The Physics and Mathematics of Evolution

[Alan Kleinman MD PhD]

The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of “survival of the fittest” and the mathematics of improving fitness.
.
The mathematics of “survival of the fittest” is addressed by the works of Haldane and Kimura. Haldane's work “The cost of natural selection” can be found at:
http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
http://www.genetics.org/content/genetics/47/6/713.full.pdf
.
These two authors in their papers use different terminology to describe the same thing. Haldane uses the word “substitution” while the Kimura paper uses the term “fixation” to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable “mutation rate”. This is because they are not addressing the mathematics of “improvement in fitness”. They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
.
On the other hand, “improvement in fitness” must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication. So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant. Bill Rogers argues that competition, “survival of the fittest”, improves that probability of that particular mutation occurring. Does it?

[Peter Nyikos]

On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of "survival of the fittest" and the mathematics of improving fitness.
> .
> The mathematics of "survival of the fittest" is addressed by the works of Haldane and Kimura. Haldane's work "The cost of natural selection" can be found at:
> http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
> And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
> http://www.genetics.org/content/genetics/47/6/713.full.pdf
> .
> These two authors in their papers use different terminology to describe the same thing. Haldane uses the word "substitution" while the Kimura paper uses the term "fixation" to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable "mutation rate". This is because they are not addressing the mathematics of "improvement in fitness". They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
> .
> On the other hand, "improvement in fitness" must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication.

You did fine until now. But now you've shown us the Achilles' Heel of
your entire rant against microevolution. You have no way of ascertaining how
many *other* mutations at how many *other* sites would also
have resulted in improved fitness.

And 'improved fitness' is so easy to achieve, that it stands to reason
there are a gargantuan number of other sites that lead to improved
fitness by the time you get to the level of even primitive vertebrates.


What you ought to concentrate on is the improbability of convergent
evolution producing hauntingly similar structures. Here is one example.

The marsupionta hypothesis had it that monotremes were more closely
related to placentals than either group was to marsupials:

Article in favor of Marsupionta hypothesis:
http://faculty.chas.uni.edu/~spradlin/SandE/Readings/Matt.pdf
J Mol Evol (2002) 54:71-80 DOI: 10.1007/s00239-001-0019-8
"Phylogenetic Analysis of 18S rRNA and the Mitochondrial Genomes of the
Wombat, Vombatus ursinus, and the Spiny Anteater, Tachyglossus aculeatus:
Increased Support for the Marsupionta Hypothesis," by Axel Janke,
Ola Magnell, Georg Wieczorek, Michael Westerman, and Ulfur Arnason

These people must have been feeling the weight of "publish or perish"
to produce such a far-out paper. One comparison of the primitive
reptilian shoulder girdle of monotremes to those of marsupials
and placentals should have made J Mol Evol reject the paper out of hand.

The scapula alone shows huge differences. The shoulder blades of humans
and opossums both have a medial ridge completely lacking in those
of the platypus, and the overall shapes are strikingly different
also.

When I told one of your most vocal and cowardly critics, John
Harshman about this, he berated me for jumping to conclusions
on the basis of "one character." Something is rotten in the
state of systematics, Harshman's specialty, when a whole scapula
is given equal footing with a single point mutation.

But more importantly: you missed a golden opportunity to hit
Harshman with the multiplication rule of probabilities AND
your "Achilles' Heel" statement. ALL those examples of hypothesized
convergence between marsupials and placentals are valid examples
where evolution really HAD to proceed according to a precise
plan in order to produce KNOWN, DOCUMENTED effects.

>So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant.

You didn't identify the mutation you are talking about below. But
what you are saying applies beautifully to the mutations responsible
for those "parallel ridges" -- the median ridge in marsupials
and the median ridge in placentals. And you might even needle
Bill Rogers about it as you do for your mysterious "that particular
mutation":

> Bill Rogers argues that competition, "survival of the fittest, improves

> that probability of that particular mutation occurring. Does it?

Peter Nyikos
Professor, Dept. of Mathematics -- standard disclaimer--
University of South Carolina
http://people.math.sc.edu/nyikos/

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 6:50:05 AM UTC-8, Peter Nyikos wrote:
> On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:

> > The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of "survival of the fittest" and the mathematics of improving fitness.
> > .
> > The mathematics of "survival of the fittest" is addressed by the works of Haldane and Kimura. Haldane's work "The cost of natural selection" can be found at:
> > http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
> > And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
> > http://www.genetics.org/content/genetics/47/6/713.full.pdf
> > .
> > These two authors in their papers use different terminology to describe the same thing. Haldane uses the word "substitution" while the Kimura paper uses the term "fixation" to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable "mutation rate". This is because they are not addressing the mathematics of "improvement in fitness". They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
> > .
> > On the other hand, "improvement in fitness" must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication.
>

> You did fine until now. But now you've shown us the Achilles' Heel of
> your entire rant against microevolution. You have no way of ascertaining how
> many *other* mutations at how many *other* sites would also
> have resulted in improved fitness.

All right, show us how to do the mathematics of your scenario.

>
> And 'improved fitness' is so easy to achieve, that it stands to reason
> there are a gargantuan number of other sites that lead to improved
> fitness by the time you get to the level of even primitive vertebrates.

Just how easy is it to achieve an improvement in fitness? Show us how to do the mathematics. And is there a difference in lineages when a beneficial mutation occurs at one site vs a beneficial mutation occurring at a different site? In other words, if one was to do extremely precise phylogenetic analysis using common descent from generation to generation, would a descendant with a beneficial mutation at one given site be in the same line of descendancy as another member with a different beneficial mutation at a different site?

>
>
> What you ought to concentrate on is the improbability of convergent
> evolution producing hauntingly similar structures. Here is one example.
>
> The marsupionta hypothesis had it that monotremes were more closely
> related to placentals than either group was to marsupials:
>
> Article in favor of Marsupionta hypothesis:
> http://faculty.chas.uni.edu/~spradlin/SandE/Readings/Matt.pdf
> J Mol Evol (2002) 54:71-80 DOI: 10.1007/s00239-001-0019-8
> "Phylogenetic Analysis of 18S rRNA and the Mitochondrial Genomes of the
> Wombat, Vombatus ursinus, and the Spiny Anteater, Tachyglossus aculeatus:
> Increased Support for the Marsupionta Hypothesis," by Axel Janke,
> Ola Magnell, Georg Wieczorek, Michael Westerman, and Ulfur Arnason
>
> These people must have been feeling the weight of "publish or perish"
> to produce such a far-out paper. One comparison of the primitive
> reptilian shoulder girdle of monotremes to those of marsupials
> and placentals should have made J Mol Evol reject the paper out of hand.

Like in the old Wendy's commercial, where's the math?

>
> The scapula alone shows huge differences. The shoulder blades of humans
> and opossums both have a medial ridge completely lacking in those
> of the platypus, and the overall shapes are strikingly different
> also.

How exactly does this relate to the mathematics of survival of the fittest and the mathematics of improvement in fitness? Comparative anatomy is one of the crudest measures of relatedness. And the selective analysis of homologous regions of genomes to determine relatedness while ignoring all the non-homologous regions of genomes is not much better than comparative anatomy to determine relatedness. Have you yet studied the Kishony video?

>
> When I told one of your most vocal and cowardly critics, John
> Harshman about this, he berated me for jumping to conclusions
> on the basis of "one character." Something is rotten in the
> state of systematics, Harshman's specialty, when a whole scapula
> is given equal footing with a single point mutation.

John has already admitted he does not take into account the mechanisms of genetic transformation in his phylogenetic analysis. This is why the classical work of paleontologists will not withstand the test of time as the mechanisms of genetic transformation are better understood.

>
> But more importantly: you missed a golden opportunity to hit
> Harshman with the multiplication rule of probabilities AND
> your "Achilles' Heel" statement. ALL those examples of hypothesized
> convergence between marsupials and placentals are valid examples
> where evolution really HAD to proceed according to a precise
> plan in order to produce KNOWN, DOCUMENTED effects.

First, you have to understand the mathematics of rmns before you can understand why the multiplication rule has such a dominant effect on the mechanisms of genetic transformation. And that mathematics is not the mathematics of survival of the fittest.

>
>
> >So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant.
>

> You didn't identify the mutation you are talking about below. But
> what you are saying applies beautifully to the mutations responsible
> for those "parallel ridges" -- the median ridge in marsupials
> and the median ridge in placentals. And you might even needle
> Bill Rogers about it as you do for your mysterious "that particular
> mutation":

It is any beneficial mutation that I'm talking about. The probability of a particular mutation occurring at a particular site in a single replication is the mutation rate. To improve the probability of that particular mutation occurring requires more replications of that genome. If you can do that calculation, that is the mathematics of improving fitness.
>
> > Bill Rogers argues that competition, "survival of the fittest, improves

> > that probability of that particular mutation occurring. Does it?
>
>

[gdgu...@gmail.com]

On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:

> Bill Rogers argues that competition, “survival of the fittest”, improves that
> probability of that particular mutation occurring. Does it?

I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?

Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
>

> > Bill Rogers argues that competition, “survival of the fittest”, improves that
> > probability of that particular mutation occurring. Does it?
>

> I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?

From the thread “Kleinman confuses probability with informal statistics ”:
On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
“Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?

>
> Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.

As long as rmns is dependent on “particular” mutations to improve fitness, it is quite appropriate to use this term. But if you think this is a flaw, point out this flaw with specificity.

[gdgu...@gmail.com]

On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
> On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> >
> > > Bill Rogers argues that competition, “survival of the fittest”, improves that
> > > probability of that particular mutation occurring. Does it?
> >
> > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
> From the thread “Kleinman confuses probability with informal statistics ”:
> On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
> “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”

That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)

> In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?
> >

> > Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
> As long as rmns is dependent on “particular” mutations to improve fitness,

It isn't.

> it is quite appropriate to use this term. But if you think this is a flaw,
> point out this flaw with specificity.

Your "math", what there is of it, demonstrates that it is vanishingly unlikely for mutation, selection and drift (evolution) to produce a *particular* target organism, with its exact DNA complement. This is due to the multiplication rule. I doubt that anyone here disagrees.

But it presents no difficulty for the idea that populations can acquire unspecified, untargeted, "un-particular" variations over time. Or the inevitable tendency for some of those variations to out-reproduce others (whether by increased fitness or by chance/drift), and thereby change the common traits of the population.

[John Harshman]

On 3/7/18 12:15 PM, gdgu...@gmail.com wrote:
> On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
>> On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
>>> On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
>>>
>>>> Bill Rogers argues that competition, “survival of the fittest”, improves that
>>>> probability of that particular mutation occurring. Does it?
>>>
>>> I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
>> From the thread “Kleinman confuses probability with informal statistics ”:
>> On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
>> “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
>
> That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)
>
>> In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?
>>>
>
>>> Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
>> As long as rmns is dependent on “particular” mutations to improve fitness,
>
> It isn't.
>
>> it is quite appropriate to use this term. But if you think this is a flaw,
>> point out this flaw with specificity.
>
> Your "math", what there is of it, demonstrates that it is vanishingly
> unlikely for mutation, selection and drift (evolution) to produce a
> *particular* target organism, with its exact DNA complement. This is
> due to the multiplication rule. I doubt that anyone here disagrees.

That isn't actually true. His math doesn't say anything at all about
selection or drift, only mutation and unsorted reproduction in a steady
state population.

[Alan Kleinman MD PhD]

John, explain to us the difference between the mathematics of survival of the fittest and the mathematics of improving fitness.

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 12:20:03 PM UTC-8, gdgu...@gmail.com wrote:
> On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
> > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> > >

> > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
> > > > probability of that particular mutation occurring. Does it?
> > >

> > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
> > From the thread “Kleinman confuses probability with informal statistics ”:
> > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
> > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
>
> That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)

That statement was made in reference to the Lenski experiment. That experiment is markedly slowed by the competition and delays the occurrence of the next beneficial mutation occurring. And if all the variants have identical fitness, the experiment would be slowed even further for the next beneficial mutation to occur. I think you don't understand why. And Bill made this statement in an earlier thread when he started a discussion on the Lenski experiment.

>
> > In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?

You apparently don't know why competition slows evolution. That's why you can't answer this question.

> > >
>
> > > Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
> > As long as rmns is dependent on “particular” mutations to improve fitness,
>
> It isn't.

Or really? So any mutation improves fitness? There are no neutral or detrimental mutations?

>
> > it is quite appropriate to use this term. But if you think this is a flaw,
> > point out this flaw with specificity.
>
> Your "math", what there is of it, demonstrates that it is vanishingly unlikely for mutation, selection and drift (evolution) to produce a *particular* target organism, with its exact DNA complement. This is due to the multiplication rule. I doubt that anyone here disagrees.

There is a target for rmns. That target is improved fitness. And it takes particular mutations to improve fitness, that is unless you think that neutral and detrimental mutations improve fitness. Neutral and detrimental mutations can increase diversity in a population but survival of the fittest removes these variants.

>
> But it presents no difficulty for the idea that populations can acquire unspecified, untargeted, "un-particular" variations over time. Or the inevitable tendency for some of those variations to out-reproduce others (whether by increased fitness or by chance/drift), and thereby change the common traits of the population.

Where is your empirical evidence for this claim? What exactly do you think that survival of the fittest does to a population? What are Haldane and Kimura calculating with their math? What "un-particular" variations over time improve fitness other than beneficial mutations?

[John Harshman]

Alan, explain to us the parameter in your mathematics that represents
the different fitnesses of different alleles.

[Alan Kleinman MD PhD]

The math that I've presented is not survival of the fittest, it is the mathematics of improving fitness, therefore there is no parameter for the differential fitness. Do you understand what Haldane and Kimura are computing and why it is not adequate for doing the mathematics of improving fitness?

[John Harshman]

I understand that you have no idea what the term "fitness" means, don't
understand that in order for fitness to improve there must be definition
be differential fitness, and that your math doesn't allow for increased
fitness even in your terms, of increased population size. Your math
assumes constant population size and has no parameter for increase.

[Alan Kleinman MD PhD]

Would you show us how to do the mathematics of the Kishony experiment based on a definition of natural selection as differential fitness to reproduce?

> and that your math doesn't allow for increased
> fitness even in your terms, of increased population size. Your math
> assumes constant population size and has no parameter for increase.

As an expediency, my published equations were based on constant population size but these equations work just fine with a variable population size, simply sum the replications over generations.
.
But since you know so much about this subject, using Haldane's model, compute the intensity of selection for the Lenski experiment. You won't do any better on this calculation than you will do using differential fitness to compute the behavior of the Kishony experiment.

[Bill Rogers]

On Wednesday, March 7, 2018 at 3:20:03 PM UTC-5, gdgu...@gmail.com wrote:
> On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
> > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> > >
> > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
> > > > probability of that particular mutation occurring. Does it?
> > >
> > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
> > From the thread “Kleinman confuses probability with informal statistics ”:
> > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
> > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
>
> That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)

Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
> On Wednesday, March 7, 2018 at 3:20:03 PM UTC-5, gdgu...@gmail.com wrote:
> > On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
> > > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> > > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> > > >
> > > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
> > > > > probability of that particular mutation occurring. Does it?
> > > >
> > > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
> > > From the thread “Kleinman confuses probability with informal statistics ”:
> > > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
> > > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
> >
> > That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)
>
> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.

Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.

[John Harshman]

That isn't a definition of natural selection.

>> and that your math doesn't allow for increased
>> fitness even in your terms, of increased population size. Your math
>> assumes constant population size and has no parameter for increase.
> As an expediency, my published equations were based on constant population size but these equations work just fine with a variable population size, simply sum the replications over generations.

Sorry, but that doesn't result in a variable population size, just in a
constant population carried through several generations. Well, at least
you now admit that you have assumed a constant population. That's progress.

So where's the selection?

> But since you know so much about this subject, using Haldane's model, compute the intensity of selection for the Lenski experiment. You won't do any better on this calculation than you will do using differential fitness to compute the behavior of the Kishony experiment.

This is you just avoiding my questions. Where is the natural selection
in your math? No allele increases in frequency, no population grows
larger, so neither the standard population-genetic definition nor your
personal definition applies. What you have dealt with is the waiting
time for a particular mutation in a bizarre bacterial population in
which each bacterium fissions once in a generation and one of the
daughter cells immediately dies. In such a system, there is no
possibility of selection.

[Alan Kleinman MD PhD]

Do the calculation with whatever definition of natural selection you wish.

>
> >> and that your math doesn't allow for increased
> >> fitness even in your terms, of increased population size. Your math
> >> assumes constant population size and has no parameter for increase.
> > As an expediency, my published equations were based on constant population size but these equations work just fine with a variable population size, simply sum the replications over generations.
>
> Sorry, but that doesn't result in a variable population size, just in a
> constant population carried through several generations. Well, at least
> you now admit that you have assumed a constant population. That's progress.
>

What you have failed to understand is the definition of the sample space. So it doesn't matter how the population varies over the generations. It the total number of replications which determines the probability of the beneficial mutation occurring.

> So where's the selection?

Selection for improvement of fitness occurs by the particular variant(s) which is/are able to amplify. Those variants which are unable to amplify either go extinct or drift.

>
> > But since you know so much about this subject, using Haldane's model, compute the intensity of selection for the Lenski experiment. You won't do any better on this calculation than you will do using differential fitness to compute the behavior of the Kishony experiment.
>
> This is you just avoiding my questions. Where is the natural selection
> in your math? No allele increases in frequency, no population grows
> larger, so neither the standard population-genetic definition nor your
> personal definition applies. What you have dealt with is the waiting
> time for a particular mutation in a bizarre bacterial population in
> which each bacterium fissions once in a generation and one of the
> daughter cells immediately dies. In such a system, there is no
> possibility of selection.

The difficulty you are having in this discussion is in your inability to understand how the mathematics of survival of the fitness works and what is computed with this mathematics. Simply put, survival of the fittest is all about the removal of the less fit variants in a population. The environment imposes limits on the population and because of these limitations, the most fit variant ultimately drives the less fit variants to extinction. This mathematics requires the notion of natural selection as the differential fitness to reproduce. However, this mathematics is not a computation of improvement in fitness. Improvement in fitness requires beneficial mutations and the probability of these mutations occurring is dependent on the total number of replications of the particular variants on their particular evolutionary trajectories. This is where natural selection must be measured by the absolute fitness to reproduce, not the relative fitness to reproduce. Try to understand the differences in the Kishony experiment where improvement in fitness occurs in a non-competitive environment and the Lenski experiment where improvement in fitness is occurring in a competitive environment.

[John Harshman]

Sorry, I don't have the data necessary to determine parameters. You
know, the sort of parameters you don't deal with.

>>>> and that your math doesn't allow for increased
>>>> fitness even in your terms, of increased population size. Your math
>>>> assumes constant population size and has no parameter for increase.
>>> As an expediency, my published equations were based on constant population size but these equations work just fine with a variable population size, simply sum the replications over generations.
>>
>> Sorry, but that doesn't result in a variable population size, just in a
>> constant population carried through several generations. Well, at least
>> you now admit that you have assumed a constant population. That's progress.
>>
> What you have failed to understand is the definition of the sample space. So it doesn't matter how the population varies over the generations. It the total number of replications which determines the probability of the beneficial mutation occurring.

What does that have to do with natural selection?

>> So where's the selection?
> Selection for improvement of fitness occurs by the particular variant(s) which is/are able to amplify. Those variants which are unable to amplify either go extinct or drift.

But you don't deal with any of that. You don't deal with drift, or
extinction, or "amplification". Just a weird constant population with no
genetic variation.

>>> But since you know so much about this subject, using Haldane's model, compute the intensity of selection for the Lenski experiment. You won't do any better on this calculation than you will do using differential fitness to compute the behavior of the Kishony experiment.
>>
>> This is you just avoiding my questions. Where is the natural selection
>> in your math? No allele increases in frequency, no population grows
>> larger, so neither the standard population-genetic definition nor your
>> personal definition applies. What you have dealt with is the waiting
>> time for a particular mutation in a bizarre bacterial population in
>> which each bacterium fissions once in a generation and one of the
>> daughter cells immediately dies. In such a system, there is no
>> possibility of selection.
> The difficulty you are having in this discussion is in your inability to understand how the mathematics of survival of the fitness works and what is computed with this mathematics. Simply put, survival of the fittest is all about the removal of the less fit variants in a population. The environment imposes limits on the population and because of these limitations, the most fit variant ultimately drives the less fit variants to extinction. This mathematics requires the notion of natural selection as the differential fitness to reproduce. However, this mathematics is not a computation of improvement in fitness. Improvement in fitness requires beneficial mutations and the probability of these mutations occurring is dependent on the total number of replications of the particular variants on their particular evolutionary trajectories. This is where natural selection must be measured by the absolute fitness to reproduce, not the relative fitness to reproduce. Try to understand the differences in the Kishony experiment where improvement in fitness occurs in a non-competitive environment and the Lenski experiment where improvement in fitness is occurring in a competitive environment.

I defy anyone to find anything in the above mess that has anything to do
with natural selection or its treatment in your math.

[Alan Kleinman MD PhD]

What parameters do you need? Write out the equation(s) you think apply to this experiment and leave any unknown quantities as variables.

>
> >>>> and that your math doesn't allow for increased
> >>>> fitness even in your terms, of increased population size. Your math
> >>>> assumes constant population size and has no parameter for increase.
> >>> As an expediency, my published equations were based on constant population size but these equations work just fine with a variable population size, simply sum the replications over generations.
> >>
> >> Sorry, but that doesn't result in a variable population size, just in a
> >> constant population carried through several generations. Well, at least
> >> you now admit that you have assumed a constant population. That's progress.
> >>
> > What you have failed to understand is the definition of the sample space. So it doesn't matter how the population varies over the generations. It the total number of replications which determines the probability of the beneficial mutation occurring.
>
> What does that have to do with natural selection?

It is the absolute fitness to reproduce. If the given variant cannot replicate sufficiently, that variant will not be able to improve fitness. This is clearly demonstrated in the Kishony experiment.

>
> >> So where's the selection?
> > Selection for improvement of fitness occurs by the particular variant(s) which is/are able to amplify. Those variants which are unable to amplify either go extinct or drift.
>
> But you don't deal with any of that. You don't deal with drift, or
> extinction, or "amplification". Just a weird constant population with no
> genetic variation.

The math I've presented describes the evolutionary trajectory. It is the total number of replications a variant can do which determines the probability of each step on that evolutionary trajectory. This is the mathematics of improving fitness, this is not the mathematics of survival of the fittest.

>
> >>> But since you know so much about this subject, using Haldane's model, compute the intensity of selection for the Lenski experiment. You won't do any better on this calculation than you will do using differential fitness to compute the behavior of the Kishony experiment.
> >>
> >> This is you just avoiding my questions. Where is the natural selection
> >> in your math? No allele increases in frequency, no population grows
> >> larger, so neither the standard population-genetic definition nor your
> >> personal definition applies. What you have dealt with is the waiting
> >> time for a particular mutation in a bizarre bacterial population in
> >> which each bacterium fissions once in a generation and one of the
> >> daughter cells immediately dies. In such a system, there is no
> >> possibility of selection.
> > The difficulty you are having in this discussion is in your inability to understand how the mathematics of survival of the fitness works and what is computed with this mathematics. Simply put, survival of the fittest is all about the removal of the less fit variants in a population. The environment imposes limits on the population and because of these limitations, the most fit variant ultimately drives the less fit variants to extinction. This mathematics requires the notion of natural selection as the differential fitness to reproduce. However, this mathematics is not a computation of improvement in fitness. Improvement in fitness requires beneficial mutations and the probability of these mutations occurring is dependent on the total number of replications of the particular variants on their particular evolutionary trajectories. This is where natural selection must be measured by the absolute fitness to reproduce, not the relative fitness to reproduce. Try to understand the differences in the Kishony experiment where improvement in fitness occurs in a non-competitive environment and the Lenski experiment where improvement in fitness is occurring in a competitive environment.
>
> I defy anyone to find anything in the above mess that has anything to do
> with natural selection or its treatment in your math.

Let's start with something simple which you should understand now. The probability of a particular mutation occurring increases with the number of replications (population size) but it does not double as the number of replication doubles. So for a given mutation rate, how large of a population is needed for there to be a reasonable probability of at least one member with that particular mutation?

[Peter Nyikos]

On Wednesday, March 7, 2018 at 10:55:04 AM UTC-5, Alan Kleinman MD PhD wrote:
> On Wednesday, March 7, 2018 at 6:50:05 AM UTC-8, Peter Nyikos wrote:
> > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> > > The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of "survival of the fittest" and the mathematics of improving fitness.
> > > .
> > > The mathematics of "survival of the fittest" is addressed by the works of Haldane and Kimura. Haldane's work "The cost of natural selection" can be found at:
> > > http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
> > > And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
> > > http://www.genetics.org/content/genetics/47/6/713.full.pdf
> > > .
> > > These two authors in their papers use different terminology to describe the same thing. Haldane uses the word "substitution" while the Kimura paper uses the term "fixation" to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable "mutation rate". This is because they are not addressing the mathematics of "improvement in fitness". They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
> > > .
> > > On the other hand, "improvement in fitness" must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication.
> >
> > You did fine until now. But now you've shown us the Achilles' Heel of
> > your entire rant against microevolution. You have no way of ascertaining how
> > many *other* mutations at how many *other* sites would also
> > have resulted in improved fitness.

> All right, show us how to do the mathematics of your scenario.

What part of "You have no way of ascertaining...resulted in improved fitness" didn't you understand?

Are you such a simpleton, that you actually think mathematics can
tell us WHICH mutations will be beneficial? It would take minute
knowledge of the genome, of the physical environment, of the species
that impact the survival of the species under study etc. that
are beyond human comprehension. Mathematics is the least of the
titanic difficulties.

If you breeze past the foregoing two paragraphs as though they
didn't exist, be prepared to be justly accused of cowardice.

> >
> > And 'improved fitness' is so easy to achieve, that it stands to reason
> > there are a gargantuan number of other sites that lead to improved
> > fitness by the time you get to the level of even primitive vertebrates.

> Just how easy is it to achieve an improvement in fitness? Show us how to do the mathematics.

More of the same idiocy, pretending that we have superhuman powers
of clairvoyance, and that mathematics is a magic entity that can
tell us things that are not within its domain.

Maybe the reason you are so incorrigibly ignorant is that you think
that vertebrates are as simple as HIV viruses, that their fitness
depends on how they can handle a tiny assortment of human-made
drugs, and that their environment is as simple as the T cells of the
host of these viruses.

If you think your chickens (goats?) are this simple, set them loose
in the woods, prevent them from returning to the farm, and see how
long they thrive in the wild.

> And is there a difference in lineages when a beneficial mutation occurs at one site vs a beneficial mutation occurring at a different site?

The probability of that is high, because just as no two snowflakes
are different, even so no two beneficial mutations can be expected
to have the exact same effect on relative or absolute fitness.

The reason this may NOT be a no-brainer for you is that in your
micro-world of HIV viruses and drug cocktails, there are only
a handful of beneficial mutations to be had.

>In other words, if one was to do extremely precise phylogenetic analysis using common descent from generation to generation, would a descendant with a beneficial mutation at one given site be in the same line of descendancy as another member with a different beneficial mutation at a different site?

NOW you are beginning to reveal that you have some minuscule
appreciation even of the complexity of your tidy little micro-world.

> >
> >
> > What you ought to concentrate on is the improbability of convergent
> > evolution producing hauntingly similar structures. Here is one example.
> >
> > The marsupionta hypothesis had it that monotremes were more closely
> > related to placentals than either group was to marsupials:
> >
> > Article in favor of Marsupionta hypothesis:
> > http://faculty.chas.uni.edu/~spradlin/SandE/Readings/Matt.pdf
> > J Mol Evol (2002) 54:71-80 DOI: 10.1007/s00239-001-0019-8
> > "Phylogenetic Analysis of 18S rRNA and the Mitochondrial Genomes of the
> > Wombat, Vombatus ursinus, and the Spiny Anteater, Tachyglossus aculeatus:
> > Increased Support for the Marsupionta Hypothesis," by Axel Janke,
> > Ola Magnell, Georg Wieczorek, Michael Westerman, and Ulfur Arnason
> >
> > These people must have been feeling the weight of "publish or perish"
> > to produce such a far-out paper. One comparison of the primitive
> > reptilian shoulder girdle of monotremes to those of marsupials
> > and placentals should have made J Mol Evol reject the paper out of hand.

> Like in the old Wendy's commercial, where's the math?

It's in the multiplication law of probabilities, silly. If you
bothered to pay attention below, you would KNOW that.

> > The scapula alone shows huge differences. The shoulder blades of humans
> > and opossums both have a medial ridge completely lacking in those
> > of the platypus, and the overall shapes are strikingly different
> > also.

> How exactly does this relate to the mathematics of survival of the fittest and the mathematics of improvement in fitness?

Crikey, are you this unintelligent? These things make it astronomically
unlikely for the scapulas of placentals and those of marsupials
evolve the same structure. If you can figure out any way those median
ridges improve fitness, and how many intermediate stages there are
between the primitive reptilian scapula and the modern placental-marsupial
scapula, and the improved fitness of each over its predecessors, you may
have the workings of a really solid research paper in anatomy.

I'm on YOUR side on this one, you silly goose. I think such a research
paper is way beyond the abilities of the best scientists.

> Comparative anatomy is one of the crudest measures of relatedness.

Not too crude for this scenario. You don't need precise calculations,
just the difference between greater fitness and reduced fitness.

> And the selective analysis of homologous regions of genomes to determine relatedness while ignoring all the non-homologous regions of genomes is not much better than comparative anatomy to determine relatedness.

I'm not trying to determine relatedness -- the evidence against
the marsupionta hypothesis is so staggering, based on what I
told you, that those authors must have either lacked all common
sense, or were really desperate to publish a research paper.

>Have you yet studied the Kishony video?

If it's about HIV viruses and drug cocktails, I think it would
be a complete waste of my time. :-)

OK, joke's over. You need to tell me just what sorts of actual
animals the video is about, and what it says about them.

> >
> > When I told one of your most vocal and cowardly critics, John
> > Harshman about this, he berated me for jumping to conclusions
> > on the basis of "one character." Something is rotten in the
> > state of systematics, Harshman's specialty, when a whole scapula
> > is given equal footing with a single point mutation.

> John has already admitted he does not take into account the mechanisms of genetic transformation in his phylogenetic analysis. This is why the classical work of paleontologists will not withstand the test of time as the mechanisms of genetic transformation are better understood.

You judge paleontologists extremely harshly if you think Harshman
is an expert in paleontology. His specialty is the systematics
of EXTANT birds. His knowledge of paleontology may be a trifle
greater than mine, but if so, why has he become so bloody lazy
about starting threads in sci.bio.paleontology?

> >
> > But more importantly: you missed a golden opportunity to hit
> > Harshman with the multiplication rule of probabilities AND
> > your "Achilles' Heel" statement. ALL those examples of hypothesized
> > convergence between marsupials and placentals are valid examples
> > where evolution really HAD to proceed according to a precise
> > plan in order to produce KNOWN, DOCUMENTED effects.

> First, you have to understand the mathematics of rmns before you can understand why the multiplication rule has such a dominant effect on the mechanisms of genetic transformation. And that mathematics is not the mathematics of survival of the fittest.

First, you need to get off your rmns hobbyhorse and look at the
huge world out there waiting for you to add to its stores of knowledge.

And you need to stop your Chinese water torture designed to get
me to read the paper you sent me. I've had my hands full with
dedicated perpetrators of injustice gunning for my scalp. I
beat off an especially loudmouthed and aggressive series of
trumped-up charges of lying by Martin Harran, aided, abetted
and comforted by Hemidactylus. But it wasn't easy. I had to
wait patiently since February 20 before Martin accumulated enough
rope to hang himself with.

You are too lamebrained and too amoral to attract such vicious assaults on
your reputation. You are content to remain a laughingstock while
you keep rocking your hobbyhorse.

> > >So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant.
> >
> > You didn't identify the mutation you are talking about below. But
> > what you are saying applies beautifully to the mutations responsible
> > for those "parallel ridges" -- the median ridge in marsupials
> > and the median ridge in placentals. And you might even needle
> > Bill Rogers about it as you do for your mysterious "that particular
> > mutation":

> It is any beneficial mutation that I'm talking about. The probability of a particular mutation occurring at a particular site in a single replication is the mutation rate.

"'any' beneficial mutation" sends up red flags all over the place. When you
move the goalposts to one particular mutation at one particular site,
all those red flags should be lowered to half mast to mourn the
death of your powers of reason.

>To improve the probability of that particular mutation occurring requires more replications of that genome. If you can do that calculation, that is the mathematics of improving fitness.

You've just put a stake through the heart of your reasoning powers.
If that stake isn't pulled out soon, they may never be reborn.

> >
> > > Bill Rogers argues that competition, "survival of the fittest, improves
> > > that probability of that particular mutation occurring. Does it?

I'm leaving you to the tender mercies of Bill Rogers and all your
other critics until Monday, March 19 unless you experience a
renaissance of your reasoning powers in a reply by noon Friday.
After Friday, I'm going to go on a posting break to coincide
with my university's Spring Break. My family deserves the break,
and so do I.

> > Peter Nyikos
> > Professor, Dept. of Mathematics -- standard disclaimer--
> > University of South Carolina
> > http://people.math.sc.edu/nyikos/

You should feel honored: you read about it HERE first -- the posting break,
I mean.

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 5:00:03 PM UTC-8, Peter Nyikos wrote:
> On Wednesday, March 7, 2018 at 10:55:04 AM UTC-5, Alan Kleinman MD PhD wrote:
> > On Wednesday, March 7, 2018 at 6:50:05 AM UTC-8, Peter Nyikos wrote:
> > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:

> > > > The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of "survival of the fittest" and the mathematics of improving fitness.
> > > > .
> > > > The mathematics of "survival of the fittest" is addressed by the works of Haldane and Kimura. Haldane's work "The cost of natural selection" can be found at:
> > > > http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
> > > > And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
> > > > http://www.genetics.org/content/genetics/47/6/713.full.pdf
> > > > .
> > > > These two authors in their papers use different terminology to describe the same thing. Haldane uses the word "substitution" while the Kimura paper uses the term "fixation" to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable "mutation rate". This is because they are not addressing the mathematics of "improvement in fitness". They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
> > > > .
> > > > On the other hand, "improvement in fitness" must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication.
> > >

> > > You did fine until now. But now you've shown us the Achilles' Heel of
> > > your entire rant against microevolution. You have no way of ascertaining how
> > > many *other* mutations at how many *other* sites would also
> > > have resulted in improved fitness.
>
> > All right, show us how to do the mathematics of your scenario.
>
> What part of "You have no way of ascertaining...resulted in improved fitness" didn't you understand?

What makes you think you have to ascertain where every mutation occurs? All you have to determine is the probability of a particular mutation occurring and all that requires is the mutation rate and the number of replications of that particular variant. All the variants are subject to this mathematics. They simply have their own particular evolutionary trajectories.

>
> Are you such a simpleton, that you actually think mathematics can
> tell us WHICH mutations will be beneficial? It would take minute
> knowledge of the genome, of the physical environment, of the species
> that impact the survival of the species under study etc. that
> are beyond human comprehension. Mathematics is the least of the
> titanic difficulties.

What mathematics tell us is how many replications for a given mutation rate for the probability of a particular mutation to occur. That's the mathematics for a single step on an evolutionary trajectory. It is that simple. And every evolutionary trajectory by rmns works that way. The physics and mathematics of improving fitness is quite simple.

>
> If you breeze past the foregoing two paragraphs as though they
> didn't exist, be prepared to be justly accused of cowardice.

Why would I want to avoid the opportunity to teach a mathematics professor a little applied mathematics?

>
>
> > >
> > > And 'improved fitness' is so easy to achieve, that it stands to reason
> > > there are a gargantuan number of other sites that lead to improved
> > > fitness by the time you get to the level of even primitive vertebrates.
>
> > Just how easy is it to achieve an improvement in fitness? Show us how to do the mathematics.
>
> More of the same idiocy, pretending that we have superhuman powers
> of clairvoyance, and that mathematics is a magic entity that can
> tell us things that are not within its domain.

I'm not asking you to be clairvoyant, understand the physics of rmns and do the math, it is just that simple.

>
> Maybe the reason you are so incorrigibly ignorant is that you think
> that vertebrates are as simple as HIV viruses, that their fitness
> depends on how they can handle a tiny assortment of human-made
> drugs, and that their environment is as simple as the T cells of the
> host of these viruses.

When it comes to rmns, the mathematics is the same for all replicators. The only thing that changes are the environment, mutation rates, selection pressures, and genes targeted. If you think that rmns differs based on whether dealing with vertebrates or viruses, explain yourself.

>
> If you think your chickens (goats?) are this simple, set them loose
> in the woods, prevent them from returning to the farm, and see how
> long they thrive in the wild.

Different selection pressures in the different environments but rmns works the same none-the-less.

>
>
> > And is there a difference in lineages when a beneficial mutation occurs at one site vs a beneficial mutation occurring at a different site?
>
> The probability of that is high, because just as no two snowflakes
> are different, even so no two beneficial mutations can be expected
> to have the exact same effect on relative or absolute fitness.

It doesn't matter, the mathematics which governs is still applicable. Two different beneficial mutations give two different lineages and two different evolutionary trajectories. And each evolutionary trajectory consists of nested binomial probability equations where each equation is linked to the others by the multiplication rule.

>
> The reason this may NOT be a no-brainer for you is that in your
> micro-world of HIV viruses and drug cocktails, there are only
> a handful of beneficial mutations to be had.

Have you ever studied the Weinreich paper, "Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins"
https://pdfs.semanticscholar.org/7d94/c58d1e7bd4f732486bbb0f5681ada85d9333.pdf
Weinreich and his co-authors identified multiple different variants, each taking their own particular evolutionary trajectory to improved fitness. Study this paper, you will learn something about the physics of rmns.

>
>
> >In other words, if one was to do extremely precise phylogenetic analysis using common descent from generation to generation, would a descendant with a beneficial mutation at one given site be in the same line of descendancy as another member with a different beneficial mutation at a different site?
>
> NOW you are beginning to reveal that you have some minuscule
> appreciation even of the complexity of your tidy little micro-world.

All evolutionary processes by rmns obey the mathematics I've presented in this tidy little micro-world. Why this math would work differently in the vertebrate world is something you claim but you offer no proof. There is empirical evidence that substantiates my claims for the vertebrate world.

>
> > >
> > >
> > > What you ought to concentrate on is the improbability of convergent
> > > evolution producing hauntingly similar structures. Here is one example.
> > >
> > > The marsupionta hypothesis had it that monotremes were more closely
> > > related to placentals than either group was to marsupials:
> > >
> > > Article in favor of Marsupionta hypothesis:
> > > http://faculty.chas.uni.edu/~spradlin/SandE/Readings/Matt.pdf
> > > J Mol Evol (2002) 54:71-80 DOI: 10.1007/s00239-001-0019-8
> > > "Phylogenetic Analysis of 18S rRNA and the Mitochondrial Genomes of the
> > > Wombat, Vombatus ursinus, and the Spiny Anteater, Tachyglossus aculeatus:
> > > Increased Support for the Marsupionta Hypothesis," by Axel Janke,
> > > Ola Magnell, Georg Wieczorek, Michael Westerman, and Ulfur Arnason
> > >
> > > These people must have been feeling the weight of "publish or perish"
> > > to produce such a far-out paper. One comparison of the primitive
> > > reptilian shoulder girdle of monotremes to those of marsupials
> > > and placentals should have made J Mol Evol reject the paper out of hand.
>
> > Like in the old Wendy's commercial, where's the math?
>
> It's in the multiplication law of probabilities, silly. If you
> bothered to pay attention below, you would KNOW that.

Whatever

>
>
> > > The scapula alone shows huge differences. The shoulder blades of humans
> > > and opossums both have a medial ridge completely lacking in those
> > > of the platypus, and the overall shapes are strikingly different
> > > also.
>
> > How exactly does this relate to the mathematics of survival of the fittest and the mathematics of improvement in fitness?
>
> Crikey, are you this unintelligent? These things make it astronomically
> unlikely for the scapulas of placentals and those of marsupials
> evolve the same structure. If you can figure out any way those median
> ridges improve fitness, and how many intermediate stages there are
> between the primitive reptilian scapula and the modern placental-marsupial
> scapula, and the improved fitness of each over its predecessors, you may
> have the workings of a really solid research paper in anatomy.
>
> I'm on YOUR side on this one, you silly goose. I think such a research
> paper is way beyond the abilities of the best scientists.

Identify the selection pressure, the genes targeted and the mutations required. That's how you do the hard mathematical science of rmns.

>
>
> > Comparative anatomy is one of the crudest measures of relatedness.
>
> Not too crude for this scenario. You don't need precise calculations,
> just the difference between greater fitness and reduced fitness.

So tell us what the selection pressure(s) is/are.

>
> > And the selective analysis of homologous regions of genomes to determine relatedness while ignoring all the non-homologous regions of genomes is not much better than comparative anatomy to determine relatedness.
>
> I'm not trying to determine relatedness -- the evidence against
> the marsupionta hypothesis is so staggering, based on what I
> told you, that those authors must have either lacked all common
> sense, or were really desperate to publish a research paper.

My work is on a much more fundamental level, how does a lineage accumulate a set of mutations.

>
> >Have you yet studied the Kishony video?
>
> If it's about HIV viruses and drug cocktails, I think it would
> be a complete waste of my time. :-)

It's about e coli and single drug therapy and how a lineage accumulates a set of mutations that allows adaptation to a selection pressure. Sorry, they don't have any scapulas.

>
> OK, joke's over. You need to tell me just what sorts of actual
> animals the video is about, and what it says about them.

Just did. The video demonstrates the fundamental physics of rmns. And that fundamental physics consists of a cycle of beneficial mutation followed by amplification of the mutation to improve the probability of the next beneficial mutation occurring. That's how replicators improve fitness to a selection pressure.

>
> > >
> > > When I told one of your most vocal and cowardly critics, John
> > > Harshman about this, he berated me for jumping to conclusions
> > > on the basis of "one character." Something is rotten in the
> > > state of systematics, Harshman's specialty, when a whole scapula
> > > is given equal footing with a single point mutation.
>
> > John has already admitted he does not take into account the mechanisms of genetic transformation in his phylogenetic analysis. This is why the classical work of paleontologists will not withstand the test of time as the mechanisms of genetic transformation are better understood.
>
> You judge paleontologists extremely harshly if you think Harshman
> is an expert in paleontology. His specialty is the systematics
> of EXTANT birds. His knowledge of paleontology may be a trifle
> greater than mine, but if so, why has he become so bloody lazy
> about starting threads in sci.bio.paleontology?

Until John takes into account the mechanism of genetic transformation, his clades will at best be a crude approximation and at worse gross over-extrapolations.

>
>
> > >
> > > But more importantly: you missed a golden opportunity to hit
> > > Harshman with the multiplication rule of probabilities AND
> > > your "Achilles' Heel" statement. ALL those examples of hypothesized
> > > convergence between marsupials and placentals are valid examples
> > > where evolution really HAD to proceed according to a precise
> > > plan in order to produce KNOWN, DOCUMENTED effects.
>
> > First, you have to understand the mathematics of rmns before you can understand why the multiplication rule has such a dominant effect on the mechanisms of genetic transformation. And that mathematics is not the mathematics of survival of the fittest.
>
> First, you need to get off your rmns hobbyhorse and look at the
> huge world out there waiting for you to add to its stores of knowledge.

This is what you have to do in order to understand rmns.

>
> And you need to stop your Chinese water torture designed to get
> me to read the paper you sent me. I've had my hands full with
> dedicated perpetrators of injustice gunning for my scalp. I
> beat off an especially loudmouthed and aggressive series of
> trumped-up charges of lying by Martin Harran, aided, abetted
> and comforted by Hemidactylus. But it wasn't easy. I had to
> wait patiently since February 20 before Martin accumulated enough
> rope to hang himself with.

I've noticed your interest in mud wrestling.

>
> You are too lamebrained and too amoral to attract such vicious assaults on
> your reputation. You are content to remain a laughingstock while
> you keep rocking your hobbyhorse.

Sometimes you have to put up with some guff if you want to advance science.

>
>
> > > >So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant.
> > >

> > > You didn't identify the mutation you are talking about below. But
> > > what you are saying applies beautifully to the mutations responsible
> > > for those "parallel ridges" -- the median ridge in marsupials
> > > and the median ridge in placentals. And you might even needle
> > > Bill Rogers about it as you do for your mysterious "that particular
> > > mutation":
>
> > It is any beneficial mutation that I'm talking about. The probability of a particular mutation occurring at a particular site in a single replication is the mutation rate.
>
> "'any' beneficial mutation" sends up red flags all over the place. When you
> move the goalposts to one particular mutation at one particular site,
> all those red flags should be lowered to half mast to mourn the
> death of your powers of reason.

What is hard for you to understand is that different beneficial mutations lead to different lineages on different evolutionary trajectories. And each of the trajectories consists of nested binomial probability equations where each equation is linked to the other by the multiplication rule. It's just that simple.

>
>
> >To improve the probability of that particular mutation occurring requires more replications of that genome. If you can do that calculation, that is the mathematics of improving fitness.
>
> You've just put a stake through the heart of your reasoning powers.
> If that stake isn't pulled out soon, they may never be reborn.

Don't you think you are being a bit over-dramatic?
>
> > >
> > > > Bill Rogers argues that competition, "survival of the fittest, improves

> > > > that probability of that particular mutation occurring. Does it?
>

> I'm leaving you to the tender mercies of Bill Rogers and all your
> other critics until Monday, March 19 unless you experience a
> renaissance of your reasoning powers in a reply by noon Friday.
> After Friday, I'm going to go on a posting break to coincide
> with my university's Spring Break. My family deserves the break,
> and so do I.

Bill still doesn't understand the difference between the mathematics of survival of the fittest and the mathematics of improving fitness. And lay off the Ouzo when you go on your break.

>
> > > Peter Nyikos
> > > Professor, Dept. of Mathematics -- standard disclaimer--
> > > University of South Carolina
> > > http://people.math.sc.edu/nyikos/
>
> You should feel honored: you read about it HERE first -- the posting break,
> I mean.

I am truly humbled by the trust you have bestowed.

[Mark Isaak]

On 3/7/18 2:53 PM, Alan Kleinman MD PhD wrote:
> On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:

>> [...]

>> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
> Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.

If removing the less fit variants from a population is not evolution,
what is?

--
Mark Isaak eciton (at) curioustaxonomy (dot) net
"Ignorance, allied with power, is the most ferocious enemy justice can
have." - James Baldwin

[jillery]

On Wed, 7 Mar 2018 14:53:03 -0800 (PST), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
>> On Wednesday, March 7, 2018 at 3:20:03 PM UTC-5, gdgu...@gmail.com wrote:
>> > On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
>> > > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
>> > > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
>> > > >
>> > > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
>> > > > > probability of that particular mutation occurring. Does it?
>> > > >
>> > > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
>> > > From the thread “Kleinman confuses probability with informal statistics ”:
>> > > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
>> > > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
>> >
>> > That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)
>>
>> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
>Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.

Since you asked, competition accelerates evolution by increasing the
intensity of selection. This necessarily speeds up the fixation and
extinction of various alleles.

Competition does not... repeat not... affect the *rate* of mutations,
favorable or otherwise, or increases the *probability* of favorable
mutations. Those are your strawmen.

You're welcome.

>> > > In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?
>> > > >
>> >
>> > > > Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
>> > > As long as rmns is dependent on “particular” mutations to improve fitness,
>> >
>> > It isn't.
>> >
>> > > it is quite appropriate to use this term. But if you think this is a flaw,
>> > > point out this flaw with specificity.
>> >
>> > Your "math", what there is of it, demonstrates that it is vanishingly unlikely for mutation, selection and drift (evolution) to produce a *particular* target organism, with its exact DNA complement. This is due to the multiplication rule. I doubt that anyone here disagrees.
>> >
>> > But it presents no difficulty for the idea that populations can acquire unspecified, untargeted, "un-particular" variations over time. Or the inevitable tendency for some of those variations to out-reproduce others (whether by increased fitness or by chance/drift), and thereby change the common traits of the population.
>

--
I disapprove of what you say, but I will defend to the death your right to say it.

Evelyn Beatrice Hall
Attributed to Voltaire

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 9:15:03 PM UTC-8, Mark Isaak wrote:
> On 3/7/18 2:53 PM, Alan Kleinman MD PhD wrote:
> > On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
> >> [...]
> >> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
> > Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.
>
> If removing the less fit variants from a population is not evolution,
> what is?

Of course, survival of the fittest is a component of evolution but it does not represent an improvement in fitness. And this process of removal of less fit variants slows the process of improvement in fitness.

[Alan Kleinman MD PhD]

On Wednesday, March 7, 2018 at 11:00:03 PM UTC-8, jillery wrote:
> On Wed, 7 Mar 2018 14:53:03 -0800 (PST), Alan Kleinman MD PhD

> wrote:
>
> >On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
> >> On Wednesday, March 7, 2018 at 3:20:03 PM UTC-5, gdgu...@gmail.com wrote:
> >> > On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
> >> > > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> >> > > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> >> > > >
> >> > > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
> >> > > > > probability of that particular mutation occurring. Does it?
> >> > > >
> >> > > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
> >> > > From the thread “Kleinman confuses probability with informal statistics ”:
> >> > > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
> >> > > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
> >> >
> >> > That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)
> >>
> >> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
> >Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.
>
>
> Since you asked, competition accelerates evolution by increasing the
> intensity of selection. This necessarily speeds up the fixation and
> extinction of various alleles.

Oh really? And how does that work? Perhaps you want to give it a shot and show us how to compute the intensity of selection for the Lenski experiment using Haldane's mathematical model?

>
> Competition does not... repeat not... affect the *rate* of mutations,
> favorable or otherwise, or increases the *probability* of favorable
> mutations. Those are your strawmen.

I never said that it does my dear. Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".

[Mark Isaak]

On 3/8/18 12:27 PM, Alan Kleinman MD PhD wrote:
> On Wednesday, March 7, 2018 at 9:15:03 PM UTC-8, Mark Isaak wrote:
>> On 3/7/18 2:53 PM, Alan Kleinman MD PhD wrote:
>>> On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
>>>> [...]
>>>> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
>>> Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.
>>
>> If removing the less fit variants from a population is not evolution,
>> what is?
> Of course, survival of the fittest is a component of evolution but it does not represent an improvement in fitness. And this process of removal of less fit variants slows the process of improvement in fitness.

This process of removal of less fit variants (plus the accumulation of
new mutations, which has nothing to do with fitness of variants or their
removal) *is* the process of improvement in fitness.

[Alan Kleinman MD PhD]

On Thursday, March 8, 2018 at 5:55:02 PM UTC-8, Mark Isaak wrote:
> On 3/8/18 12:27 PM, Alan Kleinman MD PhD wrote:
> > On Wednesday, March 7, 2018 at 9:15:03 PM UTC-8, Mark Isaak wrote:
> >> On 3/7/18 2:53 PM, Alan Kleinman MD PhD wrote:
> >>> On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
> >>>> [...]
> >>>> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
> >>> Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.
> >>
> >> If removing the less fit variants from a population is not evolution,
> >> what is?
> > Of course, survival of the fittest is a component of evolution but it does not represent an improvement in fitness. And this process of removal of less fit variants slows the process of improvement in fitness.
>
> This process of removal of less fit variants (plus the accumulation of
> new mutations, which has nothing to do with fitness of variants or their
> removal) *is* the process of improvement in fitness.

It's that "plus the accumulation of new mutations" which is not accounted for in the mathematics of survival of the fittest. And it is the accumulation of beneficial mutations which requires a different mathematical model than the mathematics of survival of the fittest. That is the mathematics on improvement in fitness I've presented.
.
Here is a little mathematical problem for you based on the Lenski experiment. Assume that e coli have a genome length of 5e6 and the mutation rate is e-8. Give us an estimate of the total number of mutations that will occur in his population in one day's growth from e6 to e8. Then based on Lenski's estimate of 1 beneficial mutation per thousand generations, what fraction of the total number of mutations is beneficial.

[Andre G. Isaak]

In article <5e626d5d-b981-4c87...@googlegroups.com>,

Alan Kleinman MD PhD <klei...@sti.net> wrote:

That's not Lenski's estimate. That's your estimate based on your
misunderstanding of Lenski's paper. Lenski was talking about fixation,
not mutation.

Andre

--
To email remove 'invalid' & replace 'gm' with well known Google mail service.

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 6:20:03 AM UTC-8, Andre G. Isaak wrote:
> In article <5e626d5d-b981-4c87...@googlegroups.com>,

From Lenski's paper:
https://telliamedrevisited.files.wordpress.com/2015/02/2004-pbr-lenski.pdf
"Assuming that beneficial mutations are neither so rare as to require a very long waiting period given the population size, nor so common that beneficial mutations often occur in minority subpopulations, then we can imagine “stringing together” 20,000/250 = 80 beneficial substitutions, each of 10% effect, in a 20,000-generation period. In fact, however, the real number of beneficial substitutions is almost certainly much less than this number, as evidenced by waiting periods between substitutions and a pronounced deceleration in the rate of adaptation over the course of the experiment. I would hazard the estimate that between 10 and 20 beneficial mutations have been substituted in each population."
The improvement in fitness is much, much less than 10%, that is why the substitution process is extremely slow. And this is quite clear if you were able to apply Haldane's math to Lenski's experimental model. The vast majority of mutations in the Lenski experiment occur on lineages that go extinct. But before they go extinct, they markedly slow the variants with the beneficial mutations ability to amplify their mutations.
Now do the computation if you can. Competition slows the rmns process by the less fit variants taking resources from the more fit variants limiting the ability of the more fit variants to replicate.

[Andre G. Isaak]

In article <0ea90e2e-80f0-4253...@googlegroups.com>,

As I said, he is talking about *fixation*.

> The improvement in fitness is much, much less than 10%, that is why the
> substitution process is extremely slow. And this is quite clear if you were
> able to apply Haldane's math to Lenski's experimental model. The vast
> majority of mutations in the Lenski experiment occur on lineages that go
> extinct. But before they go extinct, they markedly slow the variants with the
> beneficial mutations ability to amplify their mutations.
> Now do the computation if you can. Competition slows the rmns process by the
> less fit variants taking resources from the more fit variants limiting the
> ability of the more fit variants to replicate.

You still haven't answered any of the earlier requests to show how your
equations applied to this experiment, so I see no reason to do various
calculations on your behalf, especially when they are predicated on
false assumptions. If you want anyone to accept your equation as
anything other than cargo-cult science, it is incumbent on you to
demonstrate that it can actually produce meaningful results. No one is
going to do it for you.

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 7:25:02 AM UTC-8, Andre G. Isaak wrote:
> In article <0ea90e2e-80f0-4253...@googlegroups.com>,

I have posted the equation and explained the physics numerous times. I'll do it once again. The Lenski experiment consists of two physical components. The first physical component of the Lenski experiment is the survival of the fittest where for each evolutionary step, the more fit variant drives the less fit variants to extinction. The mathematics which governs this component was developed by Haldane and Kimura. The other physical component of the Lenski experiment is the improvement in fitness at each evolutionary step. This step requires the most fit variant to replicate sufficiently to have a reasonable probability of another beneficial mutation occurring on one of the members of this variant. This is the cycle of beneficial mutation followed by amplification of that mutation which is the physics of rmns. If you want me to post the governing equations again, I will.
.
If you have difficulty understanding this concept, consider the simpler experiment, the Kishony experiment, where rmns is operating without having survival of the fittest superimposed. The Kishony experiment demonstrates how rapidly rmns can operate when not operating in a competitive environment.
.
And I wouldn't expect someone to do the calculations I suggest without understanding both the physics and mathematics of the phenomena they are dealing with, and you don't.

[Andre G. Isaak]

In article <47fa4a1a-6feb-4a8b...@googlegroups.com>,

And yet once again you offer a response which fails to demonstrate a
single prediction which your equation makes with respect to the Lenski
experiment. For someone who keeps claiming to be trained in 'the hard
mathematical sciences' you really do have a hard time grasping the fact
that a request for predictions means that your answer should contain
actual numerical values which follow from your equations and which can
be compared with the actual results of Lenski's experiment.

I don't want to see your equations again. I want to see some actual
numbers which you have produced using those equations which can be
tested against actual results of an actual experiment.

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 8:20:02 AM UTC-8, Andre G. Isaak wrote:
> In article <47fa4a1a-6feb-4a8b...@googlegroups.com>,

Andre, the mathematics I've presented, for a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur for one or more selection pressures. And this mathematics applies for both competitive and non-competitive environments.

>
> I don't want to see your equations again. I want to see some actual
> numbers which you have produced using those equations which can be
> tested against actual results of an actual experiment.

This is extremely easy for the Kishony experiment. Depending on how accurately the mutation rate can be measured for this experiment, this equation predicts how large the colony needs to be for a reasonable probability of a beneficial mutation to occur. The calculation is also applicable to the Lenski experiment but measuring the size of the most fit variant will more difficult since this experiment is done in a test tube, not a petri dish. Do you want me to show you how to plug the numbers into the equation in order to do these predictions?

[Mark Isaak]

Another point you consistently miss is that mutations have been
happening essentially forever. That means populations already include a
lot of variation, including some mutations which are beneficial. You
are stuck on the idea that for a population to advance in fitness, it
must come up with the one new perfect mutation. That may be true in the
artificial situations that are all you know, but it is not true in the
wide, wide world.

[Alan Kleinman MD PhD]

It doesn't have to be a "new perfect mutation", for rmns to work, it has to be a mutation which improves fitness sufficiently that the new variant can replicate sufficiently that there is a reasonable probability that another mutation which improves fitness that occurs on one of its members. With respects to mutations occurring forever, apparently, they didn't teach you what survival of the fittest does to these less fit mutants.

[Mark Isaak]

Yawn. Where there's no recombination, or where a catastrophe is sudden
and extreme, that can sometimes be a problem for the population.
Normally, . . . Well, you never deal with normally.

> With respects to mutations occurring forever, apparently, they didn't teach you what survival of the fittest does to these less fit mutants.

Apparently, they didn't teach you.

[Alan Kleinman MD PhD]

Yea yawn. This is the same old argument trotted out when confronted with the evidence that rmns doesn't work the way you think it does in your imagination. All the empirical evidence of rmns shows that recombination has no significant effect on this process. You can start with the most studied example of rmns known, that of hiv's inability to evolve efficiently to effective 3 drug therapy. If that is not enough empirical evidence then you can look at what happens to the evolution of herbicide-resistant weeds when combination herbicides are used. Do you have any kind of evidence that shows that recombination has any significant effect on rmns? Do you even understand how recombination works? I doubt it. And what is catastrophic in the Lenski or Kishony experiment? Do you think if Lenski uses thermal stress in combination with starvation or Kishony uses 2 drug in their respective experiments that this would be catastrophic? I think if either of these experimenters did this, it would be a demonstration of two instances of the multiplication rule. This would make rmns work exponentially slower if the experiments work at all.

>
> > With respects to mutations occurring forever, apparently, they didn't teach you what survival of the fittest does to these less fit mutants.
>
> Apparently, they didn't teach you.

Clearly, I haven't been confused on this subject as you are. Did you get any instruction on rmns in your population genetics course? If so, you haven't shown any understanding of the phenomenon. So are you going to show us how to use Haldane's equation to compute the intensity of selection for the Lenski experiment? You should have learned how to do that calculation in your graduate level population genetics course. Would it help if I showed you which equation to use in the Haldane paper?

[jillery]

On Thu, 8 Mar 2018 12:35:52 -0800 (PST), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Wednesday, March 7, 2018 at 11:00:03 PM UTC-8, jillery wrote:
>> On Wed, 7 Mar 2018 14:53:03 -0800 (PST), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
>> >> On Wednesday, March 7, 2018 at 3:20:03 PM UTC-5, gdgu...@gmail.com wrote:
>> >> > On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
>> >> > > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
>> >> > > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
>> >> > > >
>> >> > > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
>> >> > > > > probability of that particular mutation occurring. Does it?
>> >> > > >
>> >> > > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
>> >> > > From the thread “Kleinman confuses probability with informal statistics ”:
>> >> > > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
>> >> > > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
>> >> >
>> >> > That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)
>> >>
>> >> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
>> >Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.
>>
>>
>> Since you asked, competition accelerates evolution by increasing the
>> intensity of selection. This necessarily speeds up the fixation and
>> extinction of various alleles.
>Oh really? And how does that work? Perhaps you want to give it a shot and show us how to compute the intensity of selection for the Lenski experiment using Haldane's mathematical model?

That's your job.

>> Competition does not... repeat not... affect the *rate* of mutations,
>> favorable or otherwise, or increases the *probability* of favorable
>> mutations. Those are your strawmen.
>I never said that it does my dear.

And I never said that you said it does, my dear. But you have said
other people have said these things, when they haven't, all still
preserved in the quote text above. That makes them your strawmen, my

dear.


>Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".

Your comments above are technically correct, but only by definition.
What you always leave out is what makes a mutation beneficial, the
environment. And competition is part of the environment. So a
mutation can be beneficial in one environment which has competition,
and be completely neutral in another environment which has no
competition. And increased competition necessarily increases said
mutation's benefit. None of these things are modeled in your
mathematics.

>> You're welcome.
>>
>>
>> >> > > In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?
>> >> > > >
>> >> >
>> >> > > > Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
>> >> > > As long as rmns is dependent on “particular” mutations to improve fitness,
>> >> >
>> >> > It isn't.
>> >> >
>> >> > > it is quite appropriate to use this term. But if you think this is a flaw,
>> >> > > point out this flaw with specificity.
>> >> >
>> >> > Your "math", what there is of it, demonstrates that it is vanishingly unlikely for mutation, selection and drift (evolution) to produce a *particular* target organism, with its exact DNA complement. This is due to the multiplication rule. I doubt that anyone here disagrees.
>> >> >
>> >> > But it presents no difficulty for the idea that populations can acquire unspecified, untargeted, "un-particular" variations over time. Or the inevitable tendency for some of those variations to out-reproduce others (whether by increased fitness or by

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 12:50:04 PM UTC-8, jillery wrote:
> On Thu, 8 Mar 2018 12:35:52 -0800 (PST), Alan Kleinman MD PhD

> wrote:
>
> >On Wednesday, March 7, 2018 at 11:00:03 PM UTC-8, jillery wrote:
> >> On Wed, 7 Mar 2018 14:53:03 -0800 (PST), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8, Bill Rogers wrote:
> >> >> On Wednesday, March 7, 2018 at 3:20:03 PM UTC-5, gdgu...@gmail.com wrote:
> >> >> > On Wednesday, March 7, 2018 at 2:55:03 PM UTC-5, Alan Kleinman MD PhD wrote:
> >> >> > > On Wednesday, March 7, 2018 at 11:30:04 AM UTC-8, gdgu...@gmail.com wrote:
> >> >> > > > On Wednesday, March 7, 2018 at 8:15:03 AM UTC-5, Alan Kleinman MD PhD wrote:
> >> >> > > >
> >> >> > > > > Bill Rogers argues that competition, “survival of the fittest”, improves that
> >> >> > > > > probability of that particular mutation occurring. Does it?
> >> >> > > >
> >> >> > > > I am quite confident that Bill does not argue that "competition" improves the odds of a mutation occurring. Cite?
> >> >> > > From the thread “Kleinman confuses probability with informal statistics ”:
> >> >> > > On Friday, March 2, 2018 at 11:25:03 AM UTC-8, Bill Rogers wrote:
> >> >> > > “Competition accelerates evolution when compared to the situation in which there is no competition, ie when all variants have identical fitness.”
> >> >> >
> >> >> > That is not a quote in which Bill argues that competition improves the probability of a particular mutation occurring. Do you have another? (I can save you some time here. You don't have such a quotation)
> >> >>
> >> >> Thank you. You are quite right. I would not argue that competition improves the probability of a particular mutation occurring.
> >> >Competition does not accelerate evolution in any way. Competition reduces the diversity of populations by removing the less fit variants. But if you think you are correct, tell us how competition accelerates evolution in any way. You won't because it doesn't.
> >>
> >>
> >> Since you asked, competition accelerates evolution by increasing the
> >> intensity of selection. This necessarily speeds up the fixation and
> >> extinction of various alleles.
> >Oh really? And how does that work? Perhaps you want to give it a shot and show us how to compute the intensity of selection for the Lenski experiment using Haldane's mathematical model?
>
>
> That's your job.

No problem, I've already done the computation. It is easy.

>
>
> >> Competition does not... repeat not... affect the *rate* of mutations,
> >> favorable or otherwise, or increases the *probability* of favorable
> >> mutations. Those are your strawmen.
> >I never said that it does my dear.
>
>
> And I never said that you said it does, my dear. But you have said
> other people have said these things, when they haven't, all still
> preserved in the quote text above. That makes them your strawmen, my
> dear.

Oh really? Where have I said that? Feel free to post those quotes.

>
>
> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
>
>
> Your comments above are technically correct, but only by definition.
> What you always leave out is what makes a mutation beneficial, the
> environment. And competition is part of the environment. So a
> mutation can be beneficial in one environment which has competition,
> and be completely neutral in another environment which has no
> competition. And increased competition necessarily increases said
> mutation's benefit. None of these things are modeled in your
> mathematics.

A beneficial mutation is one which allows improved replication against a particular selection pressure. A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.

[jillery]

Yes, it's easy to say you have done it, but you haven't posted it in
T.O.

>> >> Competition does not... repeat not... affect the *rate* of mutations,
>> >> favorable or otherwise, or increases the *probability* of favorable
>> >> mutations. Those are your strawmen.
>> >I never said that it does my dear.
>>
>>
>> And I never said that you said it does, my dear. But you have said
>> other people have said these things, when they haven't, all still
>> preserved in the quote text above. That makes them your strawmen, my
>> dear.
>Oh really? Where have I said that? Feel free to post those quotes.

Since you asked, and to accommodate your inability to read the quoted
text above
**********************************

Bill Rogers argues that competition, “survival of the fittest”,
improves that probability of that particular mutation occurring.

***********************************
You're welcome.

>> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
>>
>>
>> Your comments above are technically correct, but only by definition.
>> What you always leave out is what makes a mutation beneficial, the
>> environment. And competition is part of the environment. So a
>> mutation can be beneficial in one environment which has competition,
>> and be completely neutral in another environment which has no
>> competition. And increased competition necessarily increases said
>> mutation's benefit. None of these things are modeled in your
>> mathematics.
>A beneficial mutation is one which allows improved replication against a particular selection pressure.

Competition is a selection pressure.

>A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.

Your mathematics model none of your examples above.

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 1:25:04 PM UTC-8, jillery wrote:
> On Fri, 9 Mar 2018 13:07:31 -0800 (PST), Alan Kleinman MD PhD

I'll tell you which equation to use from the Haldane paper and you can do the computation. Does that help?

>
>
> >> >> Competition does not... repeat not... affect the *rate* of mutations,
> >> >> favorable or otherwise, or increases the *probability* of favorable
> >> >> mutations. Those are your strawmen.
> >> >I never said that it does my dear.
> >>
> >>
> >> And I never said that you said it does, my dear. But you have said
> >> other people have said these things, when they haven't, all still
> >> preserved in the quote text above. That makes them your strawmen, my
> >> dear.
> >Oh really? Where have I said that? Feel free to post those quotes.
>
>
> Since you asked, and to accommodate your inability to read the quoted
> text above
> **********************************
> Bill Rogers argues that competition, “survival of the fittest”,
> improves that probability of that particular mutation occurring.
> ***********************************

Competition doesn't accelerate evolution in any form whatsoever. All that competition does is drive the less fit variants to extinction. Competition slows evolution. Just compare the Lenski experiment which has competition between variants and the Kishony experiment which does not have competition between variants.

> You're welcome.
>
>
> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
> >>
> >>
> >> Your comments above are technically correct, but only by definition.
> >> What you always leave out is what makes a mutation beneficial, the
> >> environment. And competition is part of the environment. So a
> >> mutation can be beneficial in one environment which has competition,
> >> and be completely neutral in another environment which has no
> >> competition. And increased competition necessarily increases said
> >> mutation's benefit. None of these things are modeled in your
> >> mathematics.
> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
>
>
> Competition is a selection pressure.

The limited resources in the environment is the selection pressure. The result is competition for that limited resource.

>
>
> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
>
>
> Your mathematics model none of your examples above.

Sure it does. This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.

[Andre G. Isaak]

In article <eed38513-ed79-4885...@googlegroups.com>,

The only "non-competitive environments" are those which contain a
single, non-reproducing organism.

> > I don't want to see your equations again. I want to see some actual
> > numbers which you have produced using those equations which can be
> > tested against actual results of an actual experiment.
> This is extremely easy for the Kishony experiment. Depending on how
> accurately the mutation rate can be measured for this experiment, this
> equation predicts how large the colony needs to be for a reasonable
> probability of a beneficial mutation to occur. The calculation is also
> applicable to the Lenski experiment but measuring the size of the most fit
> variant will more difficult since this experiment is done in a test tube, not
> a petri dish. Do you want me to show you how to plug the numbers into the
> equation in order to do these predictions?

I'm not asking you to show me how to plug numbers into an equation. I
can already do that.

I'm asking you to provide me with the predictions which you yourself
generated and then to show how those predictions are confirmed by actual
experimental data. If your equation truly describes to all of evolution
as you claim, then this shouldn't be a difficult request, and yet you've
continuously avoided doing so.

[jillery]

You just derailed your own train of thought. I accept this as your
tacit admission you don't care what you're talking about and are proud
of it.

>> You're welcome.
>>
>>
>> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
>> >>
>> >>
>> >> Your comments above are technically correct, but only by definition.
>> >> What you always leave out is what makes a mutation beneficial, the
>> >> environment. And competition is part of the environment. So a
>> >> mutation can be beneficial in one environment which has competition,
>> >> and be completely neutral in another environment which has no
>> >> competition. And increased competition necessarily increases said
>> >> mutation's benefit. None of these things are modeled in your
>> >> mathematics.
>> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
>>
>>
>> Competition is a selection pressure.
>The limited resources in the environment is the selection pressure. The result is competition for that limited resource.

Resources are always finite and therefore limited, by definition. What
makes a resource *limiting* is competition for it. Without
competition, it wouldn't even be a resource.

>> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
>>
>>
>> Your mathematics model none of your examples above.
>Sure it does.

Sure it doesn't.

>This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.

Once again, without considering the environment, you have no objective
basis for declaring any mutation beneficial, nevermind its degree of
benefit.

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 9:10:02 PM UTC-8, Andre G. Isaak wrote:
> In article <eed38513-ed79-4885...@googlegroups.com>,

Then tell us what the variants in the Kishony are competing for. And tell us which variants are being fixed in that experiment. And how do you apply Haldane's and Kimura's model to this experiment?

>
> > > I don't want to see your equations again. I want to see some actual
> > > numbers which you have produced using those equations which can be
> > > tested against actual results of an actual experiment.
> > This is extremely easy for the Kishony experiment. Depending on how
> > accurately the mutation rate can be measured for this experiment, this
> > equation predicts how large the colony needs to be for a reasonable
> > probability of a beneficial mutation to occur. The calculation is also
> > applicable to the Lenski experiment but measuring the size of the most fit
> > variant will more difficult since this experiment is done in a test tube, not
> > a petri dish. Do you want me to show you how to plug the numbers into the
> > equation in order to do these predictions?
>
> I'm not asking you to show me how to plug numbers into an equation. I
> can already do that.

Then prove it, show us how to use Haldane's equation to calculate the intensity of selection for the Lenski experiment.

>
> I'm asking you to provide me with the predictions which you yourself
> generated and then to show how those predictions are confirmed by actual
> experimental data. If your equation truly describes to all of evolution
> as you claim, then this shouldn't be a difficult request, and yet you've
> continuously avoided doing so.

My mathematical model predicts the number of replications necessary for a particular variant to take a step on an evolutionary trajectory. If the mutation rate is e-8, it takes about e8 replications to take that evolutionary step for the next beneficial mutation. That applies to both the Lenski experiment and the Kishony experiment and any other example of rmns for a single selection pressure. If multiple selection pressures are acting simultaneously, it will take exponentially more replications to take a step on this more complex evolutionary trajectory because simultaneous beneficial mutations will be required to improve fitness.
.
What you are failing to understand is that when rmns is occurring in a competitive environment such as the Lenski experiment, it markedly slows the ability of the more fit variant to accumulate the necessary replications to improve fitness. This is because the less fit variants, until they are driven to extinction, are using resources that the more fit variant could be used to achieve the necessary number of replication to improve fitness. You need to learn to distinguish between the process of survival of the fittest and the process of improving fitness. These two processes have different governing mathematics and improving fitness works much more efficiently in unlimited environments than in limited environments that impose competition between the variants (such as the Kishony experiment).

[Alan Kleinman MD PhD]

On Friday, March 9, 2018 at 11:00:02 PM UTC-8, jillery wrote:
> On Fri, 9 Mar 2018 13:39:08 -0800 (PST), Alan Kleinman MD PhD

My thoughts are right on track and if you understood the differences between the Kishony experiment and the Lenski experiment you wouldn't be railing like this.

>
>
> >> You're welcome.
> >>
> >>
> >> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
> >> >>
> >> >>
> >> >> Your comments above are technically correct, but only by definition.
> >> >> What you always leave out is what makes a mutation beneficial, the
> >> >> environment. And competition is part of the environment. So a
> >> >> mutation can be beneficial in one environment which has competition,
> >> >> and be completely neutral in another environment which has no
> >> >> competition. And increased competition necessarily increases said
> >> >> mutation's benefit. None of these things are modeled in your
> >> >> mathematics.
> >> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
> >>
> >>
> >> Competition is a selection pressure.
> >The limited resources in the environment is the selection pressure. The result is competition for that limited resource.
>
>
> Resources are always finite and therefore limited, by definition. What
> makes a resource *limiting* is competition for it. Without
> competition, it wouldn't even be a resource.

If Kishony was running his experiment in a standard sized Petri dish, he would be limiting his experiment and it would not work. Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.

>
>
> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
> >>
> >>
> >> Your mathematics model none of your examples above.
> >Sure it does.
>
>
> Sure it doesn't.

Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.

>
>
> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
>
>
> Once again, without considering the environment, you have no objective
> basis for declaring any mutation beneficial, nevermind its degree of
> benefit.

What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.

[jillery]

As illustrated in the quoted text above, you started with a
misrepresentation of what Bill Rogers wrote, then jumped to a denial
of posting what you posted, and ended with a repetition of your bald
assertion about competition. You derailed yourself so often you could
manage Amtrak.

>> >> You're welcome.
>> >>
>> >>
>> >> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
>> >> >>
>> >> >>
>> >> >> Your comments above are technically correct, but only by definition.
>> >> >> What you always leave out is what makes a mutation beneficial, the
>> >> >> environment. And competition is part of the environment. So a
>> >> >> mutation can be beneficial in one environment which has competition,
>> >> >> and be completely neutral in another environment which has no
>> >> >> competition. And increased competition necessarily increases said
>> >> >> mutation's benefit. None of these things are modeled in your
>> >> >> mathematics.
>> >> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
>> >>
>> >>
>> >> Competition is a selection pressure.
>> >The limited resources in the environment is the selection pressure. The result is competition for that limited resource.
>>
>>
>> Resources are always finite and therefore limited, by definition. What
>> makes a resource *limiting* is competition for it. Without
>> competition, it wouldn't even be a resource.
>If Kishony was running his experiment in a standard sized Petri dish, he would be limiting his experiment and it would not work.

I note your assertion of facts not in evidence. The Kishony plate
shows the development of multiple distinctive populations, all
competing with each other for resources.

More to the point, the Kishony experiment is designed to show
adaptation to antibiotics, and so limits the competition for other
things. It should go without saying that well-designed experiments
deliberately limits variables.

>Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
>>
>>
>> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
>> >>
>> >>
>> >> Your mathematics model none of your examples above.
>> >Sure it does.
>>
>>
>> Sure it doesn't.
>Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.

I note your ad hominem. Whether I understand your model doesn't alter
the fact that your model doesn't model your examples.

>> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
>>
>>
>> Once again, without considering the environment, you have no objective
>> basis for declaring any mutation beneficial, nevermind its degree of
>> benefit.
>What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.

IIUC you model the probability of beneficial mutations by assuming
arbitrary values for fitness. But you do so without correlating those
values to different environments. So your fitness values are
meaningless, and so too any probabilities based on them.

>> >> >> >> You're welcome.
>> >> >> >>
>> >> >> >>
>> >> >> >> >> > > In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?
>> >> >> >> >> > > >
>> >> >> >> >> >
>> >> >> >> >> > > > Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
>> >> >> >> >> > > As long as rmns is dependent on “particular” mutations to improve fitness,
>> >> >> >> >> >
>> >> >> >> >> > It isn't.
>> >> >> >> >> >
>> >> >> >> >> > > it is quite appropriate to use this term. But if you think this is a flaw,
>> >> >> >> >> > > point out this flaw with specificity.
>> >> >> >> >> >
>> >> >> >> >> > Your "math", what there is of it, demonstrates that it is vanishingly unlikely for mutation, selection and drift (evolution) to produce a *particular* target organism, with its exact DNA complement. This is due to the multiplication rule. I doubt that anyone here disagrees.
>> >> >> >> >> >

[Alan Kleinman MD PhD]

On Saturday, March 10, 2018 at 10:45:03 AM UTC-8, jillery wrote:
> On Sat, 10 Mar 2018 06:59:11 -0800 (PST), Alan Kleinman MD PhD

Bill never explains what aspect of evolution competition accelerates. All competition does is accelerate the extinction of less fit variants. And perhaps you think that rmns is not a component of evolution?

>
>
> >> >> You're welcome.
> >> >>
> >> >>
> >> >> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
> >> >> >>
> >> >> >>
> >> >> >> Your comments above are technically correct, but only by definition.
> >> >> >> What you always leave out is what makes a mutation beneficial, the
> >> >> >> environment. And competition is part of the environment. So a
> >> >> >> mutation can be beneficial in one environment which has competition,
> >> >> >> and be completely neutral in another environment which has no
> >> >> >> competition. And increased competition necessarily increases said
> >> >> >> mutation's benefit. None of these things are modeled in your
> >> >> >> mathematics.
> >> >> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
> >> >>
> >> >>
> >> >> Competition is a selection pressure.
> >> >The limited resources in the environment is the selection pressure. The result is competition for that limited resource.
> >>
> >>
> >> Resources are always finite and therefore limited, by definition. What
> >> makes a resource *limiting* is competition for it. Without
> >> competition, it wouldn't even be a resource.
> >If Kishony was running his experiment in a standard sized Petri dish, he would be limiting his experiment and it would not work.
>
>
> I note your assertion of facts not in evidence. The Kishony plate
> shows the development of multiple distinctive populations, all
> competing with each other for resources.

How does a colony on the east side of the plate compete for resources on the west side of the plate? You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?

>
> More to the point, the Kishony experiment is designed to show
> adaptation to antibiotics, and so limits the competition for other
> things. It should go without saying that well-designed experiments
> deliberately limits variables.

That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.

>
>
> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
> >>
> >>
> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
> >> >>
> >> >>
> >> >> Your mathematics model none of your examples above.
> >> >Sure it does.
> >>
> >>
> >> Sure it doesn't.
> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
>
>
> I note your ad hominem. Whether I understand your model doesn't alter
> the fact that your model doesn't model your examples.

It does kiddo but you refuse to understand why. If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?

>
>
> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
> >>
> >>
> >> Once again, without considering the environment, you have no objective
> >> basis for declaring any mutation beneficial, nevermind its degree of
> >> benefit.
> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
>
>
> IIUC you model the probability of beneficial mutations by assuming
> arbitrary values for fitness. But you do so without correlating those
> values to different environments. So your fitness values are
> meaningless, and so too any probabilities based on them.

That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring. When you take into account the relative fitness, think survival of the fittest. When thinking improvement in fitness, think number of replications of that variant. Haven't you ever wondered why Haldane and Kimura don't have the mutation rate in their mathematics?

[Andre G. Isaak]

In article <58d92f2e-9430-4446...@googlegroups.com>,

Variants needn't necessarily be competing for resources; they are
competing to out-reproduce one another even if resources are plentiful.
And in the Kishony experiment you'll notice that the outermost zones are
highly saturated with bacteria by the time the bacteria reaches the zone
boundary. To claim there is no competition going on between variants
within this zone is rather absurd.

Kishony estimates the mutation rate to be 10E-6.7 +/- 2. Considering the
fact that the size of the E. coli genome is roughly 10E6.6 base pairs we
can safely assume that there's already been a lot of mutations in the
population by the time we actually reach the first zone boundary, and
all those variants are in competition with one another.

And, of course, multiple different strains cross each zone boundary,
which complicates your claim that we need to wait for some specific
mutation to occur on the same lineage as the first mutation.

I don't get what is so difficult about my question so let me spell it
out for you more clearly. I'm not interested in a vague description
about how to apply your equation. I'm interested in an actual example of
using your equation to make a testable *prediction*. So let me suggest
an actual format for your answer (since you claim Kishony is simpler
than Lenski, I'll use that).

"My equation predicts it should take X amount of time for the bacteria
to reach the innermost zone in the experiment" (where X is expressed as
an actual, numerical value expressed in either units of time or number
of generations)

"I derive this by plugging the following values into my equation ____"
(give actual values).

"I got these values from ___" (explain where the values come from)

This should be followed by a discussion of how closely Kishony's results
correspond to your prediction.

Now I can plug values into your equation, but I can't see how it can be
used to make any sort of testable prediction such as above. All your
equation gives is a *probability* of some *specific* mutation occurring.
Since I have no idea which specific mutations need to be considered, nor
how many different ways there are for E. coli to achieve antibiotic
resistance, nor which subpopulation you are considering (all of the
outer bands, only the population adjacent to the zone boundary, etc), I
have no idea how to apply this to a real problem. So I am relying on you
to provide an actual illustration.

So please demonstrate how you actually use that probability to make some
quantitative prediction such as the one I suggest that you tackle above.
If you cannot do that, you have no basis for claiming that Kishony's
experiment actually obeys your math.

[Andre G. Isaak]

In article <34b70e4f-0f99-4106...@googlegroups.com>,

Alan Kleinman MD PhD <klei...@sti.net> wrote:

> So what is your explanation for why the Kishony experiment can accumulate the 4
> or so mutations necessary to grow in the high concentration region in just a
> few days when it takes Lenski's experiment about 250 days for each beneficial
> mutation?

Once again, you are confusing mutation with fixation. Lenski is talking
about the time it takes for beneficial mutations to spread through the
entire population. Kishony's experiment demonstrates the occurrence of
beneficial mutations. Which, if any, of those mutations have become
fixed isn't even discussed.

[Alan Kleinman MD PhD]

On Saturday, March 10, 2018 at 11:40:03 AM UTC-8, Andre G. Isaak wrote:
> In article <58d92f2e-9430-4446...@googlegroups.com>,

To try to compare the competition occurring in the Lenski experiment with any semblance of competition in the Kishony experiment is absurd. The availability of resources in the Kishony experiment allows for much, much larger populations than the e8 population size achievable in the Lenski experiment. Why does Lenski have to replenish his experiment daily?

>
> Kishony estimates the mutation rate to be 10E-6.7 +/- 2. Considering the
> fact that the size of the E. coli genome is roughly 10E6.6 base pairs we
> can safely assume that there's already been a lot of mutations in the
> population by the time we actually reach the first zone boundary, and
> all those variants are in competition with one another.

Of course, there are a lot of mutations, but only the correct mutation at the correct site allows that variant to grow in the next higher drug concentration region. That is what my mathematics computes the probability of occurring. And which of these lineages have gone extinct in the Kishony experiment? And where do you get the estimate that the e coli genome is 10e6.6? The genome size of e coli is closer to 5e6.

>
> And, of course, multiple different strains cross each zone boundary,
> which complicates your claim that we need to wait for some specific
> mutation to occur on the same lineage as the first mutation.

The only strains which cross a drug concentration boundary are those which have a particular mutation that gives resistance to the selection pressure. The other strains happily live and reproduce in the drug-free zones as long as they have the resources. Unlike the Lenski experiment where the more fit variants replace the less fit variants over time.

Look up the mean value for the binomial distribution. From that equation, you can compute the number of trials necessary for a given mutation rate for the expected value of one beneficial mutation. The mutation rate you posted for e coli I suspect is way to high. If you look up estimates of the mutation rate for e coli, it is in the range of e-8 to e-10. Using the mean value for the binomial distribution, it gives a range of e8 to e10 replications for each beneficial mutation. Kishony can measure his colony sizes and see if that is correct.

[Alan Kleinman MD PhD]

On Saturday, March 10, 2018 at 12:20:03 PM UTC-8, Andre G. Isaak wrote:
> In article <34b70e4f-0f99-4106...@googlegroups.com>,

> Alan Kleinman MD PhD wrote:
>
> > So what is your explanation for why the Kishony experiment can accumulate the 4
> > or so mutations necessary to grow in the high concentration region in just a
> > few days when it takes Lenski's experiment about 250 days for each beneficial
> > mutation?
>
> Once again, you are confusing mutation with fixation. Lenski is talking
> about the time it takes for beneficial mutations to spread through the
> entire population. Kishony's experiment demonstrates the occurrence of
> beneficial mutations. Which, if any, of those mutations have become
> fixed isn't even discussed.

The Lenski experiment requires fixation because of the competition, what variants are fixed in the Kishony experiment? The answer to that is none because fixation is not occurring in the Kishony experiment.

[Andre G. Isaak]

In article <51179348-42fd-4c87...@googlegroups.com>,

Unless all variants reproduce at the same rate, some will be
outcompeting others.

> > Kishony estimates the mutation rate to be 10E-6.7 +/- 2. Considering the
> > fact that the size of the E. coli genome is roughly 10E6.6 base pairs we
> > can safely assume that there's already been a lot of mutations in the
> > population by the time we actually reach the first zone boundary, and
> > all those variants are in competition with one another.
> Of course, there are a lot of mutations, but only the correct mutation at the
> correct site allows that variant to grow in the next higher drug
> concentration region.

(A) Why do you assume that all variants which break through to the next
zone possess the same mutation? There is no reason to make that
assumption.

(B) Competition begins in the very first zone before the bacteria even
reach the zone boundary. Mutations may hasten or hinder reproduction
within each zone regardless of whether they are actually involved in
antibiotic resistance.

> That is what my mathematics computes the probability of
> occurring. And which of these lineages have gone extinct in the Kishony
> experiment? And where do you get the estimate that the e coli genome is
> 10e6.6? The genome size of e coli is closer to 5e6.

We're using different notations. that should be read as 1 x 10^6.6

Wikipedia claims 4.6 million base pairs, or 1 x 10^6.66

The value I gave (1 x 10 ^ 6.7 +/-2) is taken from Kishony's article in
Science (vol. 311, 17 March 2006, pp1615-1617). While that article is
dated, I doubt he'd be off by as much as you suggest).

> Using the mean value for the
> binomial distribution, it gives a range of e8 to e10 replications for each
> beneficial mutation. Kishony can measure his colony sizes and see if that is
> correct.

Why should Kishony do it for you? It's your claim, not his.

And you're still not fully addressing my questions. For which specific
mutations are you calculating the probability? Wouldn't that value
change drastically depending on whether there was only a single possible
mutation for crossing the first zone boundary (a claim which is almost
certainly wrong) versus, say, 1000 possible mutations which would allow
such zone-crossing? Are you considering the entire population as a whole
or are you treating the populations in each zone separately?

[jillery]

I accept your non sequiturs above as yet another tacit admission that

you don't care what you're talking about and are proud of it.

>> >> >> You're welcome.
>> >> >>
>> >> >>
>> >> >> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
>> >> >> >>
>> >> >> >>
>> >> >> >> Your comments above are technically correct, but only by definition.
>> >> >> >> What you always leave out is what makes a mutation beneficial, the
>> >> >> >> environment. And competition is part of the environment. So a
>> >> >> >> mutation can be beneficial in one environment which has competition,
>> >> >> >> and be completely neutral in another environment which has no
>> >> >> >> competition. And increased competition necessarily increases said
>> >> >> >> mutation's benefit. None of these things are modeled in your
>> >> >> >> mathematics.
>> >> >> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
>> >> >>
>> >> >>
>> >> >> Competition is a selection pressure.
>> >> >The limited resources in the environment is the selection pressure. The result is competition for that limited resource.
>> >>
>> >>
>> >> Resources are always finite and therefore limited, by definition. What
>> >> makes a resource *limiting* is competition for it. Without
>> >> competition, it wouldn't even be a resource.
>> >If Kishony was running his experiment in a standard sized Petri dish, he would be limiting his experiment and it would not work.
>>
>>
>> I note your assertion of facts not in evidence. The Kishony plate
>> shows the development of multiple distinctive populations, all
>> competing with each other for resources.
>How does a colony on the east side of the plate compete for resources on the west side of the plate?

Since you asked, it doesn't. Not sure why you ask such a silly
question. You're welcome.

>You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?

Since you asked, the Lenski experiment forces its 12 separate
populations through a population bottleneck every day, where only 1%
of each population is put into a new bottle. OTOH the Kishony
experiment does no deliberate reduction of its populations. Different
designs, different results, none of which your mathematics model.
You're welcome.

>> More to the point, the Kishony experiment is designed to show
>> adaptation to antibiotics, and so limits the competition for other
>> things. It should go without saying that well-designed experiments
>> deliberately limits variables.
>That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.

Incorrect. Neither experiment eliminates competition, merely
restricts what the populations compete for. There's a difference.

>> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
>> >>
>> >>
>> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
>> >> >>
>> >> >>
>> >> >> Your mathematics model none of your examples above.
>> >> >Sure it does.
>> >>
>> >>
>> >> Sure it doesn't.
>> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
>>
>>
>> I note your ad hominem. Whether I understand your model doesn't alter
>> the fact that your model doesn't model your examples.
>It does kiddo but you refuse to understand why.

To the contrary, you refuse to explain how your mathematics predict
the outcomes of these experiments. Several posters have pointed this
out, including myself. At this point, only Andre is left. And you
"still* refuse to explain.

>If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?

Your ad hominems only show you have nothing intelligent to say and are
proud of it.

>> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
>> >>
>> >>
>> >> Once again, without considering the environment, you have no objective
>> >> basis for declaring any mutation beneficial, nevermind its degree of
>> >> benefit.
>> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
>>
>>
>> IIUC you model the probability of beneficial mutations by assuming
>> arbitrary values for fitness. But you do so without correlating those
>> values to different environments. So your fitness values are
>> meaningless, and so too any probabilities based on them.
>That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring.

That's what I said, which is why your model doesn't model your
examples.

[Andre G. Isaak]

In article <f590689f-1421-4d76...@googlegroups.com>,

You're missing the point. The fact that it takes on average 250 days for
beneficial mutations to become fixed in Lenski's experiment doesn't tell
you how frequently beneficial mutations occur. There's no reason to
assume that they are occurring at a slower rate than in the Kishony
experiment.

Also, while higher rates of competition speeds fixation, that doesn't
mean that competition 'requires' fixation.

If fixation isn't occurring in the Kishony experiment, it's because the
experiment ran for a much shorter time, not because of a lack of
competition.

[Alan Kleinman MD PhD]

On Saturday, March 10, 2018 at 9:30:03 PM UTC-8, jillery wrote:
> On Sat, 10 Mar 2018 11:32:01 -0800 (PST), Alan Kleinman MD PhD

Then answer this question. Why does the colony that gives rise to a beneficial mutation still exist after that beneficial mutation produces a colony in the higher drug concentration region? Should that original colony go extinct like they do in the Lenski experiment?

>
>
> >You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?
>
>
> Since you asked, the Lenski experiment forces its 12 separate
> populations through a population bottleneck every day, where only 1%
> of each population is put into a new bottle. OTOH the Kishony
> experiment does no deliberate reduction of its populations. Different
> designs, different results, none of which your mathematics model.
> You're welcome.

And that bottleneck is created by random selection. And how should that random selection change the relative frequecy of different variants? What that bottleneck does is reduce absolute numbers of variants which you should understand by now is what is the important measure of natural selection for rmns.

>
>
> >> More to the point, the Kishony experiment is designed to show
> >> adaptation to antibiotics, and so limits the competition for other
> >> things. It should go without saying that well-designed experiments
> >> deliberately limits variables.
> >That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.
>
>
> Incorrect. Neither experiment eliminates competition, merely
> restricts what the populations compete for. There's a difference.

So what colonies are going extinct in the Kishony experiment by being driven to extinction by the more fit variants? The colonies only start going extinct when the resource of the environment are used up.

>
>
> >> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
> >> >>
> >> >>
> >> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
> >> >> >>
> >> >> >>
> >> >> >> Your mathematics model none of your examples above.
> >> >> >Sure it does.
> >> >>
> >> >>
> >> >> Sure it doesn't.
> >> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
> >>
> >>
> >> I note your ad hominem. Whether I understand your model doesn't alter
> >> the fact that your model doesn't model your examples.
> >It does kiddo but you refuse to understand why.
>
>
> To the contrary, you refuse to explain how your mathematics predict
> the outcomes of these experiments. Several posters have pointed this
> out, including myself. At this point, only Andre is left. And you
> "still* refuse to explain.

It's really not all that difficult to understand the mathematics I've presented. This math tells you how many replications are required to have a reasonable probability of a beneficial mutation to occur. Or if you want to use the mean of the binomal equation, you can compute the number of replications necessary to have an expected value of 1 beneficial mutation for a given mutation rate. But sadly, you don't want to learn introductory probability theory.

>
>
> >If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?
>
>
> Your ad hominems only show you have nothing intelligent to say and are
> proud of it.

Has it now become an insult to say you should learn introductory probability theory? If you want to discuss random processes, you should learn how they work. The basic principles are not that hard if you practice a little.

>
>
> >> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
> >> >>
> >> >>
> >> >> Once again, without considering the environment, you have no objective
> >> >> basis for declaring any mutation beneficial, nevermind its degree of
> >> >> benefit.
> >> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
> >>
> >>
> >> IIUC you model the probability of beneficial mutations by assuming
> >> arbitrary values for fitness. But you do so without correlating those
> >> values to different environments. So your fitness values are
> >> meaningless, and so too any probabilities based on them.
> >That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring.
>
>
> That's what I said, which is why your model doesn't model your
> examples.

So random mutations are not occurring in the Kishony or Lenski experiment? What exactly do you think is happening in these experiments?

[Alan Kleinman MD PhD]

On Saturday, March 10, 2018 at 10:05:02 PM UTC-8, Andre G. Isaak wrote:
> In article <f590689f-1421-4d76...@googlegroups.com>,

> Alan Kleinman MD PhD wrote:
>

> > On Saturday, March 10, 2018 at 12:20:03 PM UTC-8, Andre G. Isaak wrote:
> > > In article <34b70e4f-0f99-4106...@googlegroups.com>,

> > > Alan Kleinman MD PhD wrote:
> > >
> > > > So what is your explanation for why the Kishony experiment can accumulate
> > > > the 4
> > > > or so mutations necessary to grow in the high concentration region in
> > > > just a
> > > > few days when it takes Lenski's experiment about 250 days for each
> > > > beneficial
> > > > mutation?
> > >

> > > Once again, you are confusing mutation with fixation. Lenski is talking
> > > about the time it takes for beneficial mutations to spread through the
> > > entire population. Kishony's experiment demonstrates the occurrence of
> > > beneficial mutations. Which, if any, of those mutations have become
> > > fixed isn't even discussed.
> > The Lenski experiment requires fixation because of the competition, what
> > variants are fixed in the Kishony experiment? The answer to that is none
> > because fixation is not occurring in the Kishony experiment.
>
> You're missing the point. The fact that it takes on average 250 days for
> beneficial mutations to become fixed in Lenski's experiment doesn't tell
> you how frequently beneficial mutations occur. There's no reason to
> assume that they are occurring at a slower rate than in the Kishony
> experiment.

Don't you see the cycle going on in the Lenski experiment? Do you think there is more than 1 beneficial mutation every 250 days?

>
> Also, while higher rates of competition speeds fixation, that doesn't
> mean that competition 'requires' fixation.

So why don't you compute the intensity of selection for both the Lenski experiment and the Kishony experiment?

>
> If fixation isn't occurring in the Kishony experiment, it's because the
> experiment ran for a much shorter time, not because of a lack of
> competition.

I would say 1 beneficial mutation every 250 days vs 1 beneficial mutation every 3 days is a much shorter time. If it is not a lack of competition in the Kishony experiment that does this, then why does the Kishony experiment evolve so rapidly?

[Alan Kleinman MD PhD]

On Saturday, March 10, 2018 at 1:55:02 PM UTC-8, Andre G. Isaak wrote:
> In article <51179348-42fd-4c87...@googlegroups.com>,

> Alan Kleinman MD PhD wrote:
>

> > On Saturday, March 10, 2018 at 11:40:03 AM UTC-8, Andre G. Isaak wrote:
> > > In article <58d92f2e-9430-4446...@googlegroups.com>,

> > > Alan Kleinman MD PhD wrote:
> > >

> > > > On Friday, March 9, 2018 at 9:10:02 PM UTC-8, Andre G. Isaak wrote:
> > > > > In article <eed38513-ed79-4885...@googlegroups.com>,

> > > > > Alan Kleinman MD PhD wrote:
> > > > >

> > > > > > On Friday, March 9, 2018 at 8:20:02 AM UTC-8, Andre G. Isaak wrote:
> > > > > > > In article <47fa4a1a-6feb-4a8b...@googlegroups.com>,

> > > > > > > Alan Kleinman MD PhD wrote:
> > > > > > >

> > > > > > > > On Friday, March 9, 2018 at 7:25:02 AM UTC-8, Andre G. Isaak
> > > > > > > > wrote:
> > > > > > > > > In article
> > > > > > > > > <0ea90e2e-80f0-4253...@googlegroups.com>,

> > > > > > > > > Alan Kleinman MD PhD wrote:
> > > > > > > > >

> > > > > > > > > > On Friday, March 9, 2018 at 6:20:03 AM UTC-8, Andre G. Isaak
> > > > > > > > > > wrote:
> > > > > > > > > > > In article
> > > > > > > > > > > <5e626d5d-b981-4c87...@googlegroups.com>,

> > > > > > > > > > > Alan Kleinman MD PhD wrote:
> > > > > > > > > > >

> > > > > > > > > > > > On Thursday, March 8, 2018 at 5:55:02 PM UTC-8, Mark
> > > > > > > > > > > > Isaak
> > > > > > > > > > > > wrote:
> > > > > > > > > > > > > On 3/8/18 12:27 PM, Alan Kleinman MD PhD wrote:
> > > > > > > > > > > > > > On Wednesday, March 7, 2018 at 9:15:03 PM UTC-8, Mark
> > > > > > > > > > > > > > Isaak
> > > > > > > > > > > > > > wrote:

> > > > > > > > > > > > > >> On 3/7/18 2:53 PM, Alan Kleinman MD PhD wrote:
> > > > > > > > > > > > > >>> On Wednesday, March 7, 2018 at 2:45:02 PM UTC-8,
> > > > > > > > > > > > > >>> Bill
> > > > > > > > > > > > > >>> Rogers
> > > > > > > > > > > > > >>> wrote:

> > > > > > > > > > > > > >>>> [...]

> > > > > > > > > > > > > >>>> Thank you. You are quite right. I would not argue
> > > > > > > > > > > > > >>>> that
> > > > > > > > > > > > > >>>> competition
> > > > > > > > > > > > > >>>> improves the probability of a particular mutation
> > > > > > > > > > > > > >>>> occurring.
> > > > > > > > > > > > > >>> Competition does not accelerate evolution in any
> > > > > > > > > > > > > >>> way.
> > > > > > > > > > > > > >>> Competition
> > > > > > > > > > > > > >>> reduces the diversity of populations by removing
> > > > > > > > > > > > > >>> the
> > > > > > > > > > > > > >>> less
> > > > > > > > > > > > > >>> fit
> > > > > > > > > > > > > >>> variants.
> > > > > > > > > > > > > >>> But if you think you are correct, tell us how
> > > > > > > > > > > > > >>> competition
> > > > > > > > > > > > > >>> accelerates
> > > > > > > > > > > > > >>> evolution in any way. You won't because it doesn't.
> > > > > > > > > > > > > >>

> > > > > > > > the

> > > > > > > > less fit variants to extinction. The mathematics which governs
> > > > > > > > this
> > > > > > > > component
> > > > > > > > was developed by Haldane and Kimura. The other physical component
> > > > > > > > of
> > > > > > > > the
> > > > > > > > Lenski experiment is the improvement in fitness at each
> > > > > > > > evolutionary
> > > > > > > > step.
> > > > > > > > This step requires the most fit variant to replicate sufficiently

> > > > > > > > to
> > > > > > > > have
> > > > > > > > a

> > > > > > > > reasonable probability of another beneficial mutation occurring
> > > > > > > > on
> > > > > > > > one of
> > > > > > > > the
> > > > > > > > members of this variant. This is the cycle of beneficial mutation
> > > > > > > > followed by
> > > > > > > > amplification of that mutation which is the physics of rmns. If
> > > > > > > > you
> > > > > > > > want
> > > > > > > > me
> > > > > > > > to post the governing equations again, I will.
> > > > > > >
> > > > > > >
> > > > > > > And yet once again you offer a response which fails to demonstrate
> > > > > > > a
> > > > > > > single prediction which your equation makes with respect to the
> > > > > > > Lenski
> > > > > > > experiment. For someone who keeps claiming to be trained in 'the
> > > > > > > hard
> > > > > > > mathematical sciences' you really do have a hard time grasping the
> > > > > > > fact
> > > > > > > that a request for predictions means that your answer should
> > > > > > > contain
> > > > > > > actual numerical values which follow from your equations and which
> > > > > > > can
> > > > > > > be compared with the actual results of Lenski's experiment.

> > > > > > Andre, the mathematics I've presented, for a given mutation rate, the

> > > > > > number
> > > > > > of replications necessary for a reasonable probability of a
> > > > > > beneficial

> > > > > > mutation to occur for one or more selection pressures. And this
> > > > > > mathematics
> > > > > > applies for both competitive and non-competitive environments.
> > > > >
> > > > > The only "non-competitive environments" are those which contain a
> > > > > single, non-reproducing organism.
> > > > Then tell us what the variants in the Kishony are competing for. And tell
> > > > us
> > > > which variants are being fixed in that experiment. And how do you apply
> > > > Haldane's and Kimura's model to this experiment?
> > >
> > > Variants needn't necessarily be competing for resources; they are
> > > competing to out-reproduce one another even if resources are plentiful.
> > > And in the Kishony experiment you'll notice that the outermost zones are
> > > highly saturated with bacteria by the time the bacteria reaches the zone
> > > boundary. To claim there is no competition going on between variants
> > > within this zone is rather absurd.
> > To try to compare the competition occurring in the Lenski experiment with any
> > semblance of competition in the Kishony experiment is absurd. The
> > availability of resources in the Kishony experiment allows for much, much
> > larger populations than the e8 population size achievable in the Lenski
> > experiment. Why does Lenski have to replenish his experiment daily?
>
> Unless all variants reproduce at the same rate, some will be
> outcompeting others.

If there is any competition at all in the Kishony experiment, it is miniscule. The colony (variant) that give rise to the beneficial mutation in the Lenski experiment goes extinct by time that beneficial mutation is fixed in the population. On the other hand, the colony that gives rise to the beneficial mutation in the Kishony experiment is merrily growing on as long as there is sufficient resources.

>
> > > Kishony estimates the mutation rate to be 10E-6.7 +/- 2. Considering the
> > > fact that the size of the E. coli genome is roughly 10E6.6 base pairs we
> > > can safely assume that there's already been a lot of mutations in the
> > > population by the time we actually reach the first zone boundary, and
> > > all those variants are in competition with one another.
> > Of course, there are a lot of mutations, but only the correct mutation at the
> > correct site allows that variant to grow in the next higher drug
> > concentration region.
>
> (A) Why do you assume that all variants which break through to the next
> zone possess the same mutation? There is no reason to make that
> assumption.

You still haven't read the Weinreich paper yet? I haven't made that claim.

>
> (B) Competition begins in the very first zone before the bacteria even
> reach the zone boundary. Mutations may hasten or hinder reproduction
> within each zone regardless of whether they are actually involved in
> antibiotic resistance.

Compared to the competition in the Lenski experiment, your claim is a big nothing. Why do you refuse to see the differrence between the Kishony and Lenski experiments, and it is not the law of gravitation?

>
>
> > That is what my mathematics computes the probability of
> > occurring. And which of these lineages have gone extinct in the Kishony
> > experiment? And where do you get the estimate that the e coli genome is
> > 10e6.6? The genome size of e coli is closer to 5e6.
>
> We're using different notations. that should be read as 1 x 10^6.6

If I used your notation in Excel or other spreadsheet, 10e6.6 does not equal 1 x 10^6.6. Try using mathematical notation that is recognizable.

> > > > evolutionary step for the next beneficial mutation. That applies to both
> > > > the

Did Kishony say how he arrived at that value? Because my values are consistent with many values in the literature. I recall in one paper that Lenski wrote that the mutation rate was less than e-10. And shouldn't there be a minus sign on the exponent for the value you typed?

>
> > Using the mean value for the
> > binomial distribution, it gives a range of e8 to e10 replications for each
> > beneficial mutation. Kishony can measure his colony sizes and see if that is
> > correct.
>
> Why should Kishony do it for you? It's your claim, not his.

If Kishony wants to try and understand his own experiment, he should do it. Just like Kishony should run his experiment with two drugs so that he can learn about the multiplication rule. But just the fact that the colonies are visible without the aid of magnification should give a clue that the population sizes are huge. And note they don't go extinct after they give rise to a beneficial mutation as they do with the Lenski experiment.

>
> And you're still not fully addressing my questions. For which specific
> mutations are you calculating the probability? Wouldn't that value
> change drastically depending on whether there was only a single possible
> mutation for crossing the first zone boundary (a claim which is almost
> certainly wrong) versus, say, 1000 possible mutations which would allow
> such zone-crossing? Are you considering the entire population as a whole
> or are you treating the populations in each zone separately?

You still don't get the mathematics for rmns. You would have a better chance of understanding this mathematics if you read the Weinreich paper I linked you to. But lets say you have a variety of different mutations which give improved fitness to the selection condition. Call one A1, call another B1, call a third C1 and so on. Each beneficial mutation gives rise to a different lineage and the evolutionary trajectory for each would be written as follows:
P(A1)P(A2)P(A3)...=
P(B1)P(B2)P(B3)...=
P(C1)P(C2)P(C3)...=
Do I have to fill in the right side of the equations for you?

[jillery]

You assert facts not in evidence. On what basis do you claim the
appearance of 1 beneficial mutation every 250 days in the Lenski
experiment?

[jillery]

On Mon, 12 Mar 2018 06:30:33 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

<mercy snip>

>> >> >> >> >> >Any improvement in fitness occurs if a beneficial mutation occurs and they occur with replication. Replication of variants which ultimately end up going extinct take resources for replication from the more fit variant, reducing the number of replications that variant can do. As the less fit variants are driven to extinction, the more fit variants have more resources necessary for replication but it takes large numbers of generations for that process to occur. This is why the Lenski experiment takes 1000 generations per beneficial mutation, most of the replications in Lenski's experiment are for variants that are going extinct. This is what Haldane was talking about when he titled his paper, "Cost of Natural Selection".
>> >> >> >> >>
>> >> >> >> >>
>> >> >> >> >> Your comments above are technically correct, but only by definition.
>> >> >> >> >> What you always leave out is what makes a mutation beneficial, the
>> >> >> >> >> environment. And competition is part of the environment. So a
>> >> >> >> >> mutation can be beneficial in one environment which has competition,
>> >> >> >> >> and be completely neutral in another environment which has no
>> >> >> >> >> competition. And increased competition necessarily increases said
>> >> >> >> >> mutation's benefit. None of these things are modeled in your
>> >> >> >> >> mathematics.
>> >> >> >> >A beneficial mutation is one which allows improved replication against a particular selection pressure.
>> >> >> >>
>> >> >> >>
>> >> >> >> Competition is a selection pressure.
>> >> >> >The limited resources in the environment is the selection pressure. The result is competition for that limited resource.
>> >> >>
>> >> >>
>> >> >> Resources are always finite and therefore limited, by definition. What
>> >> >> makes a resource *limiting* is competition for it. Without
>> >> >> competition, it wouldn't even be a resource.
>> >> >If Kishony was running his experiment in a standard sized Petri dish, he would be limiting his experiment and it would not work.
>> >>
>> >>
>> >> I note your assertion of facts not in evidence. The Kishony plate
>> >> shows the development of multiple distinctive populations, all
>> >> competing with each other for resources.
>> >How does a colony on the east side of the plate compete for resources on the west side of the plate?
>>
>>
>> Since you asked, it doesn't. Not sure why you ask such a silly
>> question. You're welcome.
>Then answer this question. Why does the colony that gives rise to a beneficial mutation still exist after that beneficial mutation produces a colony in the higher drug concentration region? Should that original colony go extinct like they do in the Lenski experiment?

Your first question above is similar to the Creationist PRATT "Why are
there still monkeys?", and so the answer to it is similar: There still
existed environments where the original colony remained competitive.

Your second question asserts a fact not in evidence. To the best of
my knowledge, no colony in the Lenski experiment went extinct.
Identify your basis for that claim.

>> >You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?
>>
>>
>> Since you asked, the Lenski experiment forces its 12 separate
>> populations through a population bottleneck every day, where only 1%
>> of each population is put into a new bottle. OTOH the Kishony
>> experiment does no deliberate reduction of its populations. Different
>> designs, different results, none of which your mathematics model.
>> You're welcome.
>And that bottleneck is created by random selection.

Incorrect. The bottleneck imposes drift, not selection. Selection
implies the 1% were to some degree more fit, which is not the case.

>And how should that random selection change the relative frequecy of different variants? What that bottleneck does is reduce absolute numbers of variants which you should understand by now is what is the important measure of natural selection for rmns.

Once more time, "my understanding" isn't relevant here. The issue
here remains how your models predict those different outcomes, which
you *still* have explained. Your comments remain meaningless noise.

>> >> More to the point, the Kishony experiment is designed to show
>> >> adaptation to antibiotics, and so limits the competition for other
>> >> things. It should go without saying that well-designed experiments
>> >> deliberately limits variables.
>> >That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.
>>
>>
>> Incorrect. Neither experiment eliminates competition, merely
>> restricts what the populations compete for. There's a difference.
>So what colonies are going extinct in the Kishony experiment by being driven to extinction by the more fit variants? The colonies only start going extinct when the resource of the environment are used up.

Since you asked, to the best of my knowledge no colonies went extinct.
And you *still* don't say how your model predicts those alleged
extinctions or the appearance of those more fit variants.

>> >> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
>> >> >>
>> >> >>
>> >> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
>> >> >> >>
>> >> >> >>
>> >> >> >> Your mathematics model none of your examples above.
>> >> >> >Sure it does.
>> >> >>
>> >> >>
>> >> >> Sure it doesn't.
>> >> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
>> >>
>> >>
>> >> I note your ad hominem. Whether I understand your model doesn't alter
>> >> the fact that your model doesn't model your examples.
>> >It does kiddo but you refuse to understand why.
>>
>>
>> To the contrary, you refuse to explain how your mathematics predict
>> the outcomes of these experiments. Several posters have pointed this
>> out, including myself. At this point, only Andre is left. And you
>> "still* refuse to explain.
>It's really not all that difficult to understand the mathematics I've presented.

Perhaps that is so, but based on the fact that you *still* have
explained how your mathematics predict the outcomes of your examples,
it must be virtually impossible for your to provide said explanation.

>This math tells you how many replications are required to have a reasonable probability of a beneficial mutation to occur. Or if you want to use the mean of the binomal equation, you can compute the number of replications necessary to have an expected value of 1 beneficial mutation for a given mutation rate. But sadly, you don't want to learn introductory probability theory.

Your continued use of ad hominems shows you have nothing intelligent

to say and are proud of it.


>> >If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?
>>
>>
>> Your ad hominems only show you have nothing intelligent to say and are
>> proud of it.
>Has it now become an insult to say you should learn introductory probability theory?

Since you asked, no. You're welcome.

>If you want to discuss random processes, you should learn how they work. The basic principles are not that hard if you practice a little.

Nope. The problem here is you don't want to explain how your model
predicts the outcomes of your examples. Your ad hominem noise shows

you have nothing intelligent to say and are proud of it.

>> >> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
>> >> >>
>> >> >>
>> >> >> Once again, without considering the environment, you have no objective
>> >> >> basis for declaring any mutation beneficial, nevermind its degree of
>> >> >> benefit.
>> >> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
>> >>
>> >>
>> >> IIUC you model the probability of beneficial mutations by assuming
>> >> arbitrary values for fitness. But you do so without correlating those
>> >> values to different environments. So your fitness values are
>> >> meaningless, and so too any probabilities based on them.
>> >That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring.
>>
>>
>> That's what I said, which is why your model doesn't model your
>> examples.
>So random mutations are not occurring in the Kishony or Lenski experiment? What exactly do you think is happening in these experiments?

Your non sequiturs show you have nothing intelligent to say and are
proud of it.

[Alan Kleinman MD PhD]

On Tuesday, March 13, 2018 at 1:20:03 AM UTC-7, jillery wrote:
> On Mon, 12 Mar 2018 06:39:56 -0700 (PDT), Alan Kleinman MD PhD

That one is simple arithmetic jillery. 1 beneficial mutation for every 1000 generations, about 8 generations per day, can you take it from there?

[Alan Kleinman MD PhD]

On Tuesday, March 13, 2018 at 1:50:03 AM UTC-7, jillery wrote:

I'm trying to get you to understand when survival of the fittest is acting in an environment and when it does not. The Lenski experiment impose survival of the fittest on his populations so each branch of the phylogentic tree goes extinct when the next more fit branch takes over in the environment. The Kishony experiment on the other hand does not force the extinction of previous branches in his environment. The key difference in the evolutionary behavior of the two experiments is the availability of resources to the populations. The abundance of energy during the duration of the Kishony experiment allows much faster and larger population growth.

>
> Your second question asserts a fact not in evidence. To the best of
> my knowledge, no colony in the Lenski experiment went extinct.
> Identify your basis for that claim.

What exactly does fixation in a population mean to you? Haldane worded it like this: ‘The principle unit process in evolution is the substitution of one gene for another at the same locus’. I would call this the principle unit of survival of the fittest. And in this process of substitution, the previous branch of the evolutionary tree in Lenski's experiment are gone (unless some member devolves back but it is less fit and won't last long).

>
>
> >> >You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?
> >>
> >>
> >> Since you asked, the Lenski experiment forces its 12 separate
> >> populations through a population bottleneck every day, where only 1%
> >> of each population is put into a new bottle. OTOH the Kishony
> >> experiment does no deliberate reduction of its populations. Different
> >> designs, different results, none of which your mathematics model.
> >> You're welcome.
> >And that bottleneck is created by random selection.
>
>
> Incorrect. The bottleneck imposes drift, not selection. Selection
> implies the 1% were to some degree more fit, which is not the case.

Certainly random selection imposes drift on the population and certainly this is part of the reason Lenski's experiment runs so slowly. And consider this scenario. Consider at this phase of the evolutionary process that the fit variant has just fixed in his population and in the final generation of the day, a beneficial mutation occurs on one of it members. You now draw 99% of the members out of the population without replacement. What is the probability of that member being in that 99% removed. You do that computation using the hypergeometric distribution without replacement. You have one more-fit member in the total population size of e8, you are removing (sampling without replacement) 0.99e8. The probability of that 1 member being in that 99% removed is very high. What this does is forces the remaining fixed population to replicate for that variant to reappear. Lenski could ameliorate this effect by using large vials or smaller population bottlenecks but this bottleneck effect is on rmns, not on fixation.

>
> >And how should that random selection change the relative frequecy of different variants? What that bottleneck does is reduce absolute numbers of variants which you should understand by now is what is the important measure of natural selection for rmns.
>
>
> Once more time, "my understanding" isn't relevant here. The issue
> here remains how your models predict those different outcomes, which
> you *still* have explained. Your comments remain meaningless noise.

Try reading for comprehension but you will have difficulty comprehending unless you understand introductory probability theory, the mathematics of which governs both the Lenski and Kishony experiments and all evolution for that matter. There are other physical laws which come into play as well which determine which mathematical principles are used for which process but those shouldn't be so difficult to understand. The math that I presented for the evolutionary trajectory applies in all circumstances, whether competition is occurring or not.

>
>
>
> >> >> More to the point, the Kishony experiment is designed to show
> >> >> adaptation to antibiotics, and so limits the competition for other
> >> >> things. It should go without saying that well-designed experiments
> >> >> deliberately limits variables.
> >> >That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.
> >>
> >>
> >> Incorrect. Neither experiment eliminates competition, merely
> >> restricts what the populations compete for. There's a difference.
> >So what colonies are going extinct in the Kishony experiment by being driven to extinction by the more fit variants? The colonies only start going extinct when the resource of the environment are used up.
>
>
> Since you asked, to the best of my knowledge no colonies went extinct.
> And you *still* don't say how your model predicts those alleged
> extinctions or the appearance of those more fit variants.

My model does not apply to survival of the fittest. My model give the mathematics which governs an evolutionary trajectory (the mathematics of improving fitness). The appearance of more fit variants depends on replications. The math that I've presented tells how many replications needed of that variant to have a reasonable probability of the beneficial mutation to occur. Other lineages will have similar equations and if these variants can replicate sufficiently, they will also have a reasonable probability of a beneficial mutatioin occurring.

>
>
> >> >> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
> >> >> >>
> >> >> >>
> >> >> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
> >> >> >> >>
> >> >> >> >>
> >> >> >> >> Your mathematics model none of your examples above.
> >> >> >> >Sure it does.
> >> >> >>
> >> >> >>
> >> >> >> Sure it doesn't.
> >> >> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
> >> >>
> >> >>
> >> >> I note your ad hominem. Whether I understand your model doesn't alter
> >> >> the fact that your model doesn't model your examples.
> >> >It does kiddo but you refuse to understand why.
> >>
> >>
> >> To the contrary, you refuse to explain how your mathematics predict
> >> the outcomes of these experiments. Several posters have pointed this
> >> out, including myself. At this point, only Andre is left. And you
> >> "still* refuse to explain.
> >It's really not all that difficult to understand the mathematics I've presented.
>
>
> Perhaps that is so, but based on the fact that you *still* have
> explained how your mathematics predict the outcomes of your examples,
> it must be virtually impossible for your to provide said explanation.

I'll try to make it as simple as possible. For a beneficial mutation to occur requires replications. The math I've presented simply tells how many replications are needed.

>
>
> >This math tells you how many replications are required to have a reasonable probability of a beneficial mutation to occur. Or if you want to use the mean of the binomal equation, you can compute the number of replications necessary to have an expected value of 1 beneficial mutation for a given mutation rate. But sadly, you don't want to learn introductory probability theory.
>
>
> Your continued use of ad hominems shows you have nothing intelligent
> to say and are proud of it.

Whatever

>
>
> >> >If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?
> >>
> >>
> >> Your ad hominems only show you have nothing intelligent to say and are
> >> proud of it.
> >Has it now become an insult to say you should learn introductory probability theory?
>
>
> Since you asked, no. You're welcome.

Then learn introductory probability theory and then the mathematics of evolution will become more comprehensible.

>
>
> >If you want to discuss random processes, you should learn how they work. The basic principles are not that hard if you practice a little.
>
>
> Nope. The problem here is you don't want to explain how your model
> predicts the outcomes of your examples. Your ad hominem noise shows
> you have nothing intelligent to say and are proud of it.

I could give the explanation a thousand times and it won't make sense to you because you are unwilling to learn the logic behind the explanation. Are you proud to argue from ignorance?

>
>
> >> >> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
> >> >> >>
> >> >> >>
> >> >> >> Once again, without considering the environment, you have no objective
> >> >> >> basis for declaring any mutation beneficial, nevermind its degree of
> >> >> >> benefit.
> >> >> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
> >> >>
> >> >>
> >> >> IIUC you model the probability of beneficial mutations by assuming
> >> >> arbitrary values for fitness. But you do so without correlating those
> >> >> values to different environments. So your fitness values are
> >> >> meaningless, and so too any probabilities based on them.
> >> >That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring.
> >>
> >>
> >> That's what I said, which is why your model doesn't model your
> >> examples.
> >So random mutations are not occurring in the Kishony or Lenski experiment? What exactly do you think is happening in these experiments?
>
>
> Your non sequiturs show you have nothing intelligent to say and are
> proud of it.

My arguments are quite sequitor. You refuse to understand the logic.

>
>
> >> >When you take into account the relative fitness, think survival of the fittest. When thinking improvement in fitness, think number of replications of that variant. Haven't you ever wondered why Haldane and Kimura don't have the mutation rate in their mathematics?
> >> >> >> >> >> >> You're welcome.
> >> >> >> >> >> >>
> >> >> >> >> >> >>
> >> >> >> >> >> >> >> > > In no way does competition accelerate evolution. In fact, competition slows evolution and removes less fit variants from the population. And until these less fit variants are removed from the population, these variants are using resources from the environment. Evolution works much more rapidly in the non-competitive environment. This is due to a fundamental law of physics. Do you know which law of physics?
> >> >> >> >> >> >> >> > > >
> >> >> >> >> >> >> >> >
> >> >> >> >> >> >> >> > > > Plus, your continued use of the word "particular" demonstrates one of the conspicuous flaws in your argument.
> >> >> >> >> >> >> >> > > As long as rmns is dependent on “particular” mutations to improve fitness,
> >> >> >> >> >> >> >> >
> >> >> >> >> >> >> >> > It isn't.
> >> >> >> >> >> >> >> >
> >> >> >> >> >> >> >> > > it is quite appropriate to use this term. But if you think this is a flaw,
> >> >> >> >> >> >> >> > > point out this flaw with specificity.
> >> >> >> >> >> >> >> >
> >> >> >> >> >> >> >> > Your "math", what there is of it, demonstrates that it is vanishingly unlikely for mutation, selection and drift (evolution) to produce a *particular* target organism, with its exact DNA complement. This is due to the multiplication rule. I doubt that anyone here disagrees.
>
>

[jillery]

To rephrase for the comprehension-challenged, on what basis do you
claim the appearance of 1 beneficial mutation for every 1000
generations?

[Alan Kleinman MD PhD]

On Tuesday, March 13, 2018 at 7:00:03 AM UTC-7, jillery wrote:
> On Tue, 13 Mar 2018 05:45:09 -0700 (PDT), Alan Kleinman MD PhD

Sorry, I thought you were paying attention:
"Phenotypic and Genomic Evolution during a 20,000-Generation Experiment with the Bacterium Escherichia coli"
https://telliamedrevisited.files.wordpress.com/2015/02/2004-pbr-lenski.pdf

"I would hazard the estimate that between 10 and 20 beneficial mutations have been substituted in each population."
>

[Andre G. Isaak]

In article <d0735728-ef0d-49c8...@googlegroups.com>,

That refers to the number of mutations which have been *fixed* during
that time. There may be many other beneficial mutations which have yet
to become fixed and others which may never become fixed.

Since fixation requires time, any mutation which becomes fixed does so
long after the mutation first arose. Kishony gives evidence for
mutations occurring, but does not investigate which (if any) of those
mutations ultimately become fixed, so the two experiments are apples and
oranges. There is absolutely no reason to assume that beneficial
mutations arise any more quickly in Kishony's experiment than they do in
Lenski's experiment.

[Alan Kleinman MD PhD]

On Tuesday, March 13, 2018 at 11:55:03 AM UTC-7, Andre G. Isaak wrote:
> In article <d0735728-ef0d-49c8...@googlegroups.com>,

How do you know a mutation is beneficial?

>
> Since fixation requires time, any mutation which becomes fixed does so
> long after the mutation first arose. Kishony gives evidence for
> mutations occurring, but does not investigate which (if any) of those
> mutations ultimately become fixed, so the two experiments are apples and
> oranges. There is absolutely no reason to assume that beneficial
> mutations arise any more quickly in Kishony's experiment than they do in
> Lenski's experiment.

The point that you miss or refuse to understand is that rmns does not require fixation. This is clearly demonstrated in the Kishony experiment. Lineages accumulate mutations to give adaptation without ever becoming fixed in the population. In order for natural selection to work for rmns, the only requirement is that the particular variant must replicate sufficiently to give a reasonable probability of a beneficial mutation occurring. Fixation of variants in a population is a result of competition, ie survival of the fittest but it does not represent an improvement in the fitness of that variant.

[jillery]

That wasn't so hard after all, was it?

Now that you have identified the basis for your claim, go back to the
original issue, and explain how your model predicts the appearance of
those 10 to 20 beneficial mutations in the Lenski experiment, which is
something you *still* haven't done.

[jillery]

That may be what you think you're doing, but...

1) That's not what you're supposed to be doing, and

2) What you are doing doesn't explain anything.

>The Lenski experiment impose survival of the fittest on his populations so each branch of the phylogentic tree goes extinct when the next more fit branch takes over in the environment. The Kishony experiment on the other hand does not force the extinction of previous branches in his environment. The key difference in the evolutionary behavior of the two experiments is the availability of resources to the populations. The abundance of energy during the duration of the Kishony experiment allows much faster and larger population growth.
>>
>> Your second question asserts a fact not in evidence. To the best of
>> my knowledge, no colony in the Lenski experiment went extinct.
>> Identify your basis for that claim.
>What exactly does fixation in a population mean to you? Haldane worded it like this: ‘The principle unit process in evolution is the substitution of one gene for another at the same locus’. I would call this the principle unit of survival of the fittest. And in this process of substitution, the previous branch of the evolutionary tree in Lenski's experiment are gone (unless some member devolves back but it is less fit and won't last long).

Since you asked, from:
<https://en.wikipedia.org/wiki/Fixation_(population_genetics)>
*************************************************
In population genetics, fixation is the change in a gene pool from a
situation where there exists at least two variants of a particular
gene (allele) to a situation where only one of the alleles remains.
*************************************************

And you *still* haven't identified your basis for asserting any
population in the Lenski experiment went extinct.

You're welcome.

>> >> >You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?
>> >>
>> >>
>> >> Since you asked, the Lenski experiment forces its 12 separate
>> >> populations through a population bottleneck every day, where only 1%
>> >> of each population is put into a new bottle. OTOH the Kishony
>> >> experiment does no deliberate reduction of its populations. Different
>> >> designs, different results, none of which your mathematics model.
>> >> You're welcome.
>> >And that bottleneck is created by random selection.
>>
>>
>> Incorrect. The bottleneck imposes drift, not selection. Selection
>> implies the 1% were to some degree more fit, which is not the case.
>Certainly random selection imposes drift on the population and certainly this is part of the reason Lenski's experiment runs so slowly.

Even if true, it would be true whether or not competition existed.

>And consider this scenario. Consider at this phase of the evolutionary process that the fit variant has just fixed in his population and in the final generation of the day, a beneficial mutation occurs on one of it members. You now draw 99% of the members out of the population without replacement. What is the probability of that member being in that 99% removed. You do that computation using the hypergeometric distribution without replacement. You have one more-fit member in the total population size of e8, you are removing (sampling without replacement) 0.99e8. The probability of that 1 member being in that 99% removed is very high. What this does is forces the remaining fixed population to replicate for that variant to reappear. Lenski could ameliorate this effect by using large vials or smaller population bottlenecks but this bottleneck effect is
>on rmns, not on fixation.
>>
>> >And how should that random selection change the relative frequecy of different variants? What that bottleneck does is reduce absolute numbers of variants which you should understand by now is what is the important measure of natural selection for rmns.
>>
>>
>> Once more time, "my understanding" isn't relevant here. The issue
>> here remains how your models predict those different outcomes, which
>> you *still* have explained. Your comments remain meaningless noise.
>Try reading for comprehension but you will have difficulty comprehending unless you understand introductory probability theory, the mathematics of which governs both the Lenski and Kishony experiments and all evolution for that matter.

Your continued use of ad hominems shows you have nothing intelligent
to say and are proud of it.

>There are other physical laws which come into play as well which determine which mathematical principles are used for which process but those shouldn't be so difficult to understand. The math that I presented for the evolutionary trajectory applies in all circumstances, whether competition is occurring or not.
>>
>>
>>
>> >> >> More to the point, the Kishony experiment is designed to show
>> >> >> adaptation to antibiotics, and so limits the competition for other
>> >> >> things. It should go without saying that well-designed experiments
>> >> >> deliberately limits variables.
>> >> >That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.
>> >>
>> >>
>> >> Incorrect. Neither experiment eliminates competition, merely
>> >> restricts what the populations compete for. There's a difference.
>> >So what colonies are going extinct in the Kishony experiment by being driven to extinction by the more fit variants? The colonies only start going extinct when the resource of the environment are used up.
>>
>>
>> Since you asked, to the best of my knowledge no colonies went extinct.
>> And you *still* don't say how your model predicts those alleged
>> extinctions or the appearance of those more fit variants.
>My model does not apply to survival of the fittest. My model give the mathematics which governs an evolutionary trajectory (the mathematics of improving fitness). The appearance of more fit variants depends on replications. The math that I've presented tells how many replications needed of that variant to have a reasonable probability of the beneficial mutation to occur. Other lineages will have similar equations and if these variants can replicate sufficiently, they will also have a reasonable probability of a beneficial mutatioin occurring.


And you *still* don't say how your model predicts those alleged

extinctions or the appearance of those beneficial mutations.

>> >> >> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
>> >> >> >>
>> >> >> >>
>> >> >> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
>> >> >> >> >>
>> >> >> >> >>
>> >> >> >> >> Your mathematics model none of your examples above.
>> >> >> >> >Sure it does.
>> >> >> >>
>> >> >> >>
>> >> >> >> Sure it doesn't.
>> >> >> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
>> >> >>
>> >> >>
>> >> >> I note your ad hominem. Whether I understand your model doesn't alter
>> >> >> the fact that your model doesn't model your examples.
>> >> >It does kiddo but you refuse to understand why.
>> >>
>> >>
>> >> To the contrary, you refuse to explain how your mathematics predict
>> >> the outcomes of these experiments. Several posters have pointed this
>> >> out, including myself. At this point, only Andre is left. And you
>> >> "still* refuse to explain.
>> >It's really not all that difficult to understand the mathematics I've presented.
>>
>>
>> Perhaps that is so, but based on the fact that you *still* have
>> explained how your mathematics predict the outcomes of your examples,
>> it must be virtually impossible for your to provide said explanation.
>I'll try to make it as simple as possible. For a beneficial mutation to occur requires replications. The math I've presented simply tells how many replications are needed.

You made your reply so simple, that you forgot to explain how your
mathematics predict the outcomes of the Lenski and Kishony
experiments.

>> >This math tells you how many replications are required to have a reasonable probability of a beneficial mutation to occur. Or if you want to use the mean of the binomal equation, you can compute the number of replications necessary to have an expected value of 1 beneficial mutation for a given mutation rate. But sadly, you don't want to learn introductory probability theory.
>>
>>
>> Your continued use of ad hominems shows you have nothing intelligent
>> to say and are proud of it.
>Whatever

That's no worse than all of your replies, but it's no better either.

>> >> >If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?
>> >>
>> >>
>> >> Your ad hominems only show you have nothing intelligent to say and are
>> >> proud of it.
>> >Has it now become an insult to say you should learn introductory probability theory?
>>
>>
>> Since you asked, no. You're welcome.
>Then learn introductory probability theory and then the mathematics of evolution will become more comprehensible.


Your ad hominems only show you have nothing intelligent to say and are
proud of it.


>> >If you want to discuss random processes, you should learn how they work. The basic principles are not that hard if you practice a little.
>>
>>
>> Nope. The problem here is you don't want to explain how your model
>> predicts the outcomes of your examples. Your ad hominem noise shows
>> you have nothing intelligent to say and are proud of it.
>I could give the explanation a thousand times and it won't make sense to you because you are unwilling to learn the logic behind the explanation. Are you proud to argue from ignorance?

Since you have never given an explanation, you again assert facts not
in evidence.

>> >> >> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
>> >> >> >>
>> >> >> >>
>> >> >> >> Once again, without considering the environment, you have no objective
>> >> >> >> basis for declaring any mutation beneficial, nevermind its degree of
>> >> >> >> benefit.
>> >> >> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
>> >> >>
>> >> >>
>> >> >> IIUC you model the probability of beneficial mutations by assuming
>> >> >> arbitrary values for fitness. But you do so without correlating those
>> >> >> values to different environments. So your fitness values are
>> >> >> meaningless, and so too any probabilities based on them.
>> >> >That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring.
>> >>
>> >>
>> >> That's what I said, which is why your model doesn't model your
>> >> examples.
>> >So random mutations are not occurring in the Kishony or Lenski experiment? What exactly do you think is happening in these experiments?
>>
>>
>> Your non sequiturs show you have nothing intelligent to say and are
>> proud of it.
>My arguments are quite sequitor. You refuse to understand the logic.

To the contrary, you refuse to say anything intelligent and apparently
are proud of it.

[Alan Kleinman MD PhD]

On Tuesday, March 13, 2018 at 11:35:04 PM UTC-7, jillery wrote:

> On Tue, 13 Mar 2018 07:10:46 -0700 (PDT), Alan Kleinman MD PhD
> wrote:
>
> >On Tuesday, March 13, 2018 at 7:00:03 AM UTC-7, jillery wrote:

> >> On Tue, 13 Mar 2018 05:45:09 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Tuesday, March 13, 2018 at 1:20:03 AM UTC-7, jillery wrote:

> >> >> On Mon, 12 Mar 2018 06:39:56 -0700 (PDT), Alan Kleinman MD PhD
> >> >> wrote:
> >> >>
> >> >> >On Saturday, March 10, 2018 at 10:05:02 PM UTC-8, Andre G. Isaak wrote:
> >> >> >> In article <f590689f-1421-4d76...@googlegroups.com>,

> >> >> >> Alan Kleinman MD PhD wrote:
> >> >> >>

> >> >> >> > On Saturday, March 10, 2018 at 12:20:03 PM UTC-8, Andre G. Isaak wrote:
> >> >> >> > > In article <34b70e4f-0f99-4106...@googlegroups.com>,

> >> >> >> > > Alan Kleinman MD PhD wrote:
> >> >> >> > >
> >> >> >> > > > So what is your explanation for why the Kishony experiment can accumulate
> >> >> >> > > > the 4
> >> >> >> > > > or so mutations necessary to grow in the high concentration region in
> >> >> >> > > > just a
> >> >> >> > > > few days when it takes Lenski's experiment about 250 days for each
> >> >> >> > > > beneficial
> >> >> >> > > > mutation?
> >> >> >> > >

No, but it is repetitive, I've posted this quote many times.

>
> Now that you have identified the basis for your claim, go back to the
> original issue, and explain how your model predicts the appearance of
> those 10 to 20 beneficial mutations in the Lenski experiment, which is
> something you *still* haven't done.

DNA contains the instructions needed for an organism to develop, survive and reproduce. The sum total of the DNA is called a genome. In the process of replication, errors in the genome occur. The frequency of those errors at any site in the genome is the mutation rate. Occasionally, a mutation occurs at a particular site which gives improved ability to replicate. This is called a beneficial mutation. The mathematics I've presented describes how a lineage of variants accumulates these beneficial mutations to give a sequence of variants with improved fitness to replicate. This mathematics applies not only to the Lenski experiment where there are many different lineages competing for the same limited resources but also for other examples of evolution such as the Kishony experiment where multiple different lineages evolving to the environmental conditions but not under conditions of limited resources.
You are welcome

[Alan Kleinman MD PhD]

On Tuesday, March 13, 2018 at 11:35:04 PM UTC-7, jillery wrote:

> On Tue, 13 Mar 2018 06:43:16 -0700 (PDT), Alan Kleinman MD PhD
> wrote:
>
> >On Tuesday, March 13, 2018 at 1:50:03 AM UTC-7, jillery wrote:

If you want to understand how rmns works in different types of environments, it is what I'm supposed to be doing, if you don't want to understand how rmns, then I guess it is not what I'm supposed to be doing.

>
> 2) What you are doing doesn't explain anything.

Try paying closer attention.

>
>
> >The Lenski experiment impose survival of the fittest on his populations so each branch of the phylogentic tree goes extinct when the next more fit branch takes over in the environment. The Kishony experiment on the other hand does not force the extinction of previous branches in his environment. The key difference in the evolutionary behavior of the two experiments is the availability of resources to the populations. The abundance of energy during the duration of the Kishony experiment allows much faster and larger population growth.
> >>
> >> Your second question asserts a fact not in evidence. To the best of
> >> my knowledge, no colony in the Lenski experiment went extinct.
> >> Identify your basis for that claim.
> >What exactly does fixation in a population mean to you? Haldane worded it like this: ‘The principle unit process in evolution is the substitution of one gene for another at the same locus’. I would call this the principle unit of survival of the fittest. And in this process of substitution, the previous branch of the evolutionary tree in Lenski's experiment are gone (unless some member devolves back but it is less fit and won't last long).
>
>
> Since you asked, from:
> <https://en.wikipedia.org/wiki/Fixation_(population_genetics)>
> *************************************************
> In population genetics, fixation is the change in a gene pool from a
> situation where there exists at least two variants of a particular
> gene (allele) to a situation where only one of the alleles remains.
> *************************************************
>
> And you *still* haven't identified your basis for asserting any
> population in the Lenski experiment went extinct.

So when Lenski does his genome sequencing every 500 generations, any or all the variants that he had from the beginning of the experiment and later generations are found thousands of generations later?

>
> You're welcome.
>
>
> >> >> >You might be able to make an argument that two colonies are growing on top of each other competing for the same resources but what that will do is slow the appearance of the beneficial mutant because neither colony can grow as rapidly if they didn't have to compete. And you have to assume that the two colonies originate from different variants. So what is your explanation for why the Kishony experiment can accumulate the 4 or so mutations necessary to grow in the high concentration region in just a few days when it takes Lenski's experiment about 250 days for each beneficial mutation?
> >> >>
> >> >>
> >> >> Since you asked, the Lenski experiment forces its 12 separate
> >> >> populations through a population bottleneck every day, where only 1%
> >> >> of each population is put into a new bottle. OTOH the Kishony
> >> >> experiment does no deliberate reduction of its populations. Different
> >> >> designs, different results, none of which your mathematics model.
> >> >> You're welcome.
> >> >And that bottleneck is created by random selection.
> >>
> >>
> >> Incorrect. The bottleneck imposes drift, not selection. Selection
> >> implies the 1% were to some degree more fit, which is not the case.
> >Certainly random selection imposes drift on the population and certainly this is part of the reason Lenski's experiment runs so slowly.
>
>
> Even if true, it would be true whether or not competition existed.

Selection represents deaths of lineages. Unless you think death is an improvement in fitness to replicate, selection will always slow evolution. Only with replication is there a possibility to improve fitness in either the competitive or non-competitive environments. This is why debulking a cancer along with chemotherapy works better than chemotherapy alone. You put a bottleneck on the cancer cells and then add the chemical selection pressure and you reduce the probability of that cancer cell evolving resistance to that agent. Any action of combined selection pressures work that way. Each selection pressure imposes its own bottleneck on the population as well as making any evolutionary trajectory much more complex. That's why combination therapy works for the treatment of HIV. Three bottlenecks and a much more complex evolutionary trajectory than single drug therapy. Extremely low probabilities for that replicator.

>
>
> >And consider this scenario. Consider at this phase of the evolutionary process that the fit variant has just fixed in his population and in the final generation of the day, a beneficial mutation occurs on one of it members. You now draw 99% of the members out of the population without replacement. What is the probability of that member being in that 99% removed. You do that computation using the hypergeometric distribution without replacement. You have one more-fit member in the total population size of e8, you are removing (sampling without replacement) 0.99e8. The probability of that 1 member being in that 99% removed is very high. What this does is forces the remaining fixed population to replicate for that variant to reappear. Lenski could ameliorate this effect by using large vials or smaller population bottlenecks but this bottleneck effect is
> >on rmns, not on fixation.
> >>
> >> >And how should that random selection change the relative frequecy of different variants? What that bottleneck does is reduce absolute numbers of variants which you should understand by now is what is the important measure of natural selection for rmns.
> >>
> >>
> >> Once more time, "my understanding" isn't relevant here. The issue
> >> here remains how your models predict those different outcomes, which
> >> you *still* have explained. Your comments remain meaningless noise.
> >Try reading for comprehension but you will have difficulty comprehending unless you understand introductory probability theory, the mathematics of which governs both the Lenski and Kishony experiments and all evolution for that matter.
>
>
> Your continued use of ad hominems shows you have nothing intelligent
> to say and are proud of it.

Don't you think understanding probability theory would help you to understand something about evolution since the central principles of this subject revolve around random processes?

>
>
> >There are other physical laws which come into play as well which determine which mathematical principles are used for which process but those shouldn't be so difficult to understand. The math that I presented for the evolutionary trajectory applies in all circumstances, whether competition is occurring or not.
> >>
> >>
> >>
> >> >> >> More to the point, the Kishony experiment is designed to show
> >> >> >> adaptation to antibiotics, and so limits the competition for other
> >> >> >> things. It should go without saying that well-designed experiments
> >> >> >> deliberately limits variables.
> >> >> >That's the point I'm making. Competition slows the evolutionary process because the less fit variants are using resources that the more fit variant could use to replicate. And replication is the trial for the beneficial mutation. By the way, the Kishony experiment is more analogous to what happens in the clinical medical situation especially if the patient is immune compromised.
> >> >>
> >> >>
> >> >> Incorrect. Neither experiment eliminates competition, merely
> >> >> restricts what the populations compete for. There's a difference.
> >> >So what colonies are going extinct in the Kishony experiment by being driven to extinction by the more fit variants? The colonies only start going extinct when the resource of the environment are used up.
> >>
> >>
> >> Since you asked, to the best of my knowledge no colonies went extinct.
> >> And you *still* don't say how your model predicts those alleged
> >> extinctions or the appearance of those more fit variants.
> >My model does not apply to survival of the fittest. My model give the mathematics which governs an evolutionary trajectory (the mathematics of improving fitness). The appearance of more fit variants depends on replications. The math that I've presented tells how many replications needed of that variant to have a reasonable probability of the beneficial mutation to occur. Other lineages will have similar equations and if these variants can replicate sufficiently, they will also have a reasonable probability of a beneficial mutatioin occurring.
>
>
> And you *still* don't say how your model predicts those alleged
> extinctions or the appearance of those beneficial mutations.

The mathematics I've presented does not predict extinction. It predicts improvement in fitness. If you want the mathematics which governs survival of the fittest, study the Haldane and Kimura models.

>
>
> >> >> >> >Instead, he uses his Mega-plate which does not limit growth media until after his populations have successfully evolved against the antibiotic.
> >> >> >> >>
> >> >> >> >>
> >> >> >> >> >> >A couple examples from cases we have been discussing. A beneficial mutation in the Lenski experiment allows that variant to reproduce using less energy than the variant it descended from. A beneficial mutation in the Kishony experiment allows that variant to replicate in the environment with increased level of antibiotic toxin.
> >> >> >> >> >>
> >> >> >> >> >>
> >> >> >> >> >> Your mathematics model none of your examples above.
> >> >> >> >> >Sure it does.
> >> >> >> >>
> >> >> >> >>
> >> >> >> >> Sure it doesn't.
> >> >> >> >Sure you don't understand how it does. Do you understand Haldane's and Kimura's models? I think you don't.
> >> >> >>
> >> >> >>
> >> >> >> I note your ad hominem. Whether I understand your model doesn't alter
> >> >> >> the fact that your model doesn't model your examples.
> >> >> >It does kiddo but you refuse to understand why.
> >> >>
> >> >>
> >> >> To the contrary, you refuse to explain how your mathematics predict
> >> >> the outcomes of these experiments. Several posters have pointed this
> >> >> out, including myself. At this point, only Andre is left. And you
> >> >> "still* refuse to explain.
> >> >It's really not all that difficult to understand the mathematics I've presented.
> >>
> >>
> >> Perhaps that is so, but based on the fact that you *still* have
> >> explained how your mathematics predict the outcomes of your examples,
> >> it must be virtually impossible for your to provide said explanation.
> >I'll try to make it as simple as possible. For a beneficial mutation to occur requires replications. The math I've presented simply tells how many replications are needed.
>
>
> You made your reply so simple, that you forgot to explain how your
> mathematics predict the outcomes of the Lenski and Kishony
> experiments.

The math that I've presented describes each step on an evolutionary trajectory. As long as Lenski feeds his bacteria, he will continue to get variants with improving fitness until he exhausts all possible mutations. Perhaps you think the bacteria will get together and form an organ system or something like that. I think his experiment will reach equilibrium and stop evolving. As for the Kishony experiment, if he took his adapted variants and ran another experiment with a different drug, he could get doubly resistant variants. If he takes his drug-sensitive variants and runs his experiment with two drugs, much less likely for that evolutionary process.

>
>
> >> >This math tells you how many replications are required to have a reasonable probability of a beneficial mutation to occur. Or if you want to use the mean of the binomal equation, you can compute the number of replications necessary to have an expected value of 1 beneficial mutation for a given mutation rate. But sadly, you don't want to learn introductory probability theory.
> >>
> >>
> >> Your continued use of ad hominems shows you have nothing intelligent
> >> to say and are proud of it.
> >Whatever
>
>
> That's no worse than all of your replies, but it's no better either.

It is definitely better than the response Harshman has come to.

>
>
> >> >> >If you want to understand how rmns works, you need to understand how stochastic processes work. Are you always this stubborn?
> >> >>
> >> >>
> >> >> Your ad hominems only show you have nothing intelligent to say and are
> >> >> proud of it.
> >> >Has it now become an insult to say you should learn introductory probability theory?
> >>
> >>
> >> Since you asked, no. You're welcome.
> >Then learn introductory probability theory and then the mathematics of evolution will become more comprehensible.
>
>
> Your ad hominems only show you have nothing intelligent to say and are
> proud of it.

Whatever, but don't be surprised if you don't understand my explanations.

>
>
> >> >If you want to discuss random processes, you should learn how they work. The basic principles are not that hard if you practice a little.
> >>
> >>
> >> Nope. The problem here is you don't want to explain how your model
> >> predicts the outcomes of your examples. Your ad hominem noise shows
> >> you have nothing intelligent to say and are proud of it.
> >I could give the explanation a thousand times and it won't make sense to you because you are unwilling to learn the logic behind the explanation. Are you proud to argue from ignorance?
>
>

> Since you have never given an explanation, you again assert facts not
> in evidence.
Whatever

>
>
> >> >> >> >> >This mathematics predicts from a given mutation rate, the number of replications necessary for a reasonable probability of a beneficial mutation to occur.
> >> >> >> >>
> >> >> >> >>
> >> >> >> >> Once again, without considering the environment, you have no objective
> >> >> >> >> basis for declaring any mutation beneficial, nevermind its degree of
> >> >> >> >> benefit.
> >> >> >> >What makes up an environment? Is it not the resources available to allow for replication and the selection conditions? Then it comes down to which variants are able to survive those selection conditions and if there is any reasonable probability of those surviving variants to improve fitness against those selection conditions.
> >> >> >>
> >> >> >>
> >> >> >> IIUC you model the probability of beneficial mutations by assuming
> >> >> >> arbitrary values for fitness. But you do so without correlating those
> >> >> >> values to different environments. So your fitness values are
> >> >> >> meaningless, and so too any probabilities based on them.
> >> >> >That's not the correct understanding. All my model does is compute the probability of a particular mutation occurring.
> >> >>
> >> >>
> >> >> That's what I said, which is why your model doesn't model your
> >> >> examples.
> >> >So random mutations are not occurring in the Kishony or Lenski experiment? What exactly do you think is happening in these experiments?
> >>
> >>
> >> Your non sequiturs show you have nothing intelligent to say and are
> >> proud of it.
> >My arguments are quite sequitor. You refuse to understand the logic.
>
>
> To the contrary, you refuse to say anything intelligent and apparently
> are proud of it.

Whatever^2

[Öö Tiib]

On Wednesday, 7 March 2018 15:15:03 UTC+2, Alan Kleinman MD PhD wrote:
> The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of “survival of the fittest” and the mathematics of improving fitness.
> .
> The mathematics of “survival of the fittest” is addressed by the works of Haldane and Kimura. Haldane's work “The cost of natural selection” can be found at:
> http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
> And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
> http://www.genetics.org/content/genetics/47/6/713.full.pdf
> .
> These two authors in their papers use different terminology to describe the same thing. Haldane uses the word “substitution” while the Kimura paper uses the term “fixation” to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable “mutation rate”. This is because they are not addressing the mathematics of “improvement in fitness”. They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
> .
> On the other hand, “improvement in fitness” must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication. So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant. Bill Rogers argues that competition, “survival of the fittest”, improves that probability of that particular mutation occurring. Does it?

I still do not understand what is your objection to evolution?

Lenski's experiment does show that in a relatively tiny
environments (12 flasks) couple dozen beneficial (for those
environments) mutations did evolve with 30 years in each
flask. Fact?
That means relatively small population in relatively tight
conditions can evolve couple dozen millions of beneficial
mutations with 30 millions of years if needed? Correct
conclusion?
Couple dozen millions is several times more than there are
base pairs in whole E.coli genome. Fact?
That means it does not take absurd amounts of time to evolve
totally different organisms from E.coli. Correct conclusion?

You post hundreds of posts stating that there is some sort
of mysterious algebra somewhere that no one understands
and that does not let things to evolve. You do not post that
algebra and dodge every attempt to ask it from you so
everybody are certain that there are no such things.
But let it be. What is wrong with that simple logic above?

[jillery]

Even accepting for argument's sake that your mathematics describe how
the variants accumulate beneficial mutations, your statement above
would explain how your mathematics predict the the number of
beneficial mutations *only* if you assume that the number of
beneficial mutations are always the same in all situations. Since
that's an absurd assumption, it would explain why you're so unwilling
to post an explanation.

[jillery]

That's not it. Instead, you answer the question you want to answer,
not the question I asked. And you're proud of it.

[Alan Kleinman MD PhD]

On Wednesday, March 14, 2018 at 11:30:03 PM UTC-7, Öö Tiib wrote:
> On Wednesday, 7 March 2018 15:15:03 UTC+2, Alan Kleinman MD PhD wrote:
> > The physics and mathematics of evolution, like the physics and mathematics of any complex process often times requires more than a single set of mathematical principles to describe the complex process. For the case of evolution, this thread is intended to describe and discuss the differences between the mathematics of “survival of the fittest” and the mathematics of improving fitness.
> > .
> > The mathematics of “survival of the fittest” is addressed by the works of Haldane and Kimura. Haldane's work “The cost of natural selection” can be found at:
> > http://www.ignaciodarnaude.com/textos_diversos/Haldane,The%20cost%20of%20natural%20selection.pdf
> > And Kimura's work “On the probability of fixation of mutant genes in a population” can be found at:
> > http://www.genetics.org/content/genetics/47/6/713.full.pdf
> > .
> > These two authors in their papers use different terminology to describe the same thing. Haldane uses the word “substitution” while the Kimura paper uses the term “fixation” to describe the replacement of the less fit variants in the population by the more fit variant. What these mathematical models are addressing is the change in frequencies of variants in a population based on their relative fitness. Note that neither of these papers in their models contains the variable “mutation rate”. This is because they are not addressing the mathematics of “improvement in fitness”. They are addressing the rate at which the more fit variant will replace the less fit variants in a given population, the competition between variants for the resources of the environment. They model natural selection based on the relative fitness of the different variants.
> > .
> > On the other hand, “improvement in fitness” must take into account the mutation rate. And recall, the mutation rate is the probability of a particular mutation occurring at a particular site in a single replication. So any increase in that probability of that particular mutation occurring requires an increased number of replications of that variant. Bill Rogers argues that competition, “survival of the fittest”, improves that probability of that particular mutation occurring. Does it?
>
> I still do not understand what is your objection to evolution?

I don't object to evolution any more than I object to the motion of objects in space. And I don't object to either. They are physical phenomena and if correctly studied and understood, their behavior can be predicted mathematically. It is when someone argues that an object in space does not move in concert with the laws of motion that I object to that claim. In the same way, I object to claims that evolution works in a way in which all empirical and mathematical evidence contradicts.

>
> Lenski's experiment does show that in a relatively tiny
> environments (12 flasks) couple dozen beneficial (for those
> environments) mutations did evolve with 30 years in each
> flask. Fact?

Those tiny flasks support a population size of e8. So when you say relative, relative to what? And Lenski supports his population with the energy necessary to carry out his evolutionary process.

> That means relatively small population in relatively tight
> conditions can evolve couple dozen millions of beneficial
> mutations with 30 millions of years if needed? Correct
> conclusion?

Not correct. Since when is a population size of e8 a small population? And his populations are fixing every evolutionary step. So that member that gets that beneficial mutation in a given step, amplifies (fixes) before the next evolutionary step occurs. What you call "tight conditions" are controlled conditions. If Lenski allows other selection conditions to operate simultaneously, his experiment will only run slower. And when you use years to measure time, you must convert that to generations to do your calculations for rmns. Lenski is getting 1 beneficial mutation for every 500 to 1000 generations for his lineages. So a replicator that has a generation time of 1 year, 30,000,000 generations will give you about 30-60,000 beneficial mutations, that is if your lineage can achieve e8 for every evolutionary step and the lineage is subjected to only a single selection pressure at a time. That's the hard math Lenski's experiment is revealing.

> Couple dozen millions is several times more than there are
> base pairs in whole E.coli genome. Fact?

What fact? What evidence? Your initial premise is flawed. You assume 30,000,000 will give millions of dozens of millions of beneficial mutations? What is the basis for your claim? Certainly, it is not the Lenski experiment.

> That means it does not take absurd amounts of time to evolve
> totally different organisms from E.coli. Correct conclusion?

Incorrect conclusion.

>
> You post hundreds of posts stating that there is some sort
> of mysterious algebra somewhere that no one understands
> and that does not let things to evolve. You do not post that
> algebra and dodge every attempt to ask it from you so
> everybody are certain that there are no such things.
> But let it be. What is wrong with that simple logic above?

You almost did the algebra a while back. Where you made your mistake was in the application of the multiplication rule for the joint probability of two independent beneficial mutations. So the algebra is not so mysterious. And lots of people understand this math, I suspect even you do. And the problem with your logic above is that you don't correlate it with the mathematical and empirical evidence that the Lenski experiment provides.

[Alan Kleinman MD PhD]

On Thursday, March 15, 2018 at 3:35:03 AM UTC-7, jillery wrote:

> On Wed, 14 Mar 2018 06:32:45 -0700 (PDT), Alan Kleinman MD PhD
> wrote:
>
> >On Tuesday, March 13, 2018 at 11:35:04 PM UTC-7, jillery wrote:

> >> On Tue, 13 Mar 2018 07:10:46 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Tuesday, March 13, 2018 at 7:00:03 AM UTC-7, jillery wrote:

> >> >> On Tue, 13 Mar 2018 05:45:09 -0700 (PDT), Alan Kleinman MD PhD
> >> >> wrote:
> >> >>
> >> >> >On Tuesday, March 13, 2018 at 1:20:03 AM UTC-7, jillery wrote:

> >> >> >> On Mon, 12 Mar 2018 06:39:56 -0700 (PDT), Alan Kleinman MD PhD
> >> >> >> wrote:
> >> >> >>
> >> >> >> >On Saturday, March 10, 2018 at 10:05:02 PM UTC-8, Andre G. Isaak wrote:
> >> >> >> >> In article <f590689f-1421-4d76...@googlegroups.com>,

> >> >> >> >> Alan Kleinman MD PhD wrote:
> >> >> >> >>

> >> >> >> >> > On Saturday, March 10, 2018 at 12:20:03 PM UTC-8, Andre G. Isaak wrote:
> >> >> >> >> > > In article <34b70e4f-0f99-4106...@googlegroups.com>,

> >> >> >> >> > > Alan Kleinman MD PhD wrote:
> >> >> >> >> > >

> >> >> >> >> > > > So what is your explanation for why the Kishony experiment can accumulate
> >> >> >> >> > > > the 4
> >> >> >> >> > > > or so mutations necessary to grow in the high concentration region in
> >> >> >> >> > > > just a
> >> >> >> >> > > > few days when it takes Lenski's experiment about 250 days for each
> >> >> >> >> > > > beneficial
> >> >> >> >> > > > mutation?
> >> >> >> >> > >

My equations do not predict the number of beneficial mutations. And your statement is ambiguous. Are you talking about the number of possible beneficial mutations and a given evolutionary step or the possible number of beneficial mutations for a particular evolutionary trajectory? In the former case, the total number of possible mutation for a given gene of base length "N" would be 4^N. That number actually could be larger if you include insertions, deletions, and other possible mutations but obviously, the subset of beneficial mutations would be much, much smaller. But the point you miss, each beneficial mutation for this circumstance represents a different evolutionary trajectory and therefore a different lineage. But the mathematics of that lineage would be analogous to any other lineage subject to the same beneficial mutation/amplification of mutation cycle. With respects to the total number of beneficial mutations in an evolutionary trajectory, such as the Lenski experiment, that would be limited by the number of sites in the entire genome, obviously, a much larger number than in the former case. But again, each evolutionary step must operate in a beneficial mutation/amplification of the beneficial mutation cycle.

[Alan Kleinman MD PhD]

On Thursday, March 15, 2018 at 3:35:03 AM UTC-7, jillery wrote:
> On Wed, 14 Mar 2018 07:12:26 -0700 (PDT), Alan Kleinman MD PhD

I'm answering how rmns works. If you object to this answer, try being more explicit in your objections.

[jillery]

Who do you think you're fooling?

[jillery]

That's exactly what Andre and Bill Rogers and I and just about every
poster who has replied to you, have been telling you for months. Thank
you for finally admitting it.

[Alan Kleinman MD PhD]

On Thursday, March 15, 2018 at 3:05:03 PM UTC-7, jillery wrote:
> On Thu, 15 Mar 2018 10:18:42 -0700 (PDT), Alan Kleinman MD PhD

I'm not trying to fool anyone. The mathematics and emperical evidence is clear enough to see.

[Alan Kleinman MD PhD]

On Thursday, March 15, 2018 at 3:05:04 PM UTC-7, jillery wrote:
> On Thu, 15 Mar 2018 10:14:20 -0700 (PDT), Alan Kleinman MD PhD

Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.

[jillery]

On Thu, 15 Mar 2018 15:32:44 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>> Who do you think you're fooling?
>I'm not trying to fool anyone. The mathematics and emperical evidence is clear enough to see.

To be accurate, your excuses are clear enough to see. That other
stuff is just spam.

[jillery]

On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.

Non-sequiturs "R" DrDr.

[Alan Kleinman MD PhD]

On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
> On Thu, 15 Mar 2018 15:32:44 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >> Who do you think you're fooling?
> >I'm not trying to fool anyone. The mathematics and emperical evidence is clear enough to see.
>
>
> To be accurate, your excuses are clear enough to see. That other
> stuff is just spam.

No excuses, just hard mathematical facts of life which explains the Lenski experiment, the Kishony experiment, why combination therapy works for the treatment of hiv, in fact, all real, measurable and repeatable examples of rmns. And please note, rmns is not survival of the fittest. Survival of the fittest slows rmns as clearly seen with the differences between the Lenski and Kishony experiment.
You are welcome.

[Alan Kleinman MD PhD]

On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:

> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
>
>
> Non-sequiturs "R" DrDr.

So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?

[jillery]

On Fri, 16 Mar 2018 06:36:02 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
>> On Thu, 15 Mar 2018 15:32:44 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >> Who do you think you're fooling?
>> >I'm not trying to fool anyone. The mathematics and emperical evidence is clear enough to see.
>>
>>
>> To be accurate, your excuses are clear enough to see. That other
>> stuff is just spam.
>No excuses, just hard mathematical facts of life which explains the Lenski experiment, the Kishony experiment, why combination therapy works for the treatment of hiv, in fact, all real, measurable and repeatable examples of rmns.

Of course, your hard mathematical facts are at best descriptive, not
prescriptive, and so explain nothing by themselves.

>And please note, rmns is not survival of the fittest. Survival of the fittest slows rmns as clearly seen with the differences between the Lenski and Kishony experiment.

More of your non-sequitur spam.

[jillery]

On Fri, 16 Mar 2018 06:41:07 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
>> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
>>
>>
>> Non-sequiturs "R" DrDr.
>So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?

Since you asked, from the same place your MRSA got their genes. You're
welcome.

[Alan Kleinman MD PhD]

On Friday, March 16, 2018 at 10:45:03 AM UTC-7, jillery wrote:
> On Fri, 16 Mar 2018 06:36:02 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
> >> On Thu, 15 Mar 2018 15:32:44 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >> Who do you think you're fooling?
> >> >I'm not trying to fool anyone. The mathematics and emperical evidence is clear enough to see.
> >>
> >>
> >> To be accurate, your excuses are clear enough to see. That other
> >> stuff is just spam.
> >No excuses, just hard mathematical facts of life which explains the Lenski experiment, the Kishony experiment, why combination therapy works for the treatment of hiv, in fact, all real, measurable and repeatable examples of rmns.
>
>
> Of course, your hard mathematical facts are at best descriptive, not
> prescriptive, and so explain nothing by themselves.

So you have an empirical example of rmns that is not governed by the multiplication rule? Please post that example.

>
>
> >And please note, rmns is not survival of the fittest. Survival of the fittest slows rmns as clearly seen with the differences between the Lenski and Kishony experiment.
>
>
> More of your non-sequitur spam.

Only the hard mathematical scientific facts.

[Alan Kleinman MD PhD]

On Friday, March 16, 2018 at 10:45:03 AM UTC-7, jillery wrote:
> On Fri, 16 Mar 2018 06:41:07 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
> >> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
> >>
> >>
> >> Non-sequiturs "R" DrDr.
> >So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?
>
>
> Since you asked, from the same place your MRSA got their genes. You're
> welcome.

MRSA got their genes from frogs? I think you are telling a fish story. Who do you think you are fooling?

[jillery]

On Fri, 16 Mar 2018 11:06:18 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>Only the hard mathematical scientific facts.

Quadratic formulae are also hard mathematical scientific facts, and
are also not an explanation of how your model predicts the outcomes in
your examples.

[jillery]

On Fri, 16 Mar 2018 11:10:02 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, March 16, 2018 at 10:45:03 AM UTC-7, jillery wrote:
>> On Fri, 16 Mar 2018 06:41:07 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
>> >> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
>> >> wrote:
>> >>
>> >> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
>> >>
>> >>
>> >> Non-sequiturs "R" DrDr.
>> >So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?
>>
>>
>> Since you asked, from the same place your MRSA got their genes. You're
>> welcome.
>MRSA got their genes from frogs? I think you are telling a fish story. Who do you think you are fooling?

Apparently you don't have the genes to parse written English.

[Alan Kleinman MD PhD]

On Friday, March 16, 2018 at 10:55:02 PM UTC-7, jillery wrote:
> On Fri, 16 Mar 2018 11:06:18 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >Only the hard mathematical scientific facts.
>
>
> Quadratic formulae are also hard mathematical scientific facts, and
> are also not an explanation of how your model predicts the outcomes in
> your examples.

You need to learn how formulas work, not just to plug numbers into formulas.

[Alan Kleinman MD PhD]

On Friday, March 16, 2018 at 10:55:02 PM UTC-7, jillery wrote:
> On Fri, 16 Mar 2018 11:10:02 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Friday, March 16, 2018 at 10:45:03 AM UTC-7, jillery wrote:
> >> On Fri, 16 Mar 2018 06:41:07 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
> >> >> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
> >> >> wrote:
> >> >>
> >> >> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
> >> >>
> >> >>
> >> >> Non-sequiturs "R" DrDr.
> >> >So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?
> >>
> >>
> >> Since you asked, from the same place your MRSA got their genes. You're
> >> welcome.
> >MRSA got their genes from frogs? I think you are telling a fish story. Who do you think you are fooling?
>
>
> Apparently you don't have the genes to parse written English.

Perhaps you should have asked where MRSA got their alleles?

[jillery]

On Mon, 19 Mar 2018 05:52:33 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, March 16, 2018 at 10:55:02 PM UTC-7, jillery wrote:
>> On Fri, 16 Mar 2018 11:10:02 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Friday, March 16, 2018 at 10:45:03 AM UTC-7, jillery wrote:
>> >> On Fri, 16 Mar 2018 06:41:07 -0700 (PDT), Alan Kleinman MD PhD
>> >> wrote:
>> >>
>> >> >On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
>> >> >> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
>> >> >> wrote:
>> >> >>
>> >> >> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
>> >> >>
>> >> >>
>> >> >> Non-sequiturs "R" DrDr.
>> >> >So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?
>> >>
>> >>
>> >> Since you asked, from the same place your MRSA got their genes. You're
>> >> welcome.
>> >MRSA got their genes from frogs? I think you are telling a fish story. Who do you think you are fooling?
>>
>>
>> Apparently you don't have the genes to parse written English.
>Perhaps you should have asked where MRSA got their alleles?

My impression is it would have made no difference to your reply.

[jillery]

On Mon, 19 Mar 2018 05:50:28 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, March 16, 2018 at 10:55:02 PM UTC-7, jillery wrote:
>> On Fri, 16 Mar 2018 11:06:18 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >Only the hard mathematical scientific facts.
>>
>>
>> Quadratic formulae are also hard mathematical scientific facts, and
>> are also not an explanation of how your model predicts the outcomes in
>> your examples.
>You need to learn how formulas work, not just to plug numbers into formulas.

That's exactly the problem others have pointed out about your RMNS
applied to Evolution in general. So now that you admit what your
problem is, what are you going to do to fix it?

[Alan Kleinman MD PhD]

On Monday, March 19, 2018 at 10:40:02 PM UTC-7, jillery wrote:
> On Mon, 19 Mar 2018 05:52:33 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Friday, March 16, 2018 at 10:55:02 PM UTC-7, jillery wrote:
> >> On Fri, 16 Mar 2018 11:10:02 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Friday, March 16, 2018 at 10:45:03 AM UTC-7, jillery wrote:
> >> >> On Fri, 16 Mar 2018 06:41:07 -0700 (PDT), Alan Kleinman MD PhD
> >> >> wrote:
> >> >>
> >> >> >On Thursday, March 15, 2018 at 10:35:03 PM UTC-7, jillery wrote:
> >> >> >> On Thu, 15 Mar 2018 15:36:56 -0700 (PDT), Alan Kleinman MD PhD
> >> >> >> wrote:
> >> >> >>
> >> >> >> >Then it should be clear why reptiles cannot grow feathers. They don't have the correct genes and control modules and rmns cannot produce the correct genetics to grow these feathers.
> >> >> >>
> >> >> >>
> >> >> >> Non-sequiturs "R" DrDr.
> >> >> >So reptiles do have the genes and control modules necessary to grow feathers? Where did they get them from, frogs?
> >> >>
> >> >>
> >> >> Since you asked, from the same place your MRSA got their genes. You're
> >> >> welcome.
> >> >MRSA got their genes from frogs? I think you are telling a fish story. Who do you think you are fooling?
> >>
> >>
> >> Apparently you don't have the genes to parse written English.
> >Perhaps you should have asked where MRSA got their alleles?
>
>
> My impression is it would have made no difference to your reply.

There certainly is a difference with respects to genetic transformation. In one case it is the transformation of a gene from one form to another. In the other case, it is the acquisition of genetic material that doesn't exist in the parent.

[jillery]

On Tue, 20 Mar 2018 05:28:04 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>There certainly is a difference with respects to genetic transformation. In one case it is the transformation of a gene from one form to another. In the other case, it is the acquisition of genetic material that doesn't exist in the parent.

Once again you show you have no idea what you're talking about.

[Alan Kleinman MD PhD]

On Tuesday, March 20, 2018 at 9:50:04 AM UTC-7, jillery wrote:
> On Tue, 20 Mar 2018 05:28:04 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >There certainly is a difference with respects to genetic transformation. In one case it is the transformation of a gene from one form to another. In the other case, it is the acquisition of genetic material that doesn't exist in the parent.
>
> Once again you show you have no idea what you're talking about.

Try google translate.

[wpih...@gmail.com]

Standard crank stuff.


Non-crank

A is true

A does not imply B

B is false.




Crank

We know A implies B (the crank will never discuss this just claim it)

You say A is true.

You think B is true.





Here A is: competition accelerates evolution

B is: competition increases the probability of a beneficial mutation

(Dr^2 thinks A implies B because the only way he can see evolution accelerating
is if the probability of a beneficial mutation increases)

[Andre G. Isaak]

In article <8af77bd4-ccff-4249...@googlegroups.com>,

wpih...@gmail.com wrote:

> Standard crank stuff.
>
>
> Non-crank
>
> A is true
>
> A does not imply B
>
> B is false.

One would hope that your hypothetical non-crank wouldn't try to pass
that off as a valid syllogism, the truth of the conclusion
notwithstanding.

Andre

--
To email remove 'invalid' & replace 'gm' with well known Google mail service.

[wpih...@gmail.com]

On Saturday, March 24, 2018 at 12:05:02 AM UTC-3, Andre G. Isaak wrote:
> In article <8af77bd4-ccff-4249...@googlegroups.com>,
> wpih...@gmail.com wrote:
>
> > Standard crank stuff.
> >
> >
> > Non-crank
> >
> > A is true
> >
> > A does not imply B
> >
> > B is false.
>
>
> One would hope that your hypothetical non-crank wouldn't try to pass
> that off as a valid syllogism, the truth of the conclusion
> notwithstanding.

Indeed. These are three independent statements, not a syllogism.

[Andre G. Isaak]

In article <9af122ea-4194-4429...@googlegroups.com>,

My Bad.