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Author Topic:   Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 1921 of 2926 (902163)
11-18-2022 12:11 PM
Reply to: Message 1919 by ringo
11-18-2022 11:58 AM


Re: Kleinman does not know asexual vs sexual
Kleinman:
Good for you, your friends can't explain biological evolution, the evolution of drug resistance, and why cancer treatments fail.
ringo:
They can explain it to everybody's satisfaction but yours.

Tell that to the people dying of drug-resistant infections and failed cancer treatments.
Kleinman:
Your friend are really smart.
ringo:
And you're not.

At least I can explain how bacteria evolve drug resistance and why cancer treatments fail. Your friends have failed at their job. Of course, they are really smart.

This message is a reply to:
 Message 1919 by ringo, posted 11-18-2022 11:58 AM ringo has replied

Replies to this message:
 Message 1922 by ringo, posted 11-18-2022 12:23 PM Kleinman has not replied

  
ringo
Member (Idle past 412 days)
Posts: 20940
From: frozen wasteland
Joined: 03-23-2005


Message 1922 of 2926 (902164)
11-18-2022 12:23 PM
Reply to: Message 1921 by Kleinman
11-18-2022 12:11 PM


Re: Kleinman does not know asexual vs sexual
Kleinman writes:
They can explain it to everybody's satisfaction but yours.
Tell that to the people dying of drug-resistant infections and failed cancer treatments.
People die from car accidents too. That doesn't mean Ford and Suzuki don't know what they're doing.
Kleinman writes:
At least I can explain how bacteria evolve drug resistance and why cancer treatments fail.
To nobody's satisfaction but your own.
Kleinman writes:
Your friends have failed at their job.
In nobody's opinion but yours.

Come all of you cowboys all over this land,
I'll teach you the law of the Ranger's Command:
To hold a six shooter, and never to run
As long as there's bullets in both of your guns.
-- Woody Guthrie

This message is a reply to:
 Message 1921 by Kleinman, posted 11-18-2022 12:11 PM Kleinman has not replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 1923 of 2926 (902165)
11-18-2022 12:37 PM


Illustration of Adaptation in Asexual and Sexual Populations
The Peabody et. al. (2017) paper mentioned earlier has a great illustration of how adaptation differs in asexual and sexual populations:

from the paper:
Theoretical impacts of mutation rate and sexual recombination on population structures. a Mutationally limited fitness landscape, where most mutations fix in a single sweep with very little inter-clonal competition. b Increased mutation rate over (a), more competition and faster evolution observed, but some mutations are lost due to inter-clonal competition. c Adding sexual recombination to (a), due to few available beneficial mutations, no strong influence on evolution is observed. d Both sexual recombination and increase in mutation rate from (a), more rapid evolution is observed and fewer beneficial mutations are lost due to clonal interference
The two variables here are mutation rate and recombination. The two plots on the left are with the lower mutation rate. The two plots at the bottom are with sexual recombination.
a. low mutation, asexual
b. low mutation, sexual
c. high mutation, asexual
d. high mutation, sexual
Even at low mutation rates, you can see that the sexual population gets all 5 beneficial mutations which the asexual population is limited to 4 because clonal interference drove the ABD lineage to extinction. In the sexual population, recombination between the ABC and ABD lineages put all 5 beneficial mutations into the same background. When mutation rates are even higher, the differences can be even more stark.

Replies to this message:
 Message 1925 by Kleinman, posted 11-18-2022 12:51 PM Taq has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 1924 of 2926 (902166)
11-18-2022 12:43 PM
Reply to: Message 1920 by Taq
11-18-2022 12:09 PM


Kleinman:
You are so stupid. The Kishony experiment works quickly because his lineages can accumulate their 1/(mutation rate) replications without having to deal with biological competition.
Taq:
You didn't address what I said. Here it is again.

The Lenski experiment had a constant environment for 10's of thousands of generations. Are you saying that a constant environment does not disqualify an experiment?

As to the Kishony experiment, what would the dynamics of adaption to chloramphenicol look like if the E. coli in the experiment were undergoing sexual recombination? How would it compare to a population of asexual E. coli adapting to the same environment?

Imagine if scientists published a paper on that very experiment? Well we don't have to imagine.

If you understood the Kishony or Lenski experiments, you would have done the mathematics long ago, but you don't. The only way that Desai could get his experiment to work was to use a constant environment, let adaptive alleles increase in frequencies for 90 generations in a constant environment, and then induce sexual reproduction. You are just too stupid to understand this.
quote:
From the evolution experiments in each fitness landscape, we find that increased mutation rate expedite adaptation in some environments tested, and that sexual recombination further speed up adaptive evolution in some environments. We also observe strong evidence of an in situ recombination event that help to alleviate clonal interference and generate a superior genotype in a sexual E. coli.

Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes
Taq:
Look at the title of that paper. Wouldn't you know it, sexual recombination speeds up adaptation, and it does so by alleviating clonal inteference. More from the paper:

You are so stupid, you think that recombination works the same way in a varying environments. You stupidly extrapolate a constant environment to all environments.
quote:
The results suggest that sexual recombination facilitates a more swift increase in resistance, probably by combining compatible determinants of CM tolerance.
Taq:
CM tolerance is chloramphenicol resistance. Sexual recombination combines different beneficial mutations in different genes into the same genetic background, thereby speeding up adaptation to chloramphenicol.

It doesn't work with HIV, weeds, and insects. You extrapolate a result and you get garbage.
Kleinman:
The only reason that Desai's population doesn't see the effect of clonal interference is that he lets his population increase the frequencies of a few adaptive alleles and then induces sexual reproduction after 90 generations of constant selection.
Taq:
Yes, it is sexual recombination that alleviates clonal interference.

And you are so stupid, you extrapolate this result to all evolution. You are a mathematically incompetent idiot.
Kleinman:
If Desai allowed his environment to change, who knows if any alleles would have increased in frequencies and who knows what kind of recombination events would have happened.
Taq:
Why wouldn't those same beneficial mutations increase in frequency if there was sexual recombination in every generation?

Because they aren't increasing in frequency. The adaptive alleles change as the environment changes, moron. Do you think these alleles increase in frequency in one generation? Why did Desai use 90 generations of constant selection? Since you are too stupid to answer that question, here's the answer, it takes time (many generations to increase the frequencies of adaptive alleles) and that process is disrupted by a changing environment and changing selection conditions.
Kleinman:
Why don't you do the math with a varying environment and see how much recombination helps?
Taq:
The experiment was already run. It helps.

Yeah, you simpleton, in a constant environment you get a slight increase in relative fitness. Now, learn that this principle doesn't apply when the environment and selection conditions are changing.

This message is a reply to:
 Message 1920 by Taq, posted 11-18-2022 12:09 PM Taq has replied

Replies to this message:
 Message 1926 by Taq, posted 11-18-2022 1:00 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 1925 of 2926 (902167)
11-18-2022 12:51 PM
Reply to: Message 1923 by Taq
11-18-2022 12:37 PM


Re: Illustration of Adaptation in Asexual and Sexual Populations
Taq:
Theoretical impacts of mutation rate and sexual recombination on population structures.
The problem is their theory doesn't match up with reality, just like your claim of constant selection being a realistic model for recombination. Try dealing with reality, we already know your reality of Covid.

This message is a reply to:
 Message 1923 by Taq, posted 11-18-2022 12:37 PM Taq has replied

Replies to this message:
 Message 1927 by dwise1, posted 11-18-2022 1:06 PM Kleinman has not replied
 Message 1928 by Taq, posted 11-18-2022 1:07 PM Kleinman has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(4)
Message 1926 of 2926 (902168)
11-18-2022 1:00 PM
Reply to: Message 1924 by Kleinman
11-18-2022 12:43 PM


Kleinman writes:
If you understood the Kishony or Lenski experiments, you would have done the mathematics long ago, but you don't.
You still haven't addressed what I said.
The Lenski experiment had a constant environment for 10's of thousands of generations. Are you saying that a constant environment does not disqualify an experiment?
The only way that Desai could get his experiment to work was to use a constant environment, let adaptive alleles increase in frequencies for 90 generations in a constant environment, and then induce sexual reproduction.
The adaptive alleles would increase in frequency if there was sexual reproduction in every generation.
You are so stupid, you think that recombination works the same way in a varying environments.
How does recombination work differently in varying environments?
You stupidly extrapolate a constant environment to all environments.
The Lenski experiment used a constant environment of 10's of thousands of generations.
"The Kishony and Lenski experiments demonstrate exactly how descent with modification operates."--Kleinman
quote:
It doesn't work with HIV, weeds, and insects.
Yes, it does.
quote:
These findings emphasize that recombination can participate in the adaptation of HIV to changing selective pressure, both by generating novel combinations of resistance mutations and by maintaining diversity in genomic regions outside those implicated in a selective sweep.
Just a moment...
And you are so stupid, you extrapolate this result to all evolution.
So says the person who extrapolates the Kishony/Lenski experiment to all of evolution.
Because they aren't increasing in frequency. The adaptive alleles change as the environment changes, moron.
You are really mixed up now. You were saying that Desai had to asexual reproduction in a constant environment in order to increase the frequency of beneficial alleles. Why wouldn't those same alleles increase in fitness with sexual reproduction in every generation and a constant environment?
Why did Desai use 90 generations of constant selection?
Why did Lenski use 10's of thousands of generations of constant selection?
Yeah, you simpleton, in a constant environment you get a slight increase in relative fitness. Now, learn that this principle doesn't apply when the environment and selection conditions are changing.
Why don't you show us the principle. Show us a real world example that compares asexual and sexual reproduction in a changing environment. Show us the math.
Put up or shut up.

This message is a reply to:
 Message 1924 by Kleinman, posted 11-18-2022 12:43 PM Kleinman has replied

Replies to this message:
 Message 1930 by Kleinman, posted 11-18-2022 2:10 PM Taq has replied

  
dwise1
Member
Posts: 5930
Joined: 05-02-2006
Member Rating: 5.8


Message 1927 of 2926 (902169)
11-18-2022 1:06 PM
Reply to: Message 1925 by Kleinman
11-18-2022 12:51 PM


Re: Illustration of Adaptation in Asexual and Sexual Populations






And yet you still cannot understand the simple reality that sexual reproduction is different than asexual reproduction?






And you still cannot understand that a math model for asexual reproduction will not work to model sexual reproduction?



You silly creationists say the stupidest things!






This message is a reply to:
 Message 1925 by Kleinman, posted 11-18-2022 12:51 PM Kleinman has not replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 1928 of 2926 (902170)
11-18-2022 1:07 PM
Reply to: Message 1925 by Kleinman
11-18-2022 12:51 PM


Re: Illustration of Adaptation in Asexual and Sexual Populations
Kleinman writes:
The problem is their theory doesn't match up with reality,
Except that it does. Peabody et al. observed those same effects in their experiment.
Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes
Beneficial mutations for CM resistance can occur in different genes which makes it a candidate for studies on sexual recombination. They found that the combination of a faster mutation rate and sexual recombination increased the speed of adaptation to CM resistance.
The genderless are the sexual reproducers, and higher mutation rates were induced with arabinose (ara). Therefore, the sexual reproducers with high mutation rates are the genderless ara+, and they adapted to CM the fastest.

This message is a reply to:
 Message 1925 by Kleinman, posted 11-18-2022 12:51 PM Kleinman has replied

Replies to this message:
 Message 1931 by Kleinman, posted 11-18-2022 2:11 PM Taq has not replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 1929 of 2926 (902172)
11-18-2022 1:44 PM


Yet Another Example
The more you look around the more examples you can find of sexual recombination increasing the efficiency of adaptation.
quote:
The findings presented above indicate that multiple beneficial mutations were present in the evolving populations and that, as required by the FM model, in the absence of recombination, competition between these mutations was associated with slower fixation times. Indeed, this competition was so strong that in the rec− lines, the relative effect of the focal spoTEv mutations became negative, such that additional beneficial mutations must have occurred on the same background in order for the focal mutation to fix. The possible existence of linked deleterious mutations cannot explain this result by itself, because the deleterious mutations would impose a constant cost to the focal mutation. By contrast, in the rec+ lines, the relative advantage conferred by the spoTEv mutations showed no overall change, indicating that recombination effectively reduced the effect of competition between beneficial mutations. This reduction in competition is consistent with recombination bringing competing beneficial mutations together into one lineage, the mechanism proposed by the FM model.
Recombination Speeds Adaptation by Reducing Competition between Beneficial Mutations in Populations of Escherichia coli | PLOS Biology
The rec+ populations were recombination positive. Wouldn't you know it, recombination alleviated clonal interference and sped up adaptation by putting beneficial mutations from different lineages into the same genetic background. Seems to be a repeating theme.

Replies to this message:
 Message 1932 by Kleinman, posted 11-18-2022 2:21 PM Taq has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 1930 of 2926 (902173)
11-18-2022 2:10 PM
Reply to: Message 1926 by Taq
11-18-2022 1:00 PM


Kleinman:
If you understood the Kishony or Lenski experiments, you would have done the mathematics long ago, but you don't.
Taq:
You still haven't addressed what I said.

The Lenski experiment had a constant environment for 10's of thousands of generations. Are you saying that a constant environment does not disqualify an experiment?

I've said it many times, you just don't get it. It takes 1/(mutation rate) replications in a single selection pressure environment to get an adaptive mutation. Change the environment as much as you want and it still takes 1/(mutation rate) replications to get an adaptive mutation. When recombination is a possibility, a changing environment reduces the probability because the selection condition is changing therefore, the adaptive alleles are changing. Lenski's experiment would have been even slower if the environment was changing. Learn this math you dummy.
Kleinman:
The only way that Desai could get his experiment to work was to use a constant environment, let adaptive alleles increase in frequencies for 90 generations in a constant environment, and then induce sexual reproduction.
Taq:
The adaptive alleles would increase in frequency if there was sexual reproduction in every generation.

So you dream. None of the adaptive alleles would have had a chance to increase in frequency. Of course, you think they magically do increase in frequencies.
Kleinman:
You are so stupid, you think that recombination works the same way in a varying environments.
Taq:
How does recombination work differently in varying environments?

You should know the answer to this one dummy, even Tany blundered into this one. The adaptive alleles change depending on the selection conditions. Only in your imagination do alleles increase in a changing environment.
Kleinman:
You stupidly extrapolate a constant environment to all environments.
Taq:
The Lenski experiment used a constant environment of 10's of thousands of generations.

"The Kishony and Lenski experiments demonstrate exactly how descent with modification operates."--Kleinman

And you are supposed to be in the varsity. The Lenski experiment would operate more slowly in a changing environment. Change the temperature, change the osmotic pressure, change any selection condition you want and evolution will work more slowly because of the changing evolutionary trajectories. You know, Lenski did run experiments in non-optimal conditions and it required different mutations than his starvation condition experiment. Of course, in your twisted imagination, evolution would occur more quickly.
Kleinman:
It doesn't work with HIV, weeds, and insects.
Taq:
Yes, it does.
quote:
These findings emphasize that recombination can participate in the adaptation of HIV to changing selective pressure, both by generating novel combinations of resistance mutations and by maintaining diversity in genomic regions outside those implicated in a selective sweep.
Just a moment...


The genius virologist has just proven that 3 drug combination therapy does not work for the treatment of HIV. You are a blithering genius.
Kleinman:
And you are so stupid, you extrapolate this result to all evolution.
Taq:
So says the person who extrapolates the Kishony/Lenski experiment to all of evolution.

Biological evolution only gets slower with changing environments and multiple selection pressures. You really don't know anything about biological evolution.
Kleinman:
Because they aren't increasing in frequency. The adaptive alleles change as the environment changes, moron.
Taq:
You are really mixed up now. You were saying that Desai had to asexual reproduction in a constant environment in order to increase the frequency of beneficial alleles. Why wouldn't those same alleles increase in fitness with sexual reproduction in every generation and a constant environment?

You think it would increase the frequencies of adaptive alleles but that just proves you speculate.
Kleinman:
Why did Desai use 90 generations of constant selection?
Taq:
Why did Lenski use 10's of thousands of generations of constant selection?

You are so dumb. Lenski's experiment would have worked far more slowly if he had a changing environment with changing selection conditions. Instead of taking 30 years to get 100 adaptive mutations, it might have taken much longer. You simply don't understand what combination selection pressures do to an evolutionary process. It imposes more instances of the multiplication rule on the population and requires exponentially more replication to evolve. That's why HIV cannot evolve to 3 drug therapy, even with recombination, it can't achieve the population size necessary to give a reasonable probability of a 3 drug resistant variant. Learn how to do the math.
Kleinman:
Yeah, you simpleton, in a constant environment you get a slight increase in relative fitness. Now, learn that this principle doesn't apply when the environment and selection conditions are changing.
Taq:
Why don't you show us the principle. Show us a real world example that compares asexual and sexual reproduction in a changing environment. Show us the math.

Put up or shut up.

I've given you many empirical examples, HIV, insects, and weeds. You have this strange imagination that evolution occurs in a constant environment when it doesn't. Experiments in constant environments show how slow the process is with the constant environments and single selection conditions. Multiple selection conditions give treatment for HIV, insects, and weeds. These are real examples and I've given the correct mathematics that explains why this works. Take a course in introductory probability theory and learn how biological evolution works.

This message is a reply to:
 Message 1926 by Taq, posted 11-18-2022 1:00 PM Taq has replied

Replies to this message:
 Message 1934 by Taq, posted 11-18-2022 3:25 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 1931 of 2926 (902174)
11-18-2022 2:11 PM
Reply to: Message 1928 by Taq
11-18-2022 1:07 PM


Re: Illustration of Adaptation in Asexual and Sexual Populations
Kleinman:
The problem is their theory doesn't match up with reality,
Taq:
Except that it does. Peabody et al. observed those same effects in their experiment.

Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes


Hey, dummy, why do lab tests done in vitro show drug resistance, and yet in vivo, the drugs sometimes work? When you can't figure that out, I'll explain it to you and perhaps you will understand.

This message is a reply to:
 Message 1928 by Taq, posted 11-18-2022 1:07 PM Taq has not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 1932 of 2926 (902175)
11-18-2022 2:21 PM
Reply to: Message 1929 by Taq
11-18-2022 1:44 PM


Re: Yet Another Example
Taq:
The more you look around the more examples you can find of sexual recombination increasing the efficiency of adaptation.
Is that all you can find is constant environment experiments with a single selection pressure. No wonder you don't understand biological evolution when everything evolves in a constant environment single selection pressure environment. And it still takes thousands of generations to evolve.

This message is a reply to:
 Message 1929 by Taq, posted 11-18-2022 1:44 PM Taq has replied

Replies to this message:
 Message 1933 by Taq, posted 11-18-2022 3:14 PM Kleinman has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 1933 of 2926 (902177)
11-18-2022 3:14 PM
Reply to: Message 1932 by Kleinman
11-18-2022 2:21 PM


Re: Yet Another Example
Kleinman writes:
Is that all you can find is constant environment experiments with a single selection pressure.
The Lenski experiment used a constant environment and a single selection pressure for 50,000 generations.
"The Kishony and Lenski experiments demonstrate exactly how descent with modification operates."--Kleinman

This message is a reply to:
 Message 1932 by Kleinman, posted 11-18-2022 2:21 PM Kleinman has replied

Replies to this message:
 Message 1937 by Kleinman, posted 11-18-2022 4:37 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 1934 of 2926 (902178)
11-18-2022 3:25 PM
Reply to: Message 1930 by Kleinman
11-18-2022 2:10 PM


Kleinman writes:
I've said it many times, you just don't get it. It takes 1/(mutation rate) replications in a single selection pressure environment to get an adaptive mutation.
Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:
REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMC
Luria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.
There is one interesting observation in the Lederberg paper:
"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."
In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.
Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.
If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species?
When recombination is a possibility, a changing environment reduces the probability because the selection condition is changing therefore, the adaptive alleles are changing.
Reduces the probability of what, and compared to what?
Would a changing environment cause clonal interference in a sexually reproducing population? NO.
Would beneficial alleles in the new environment increase in frequency in the new environment in sexually reproducing populations? YES
Would you get a combination of beneficial alleles faster in a changing environment with a sexually reproducing population compared to an asexual population? YES
So you dream. None of the adaptive alleles would have had a chance to increase in frequency.
In a constant environment, why wouldn't beneficial alleles increase in frequency in a sexually reproducing population?
You should know the answer to this one dummy, even Tany blundered into this one.
I do know the answer. Sexual recombination doesn't change in a changing environment. It works the same way. When humans move to a different environment their gametes still work in the very same way.
The Lenski experiment would operate more slowly in a changing environment.
You said the Lenski experiment demonstrates exactly how descent with modification works, and it had 50,000 generations in the same exact environment. You reject the Desai experiment because it had a constant environment for 90 generations.
Hypocrisy much?
The genius virologist has just proven that 3 drug combination therapy does not work for the treatment of HIV.
I'm not the one rejecting published science. You are.
Biological evolution only gets slower with changing environments and multiple selection pressures. You really don't know anything about biological evolution.
Then show it in a real population. Show how an asexual and sexual population evolve in changing environments with multiple selection pressures.
I've given you many empirical examples, HIV, insects, and weeds.
All of which increase their rate of adaptation through sexual recombination.

This message is a reply to:
 Message 1930 by Kleinman, posted 11-18-2022 2:10 PM Kleinman has replied

Replies to this message:
 Message 1938 by Kleinman, posted 11-18-2022 4:44 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 1935 of 2926 (902179)
11-18-2022 3:36 PM


Evolution of Multiple Herbicide Resistance
quote:
The acquired inheritable trait of plants to survive and reproduce under herbicide exposure is defined as resistance. Herbicide resistance is an extraordinary example of adaptive evolution in weed species infesting agroecosystems with clear detrimental consequences on agriculture sustainability around the globe (Palumbi, 2001; Llewellyn et al., 2016). Multiple herbicide resistance is a compelling evolutionary process in which distinct survival mechanisms are present in a population or are combined within single plants, each endowing resistance to dissimilar site of action herbicides (Hall et al., 1994; Gaines et al., 2020). These multiple mechanisms may involve either target site (TSR) or non-target site resistance (NTSR) mechanisms or any combination endowing multiple resistance. Multiple resistance can evolve through unique events that sequentially select for resistance alleles within single plants and/or genetic exchange of independently evolved resistance mutations through pollen outcrossing among plants within or between populations.
Frontiers | Editorial: Multiple Herbicide-Resistant Weeds and Non-target Site Resistance Mechanisms: A Global Challenge for Food Production


Wouldn't you know it, recombination can speed up the acquisition of multi-herbicide resistance.

Replies to this message:
 Message 1939 by Kleinman, posted 11-18-2022 4:45 PM Taq has replied

  
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