|
Register | Sign In |
|
QuickSearch
Summations Only | Thread ▼ Details |
|
Thread Info
|
|
|
Author | Topic: Explaining the pro-Evolution position | |||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6
|
Kleinman writes: Do all modern reptiles also have genes for scales and feathers as well? Can you point to any step in the evolution of feathers that required 2 simultaneous mutations? If not, WHAT ARE YOU GOING ON ABOUT???????
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Kleinman writes: What each of the different variants share in common is that they must amplify (increase in number) before there is a reasonable probability of another beneficial mutation occurring on a member of that lineage. And this is a problem how?
What determines if a mutation is beneficial or not is whether the variant can amplify (increase in number). In a very limited sense, amplification does not have to occur to improve the probability of a beneficial mutation occurring, a small number lineage which doesn't grow in size over the generations can have enough replications (the random trial) over many generations to improve the probability of another beneficial mutation occurring on a member of that lineage. I am still waiting for you to explain how this is a problem for rmns.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6
|
My mathematical model predicts the behavior of every real, measurable and repeatable example of rmns. Then please use that model on vertebrate genomes and show us which genetic differences between species could not be produced by rmns. If you can't do that, THEN WHAT ARE YOU GOING ON ABOUT?
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Kleinman writes: So you have the genetic sequences for dinosaurs? We have plenty of living species whose genomes we can compare. For example, we have chimps and humans. When we use mutation rate, population size, and generation time to calculate the divergence time for genetic data you get 5-8 million years which matches the hominid fossil record.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6
|
Kleinman writes: It took 5 mutations to achieve high resistance to the drug but different combinations of mutations could accomplish this. Can you name a single beneficial difference between any two vertebrate species that required 5 simultaneous mutations? If not, THEN WHAT ARE YOU GOING ON ABOUT??????
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6
|
Dr Adequate writes: So far, you have said --- at what is perhaps unnecessary length --- that the probability of a particular mutation at a given locus is the probability of there being any mutation at that locus multiplied by the probability that if there is a mutation at that locus it will be that particular mutation. I don't think there's a single person here who needed to have that explained to them. So my question would be ... when do we get to the dinosaurs?
In an attempt to communicate your's, mine, and other's confusion over the argument being made by Kleinman in this thread, I will attempt to configure the argument in terms of the lottery.
Me: Why do you say that random chance can't explain people winning the lottery? Kleinman: In order to win the lottery, you have to get 6 matches to 6 numbers simultaneously. Me: Why is that a problem? Kleinman: The chances of that occurring are one in 175 million. Me: I think we all agree with that. Why is that a problem? Kleinman: My mathematical model shows that people shouldn't win the lottery by random good luck. That's the problem. Such a thing would require the sale of millions of tickets, afterall. In fact, I can find instances where people have won the lottery, and it has taken the sale of millions of tickets before there is a winner. Me: Hold on. You said it was impossible for people to win the lottery through blind luck, and then you cite examples of people winning through blind luck? Kleinman: That's right. It took lots of tries before someone actually won through blind luck which proves they can't win through blind luck. It is at this point that we all just scratch our heads and wonder what in the world he is arguing against. Edited by Taq, : No reason given. Edited by Taq, : No reason given.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6
|
Kleinman writes: I happen to use this bacterial example because we have empirical data. But the governing mathematics is applicable to any arbitrary example of rmns. The problem is that the bacterial examples you use show that RMNS can produce the observed evolution of adaptations in those bacteria. You have yet to show a real example in a real species where RMNS can not produce the observed differences between two species or a species and its ancestors. You claim that RMNS can not produce the differences we do see, but you have yet to show us a single example where this is true.
What I've done (and doing here) is describing the physics and mathematics of rmns. You need to describe why the physics and mathematics of RMNS disqualifies RMNS as the mechanism behind the divergence of species with reference to specific genetic differences.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Kleinman writes:
In case you don't recognize it, these probability equations are the general solution for rmns and apply to all replicators. I'll show you how to do the calculation for multiple simultaneous selection pressures after we finish with the single selection pressure model. When will be getting to real replicators and real genomes?
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
The mathematics I'm presenting here is the mathematics of rmns by common descent. How do you think replicators accumulate the mutations necessary to adapt to selection pressures by rmns? Perhaps you think that lateral transfer of genetic material is the way it is done? Try doing the mathematics of random ecombination. If you can't do it, I'll show you. They accumulate through selection, so I don't see how the mathematics of random recombination are applicable. The non-random rates of survival and reproduction seem to be more applicable in this instance.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6
|
Kleinman writes: Once you get above the transformation of a single gene by a single selection pressure, rmns is stifled. How much is it stifled? Consider the evolution of HIV where only 2 genes are targeted by 3 selection pressures and you have people surviving for decades instead of weeks. The main problem with your HIV example is that the beneficial mutations are not additive. In most situations, beneficial mutations are additive. What I mean by additive is if A and B are both beneficial mutations on their own, then an individual with both A and B will be more fit than individuals with just A or B. In the case of multi-drug treatment and HIV, there is no way for an amplification of just A or just B because the individual viruses with just one potentially beneficially mutation do not reproduce at a higher rate. We could use an example in humans to show why your HIV example doesn't work. In humans, there has been selection for both malaria resistance and melanin production. Individuals with either darker skin or resistance to malaria will do better than individuals without either trait in lower latitudes that experience endemic rates of malaria. Both traits will be selected for independently. Individuals who receive both traits will be even fitter than individuals with just one of those traits. As we can see, your HIV model fails to model real life, both because it lacks additive fitness and it lacks sexual recombination. In human populations, you don't have to wait for dark skin to become fixed before malaria resistance can be selected for. Both can be selected for in individual lineages, and through sexual recombination you can have individuals inherit both beneficial mutations. Edited by Taq, : No reason given.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Dr Adequate writes: Do you have a reference for this? I don't have a reference at hand, but I may find time to find one. I think my example of melanin production and malaria resistance should suffice, unless someone can explain how darker skin will not be selected for unless someone also has mutations that confer malarial resistance (and visa versa).
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Kleinman writes: It is the theory of evolution, the notion that some primordial replicator through rmns evolved into all the life forms we see today is a mathematically irrational belief system. Then let's see your math with specific examples in real genomes.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Kleinman writes:
I think you will find some disagreement with other posters on this thread. As long as mutation are random events, beneficial mutations are just a subset of all mutations. I don't see how that addresses anything in my post. Let's use military tanks as an example. Let's say that two possible upgrades for a tank are thicker armor and a more powerful main gun. A tank with either thicker armor or a more powerful gun would be better. A tank with BOTH thicker armor and a more powerful gun would be better than a tank with just one upgrade. The upgrades are additive in that both upgrades add up to a better tank than a single upgrade by itself. This is often how beneficial mutations work. A beneficial mutation is beneficial all by itself. When it is combined with another beneficial mutation, the individual with two beneficial mutations is more fit than an individual with just one of those beneficial mutations. The problem with your HIV model is that it doesn't take this into account. You are only looking at situations where you need both mutations in order to see an increase in fitness. As discussed earlier, this isn't always the case in the real world. Edited by Taq, : No reason given.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Kleinman writes: Don't get me wrong, there's more than one way replicators can adapt to selection pressures other than rmns. Recombination is a much faster way replicators can adapt and they can do it to multiple selection pressures simultaneously. But they have to have the correct alleles already in the gene pool. Recombination events are random mutations, and recombination events can produce new alleles.
|
|||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Dr Adequate writes: I meant specifically for the bit where you said "the individual viruses with just one potentially beneficially mutation do not reproduce at a higher rate". Sorry for the confusion. With multidrug therapy, if a virus gains a mutation that confers resistance to just one of the drugs it will not be fitter than other viruses without that same mutation. This means that individual viral particles with just one mutation to one drug will replicate at the same rate as those without the mutation.
|
|
|
Do Nothing Button
Copyright 2001-2023 by EvC Forum, All Rights Reserved
Version 4.2
Innovative software from Qwixotic © 2024