection pressures are the rule in nature. Drought, starvation, thermal stress, disease, predation,...
You admitted that conservative selection pressures don't count. Just thought I should remind you.
You think that drought, starvation, thermal stress, disease, predation,... are conservative selection pressures? NOT
quote:
How large is that population size for dinosaurs?
That's one of the many things you don't know that has prevented you from actually proving anything about dinosaurs.
Yes, one of the many things you do not know. I thought the theory of evolution was settled science? Well, at least you know that fixation and amplification aren't the same thing now.
quote:
That's not your fixation calculation again?
No, that's the result of simulations, as I said in the post to which you are ostensibly replying.
It is your fixation calculation again.
quote:
Do you think the intensity of selection in the Lenski experiment is hard or soft?
Lenski takes a random sample of 1% of the population every day to start a new colony and discards the rest. Insofar as it's meaningful to ask under such circustances whether the environmental pressures are hard or soft, they're soft.
Are you sure about that, it has been a while since I read his papers but I think he uses 10%. So if you think he increases his intensity of selection the evolutionary process will go faster or slower?
quote:
Again?
Well, so far all you've shown us could have been knocked off in half an hour by a bright middle schooler and comes nowhere close to proving your point, so yeah, some more math would be nice.
Actually elementary. So I left off in the mathematics after computing the probability of mutation A occurring in the population. I was just about to compute the probability of mutation B occurring on a member with mutation A. I think I'll start this mathematics tomorrow.
quote:
Now I would like to see some empirical evidence of that, you obviously have that.
Try considering the case where the intensity is 0.
Reducing selection pressure only increases the diversity of populations. No directional selection there.
quote:
Why might that happen?
Adaptive evolution is often a tradeoff. If there is more of an upside associated with making a change, then it's more likely to outweigh the potential downside.
Adaptive evolution, meet nested binomial probability problems and the multiplication rule of probabilities.
But the populations are amplifying improving the probability that the first beneficial mutation will land on some member of a population
And if the population started high rather than built up, that would have increased the probability sooner. So what? How is rmns working 'better'? If we removed the poison and let them grow with very little competition and then poured anti-biotic at 1,000 times the normal required dosage into the mix...do you think that more bacteria would survive it? Is that what you mean by 'better'?
I disagree with you. I think combination selection pressures are the rule in nature. Drought, starvation, thermal stress, disease, predation,...
Then you agree with me.
Back to the point, however, you haven't determined the magnitude of the selection pressures faced by the ancestors of feathered dinosaurs. The number of pressures and that they act in concert is irrelevant. There are thousands of selection pressures acting ALL the time everywhere. The question is of magnitude.
How large is that population size for dinosaurs?
Very large.
And remember, or learn, that rmns occurs on lineages, you know, common descent.
I am remembering that it's populations.
And that quadrillion population is now reduced to a new lineage of 1 with that first beneficial mutation.
No it isn't. All the dinosaurs still count. You don't ignore their lottery entries just because one won. That would imply all dinosaurs went extinct. This is not true. A thousand different lineages could independently mutate in the direction of feathers. That you think you can discount these suggests your maths training was poorer than you've been letting on.
And until that variant amplifies, the probabilities are very low that the 2nd beneficial mutation will occur on one of its descendants.
Because of sex, it doesn't have to occur in one of its descendants. Did you forget dinosaurs were sexual organisms?
Well then how did Weinreich measure so many different variants from his one targeted antibiotic selection pressure?
Did he measure all variants to have increased by the same amount in lockstep? His population must have exploded.
What do you think you are seeing in the video. Do you think that all the colonies are giving the same variants?
The first question is too vague, but I've answered it already where it seems relevant. No, the colonies are not giving the same variants, why do you ask?
The non-antibiotic resistant variants amplify until the resources of the plate are exhausted
Are you certain? Do they never reach an equilibrium condition when the number that die without reproducing equals the number that reproduce before the sum total food is exhausted? Given that not all food is available to any given bacteria, is there not a certain density at which not all bacteria are able to acquire enough food to reproduce? Where they are basically getting in each others way (deliberately or otherwise)?
Let's suppose that simultaneously, 10 bacteria evolve an anti-biotic resistant mutation. This is best case for your argument, lowering this number hurts you. Let's say there are a billion non-resistant varieties. That means the frequency of resistant types is is 10 in a billion. Each variant is individual and so each variant has a frequency of 1 in a billion.
In order that these variants all amplify while keeping this frequency this is what you say we should expect:
Population of resistant variants 100. Population of non-resistant variants: 10 billion. Population of RV 1000. Population of nRV: 100 billion. Pop RV 10,000. Pop nRV: 1 trillion. RV 100,000. Pop nRV: 10 trillion.
I believe culture density maximums are usually around a million to a billion bacteria per ml. There aren't a lot of ml even on the megaplate, there are less that have no poison.
Given the resistant variety has twice as much food and therefore space, what happens when the non-resistant variant reaches saturation?
RV 1,000,000 (approx 1 ml of volume): Pop nRV: 100 trillion. (100,000 litres required)
Are you seriously telling me that the frequencies stay the same? Because that seems extraordinary when we examine the numbers.
Interesting to you, because it shows the type of multi-mutation adaptation that you seem to think highly improbable happening repeatedly with ease.
K writes:
So do you agree with them when they said, "We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
I agree with the first sentence, but not with the "information" waffle.
Kleinman writes:
These calculations simply describe what populations have to do to accumulate beneficial mutations in order to adapt to selection pressures.
So tell me, can numerous beneficial mutations be facing positive selection in one species at the same time?
You think that drought, starvation, thermal stress, disease, predation,... are conservative selection pressures?
Often. Unless they're new.
Yes, one of the many things you do not know. I thought the theory of evolution was settled science? Well, at least you know that fixation and amplification aren't the same thing now.
Perhaps you meant something when you wrote that.
It is your fixation calculation again.
No, that's the result of simulations, as I said in the post to which you are ostensibly replying.
Are you sure about that, it has been a while since I read his papers but I think he uses 10%. So if you think he increases his intensity of selection the evolutionary process will go faster or slower?
What do you mean by "his intensity of selection"?
Actually elementary. So I left off in the mathematics after computing the probability of mutation A occurring in the population. I was just about to compute the probability of mutation B occurring on a member with mutation A. I think I'll start this mathematics tomorrow.
Good, good. And maybe some time this month we could get on to the interesting bit?
Reducing selection pressure only increases the diversity of populations. No directional selection there.
And hence the population will follow a different evolutionary trajectory than if the intensity was not zero. Proving that the intensity matters.
Adaptive evolution, meet nested binomial probability problems and the multiplication rule of probabilities.
Would these be the "nested binomial probability problems" that you've spent the past week not actually posting about?
Yes, one of the many things you do not know {about dinosaurs} I thought the theory of evolution was settled science?
You have confused theory with application. The details about the dinosaurs is a practical problem we can apply theory to. The theory of evolution is not that dinosaurs evolved into birds. The theory of evolution provides an explanation for how dinosaurs evolved into birds.
The theory of relativity does not say that a planet mercury exists, and that the precession of the perihelion of its orbit should advance in such a way.
It instead can provide an answer as to what the precession should be, given the existence of Mercury.
There are still many unanswered questions about our cosmological history, even in our own solar system. That doesn't mean all the associated theories are not settled, it may be a lack of data that results in unanswered questions. We have a perfectly understandable lack of data about dinosaurs. What we do have is consistent with, indeed highly suggestive of, the notion that some of them evolved into birds.
We do not have the data you require to apply your simple mathematics in order to prove the whole thing a charade. And neither do you.
Re: Mathematics cannot change reality and when done incorrectly predicts nothing
quote:
... What I do remember is that they listed at least 8 genes necessary to be transformed. ...
Excuse me for coming in late in the discussion. I have received your pdfs but not had time to look them over yet. Can you answer a simple question for me, even if it has already been asked?
What is the probability that a mutation will be beneficial?
Your question hasn't been asked and my answer is I don't know. ...
If you don't know then you cannot invalidate evolution with your calculations.
... But this is not a number which you have to know to understand how rmns works.
Evolution works by beneficial mutations being selected by natural processes -- success in living and breeding. The probability of a mutation being beneficial would seem to be central to any mathematical approach trying to show that evolution is broken.
quote:I think we can all agree that mutations are random -- leaving aside for the moment that the probability of mutations varies with the section of DNA involved -- and that some are immediately deleterious or immediately beneficial, while others are immediately neutral and their relative deleterious\beneficial value can be important later.
We also have cases where a mutation is somewhat deleterious but leads later to beneficial results because of changing environmental conditions.
So how can we predict the probability of a mutation being beneficial?
Most people say that most mutations are neutral. ...
Which leaves the door open to later mutations that can build on them.
... Mutations are fairly rare to begin with. ...
Yet every individual in every species has several.
... Most DNA replication is done with high fidelity. ...
For individuals that survive from zygote to born young. All those that die from birth defects are because of less than sufficient fidelity.
... As you read my papers on rmns, you will see that I address the possibility that even though a mutation occurs at the correct site in a genome, it has to be the correct mutation to improve fitness. ...
This is confused. There is one mutation, it occurs randomly, and that means both location and format\type are part of the same mutation, not two separate problems. The same type in a different location would be a different mutation.
There is no "correct mutation" -- the mutation happens and then selection operates on that mutation, whether it is in location A or location B, whether it is type K or type L. Whether or not it is beneficial is that probability discussed above that you admit you don't know.
This seems to be the root of your problem, trying to make a single mutation event into a two event process.
It also seems from this that you are calculating the probability of a given mutation occurring in a second individual. Certainly when you go to two mutations occurring independently in different individuals the maths would give an extremely low probability for occurrence, but that is not how evolution works.
... Just getting an accurate mutation rate is a challenging problem and then determining the fraction of the mutations which are beneficial, neutral and detrimental is even more challenging. ...
Yet we know that they all occur every generation of every species. All natural selection needs are some beneficial mutations and a low rate of death/fertility problems (where selection pressure enters the picture).
... But the mutation rate is not the dominant factor in the rmns problem, it is the multiplication rule of probabilities that drives this phenomenon. ...
This too is confused. If I take a coin and toss it 53 times I end up with a pattern of heads and tails, and the probability of my getting that specific pattern is 1.
If I try to match that pattern with another 53 tosses the probabilities are, by the multiplication rule, extremely minute. You only use multiplication when the same steps need to be reproduced. Evolution does not work that way.
... It is the joint probability that two or more beneficial mutation occur on a lineage which drives this problem.
Again, we get back to the question of the probability that a mutation will be beneficial, which you admitted you don't know ... certainly then you can't know the probability of a second mutation being beneficial, but that isn't the worst of your problem.
There are actual documented experiments (one involving E. coli) where a neutral mutation occurs in one generation and then in a later generation a second mutation occurs where the combination is beneficial, meaning that the original mutation is now beneficial. Calculating the probability that those two specific mutations would occur (the "correct mutations" at the "correct locations") would result in a very small number, but the probability that it occurred is 1: it happened.
Your model is wrong because there is an assumption of structure to the mutation process being necessary to evolution, and that assumption is false.
I have figured it out, I published the mathematics of random mutation and natural selection for multiple simultaneous selection pressures. But in order to understand this paper, you need to understand the difference between complementary events and additive events.
As I expected, the debate has become very repetitive. One frequently seen pattern is for people to argue that the example of fatal selection pressures on bacteria and viruses cannot be generalized to other levels of selection, and for you to reply that your papers show otherwise. But your papers are not accessible to the people here, so you must stop citing them. Even if they were accessible you must still present your evidence and arguments in the thread, using links only as references. Arguing, in effect, "This link shows I'm right" or "This link shows you're wrong," is strongly discouraged here at EvC Forum.
What you must do is substitute actual values into this equation demonstrating evolution impossible. If I don't see this presentation very soon I will drop this thread into summation mode.
Edited by Admin, : Typo.
Edited by Admin, : Fix equation to eliminate the smilie.
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