Darwin and Mendel

[mark kennedy]

Then why do you keep talking about how frameshifts are lethal when I cite examples of substitutions?

The amino acid substitution is where this all started so you don't get to bury it in these tangents. We are talking about the color of mice in case you have forgotten and the amino acid change was sufficient to produce the change in color. Since that came up I've shown you again and again that changes in the amino acid sequence of protein coding genes are going to cause frameshifts the vast majority of the time. With that you have continually tried to derail the thread which would appear to be you only purpose in these discussions.

We are talking about SUBSTITUTION MUTATIONS in a mouse gene, not indels.

Which is based on the artificial substitution of an amino acid, now we are talking about what happens when the protein coding sequence is changed by a spontaneous mutation and the result is going to be a frameshift the vast majority of the time.

If we were talking about substitutions, THEN WHY DID YOU BRING UP INDELS?

We are not talking about them, you are talking in circles around them.

If most mutations do nothing, then why did you say that 98% are deleterious?

Why do you insist on wasting time chasing down tangents.

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. Some are neutral, that is, they produce no effect strong enough to permit selection for or against (Rates of Spontaneous Mutation)​

The definition for mutations has been offered, ignored and now it's going to be repeated until you acknowledge that we are talking about two different things here.

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. Mutations​

You have two choices here, either accept this definition or provide another one. If you want to argue semantics then define your terms or quit correcting mine.

Then stop bringing up indels when we are talking about substitution mutations.

I'm not the one conflating my terms, when the smoke clears you are going to be left with an inescapable fact. Mutations are a terrible explanation for the change of color in mice. Indeed, there are variant sequences but it's a lot like the Nylon eating bacteria the evolutionists on here used to love to bring up. When you track it down it's not a mutation at all, the genome was swapping out in tact reading frames.

Unless or until you learn something about the difference between an adaptation and a mutation semantics is going to do nothing but expose the fallacious nature of your arguments.

But please, continue spamming these pedantic one liners and intermittent random links, you prove my point with every post.

Have a nice day
Mark

 

[keith99]

Very interesting post. Thanks for posting it.

A pedantic add on.

Stalin was a follower of Lysenko who was a follower of Lamarck and rejected Darwinian evolution much to the detriment of Russian agriculture.

A point that comes up every so often with statements about the atheist Stalin being a follower of Darwin.

Dizredux

A second level pedantic point.

Much of the time opponents of Evolution make statements that are objecting to Lamarck or ancient Greek philosophers, not Darwin. Sometimes even demanding supporters show something that would in fact discredit Darwinian evolution.

 

[mark kennedy]

A second level pedantic point.

Much of the time opponents of Evolution make statements that are objecting to Lamarck or ancient Greek philosophers, not Darwin. Sometimes even demanding supporters show something that would in fact discredit Darwinian evolution.

There is nothing about opposing Darwinism that is opposed to evolution. The point is that Darwinian political and social movements, especially national socialist movements, are opposed the genuine article of science.

They were not receiving Western journals. And Western ideas were considered bourgeois, erroneous and that they had to be abandoned, including - and this is what shocked Monod - 50 years of genetics. So this - there was a public announcement in the Soviet Union that Mendelian genetics, the genetics of Gregor Mendel and the chromosomal theories of genetics...It gutted Soviet biology, I would say, really, since that time; that Soviet biology never really recovered from this long episode of genetics being suppressed in the Soviet Union. ( 'Brave Genius': A Tale of Two Nobelists NPR)​

They do so at great intellectual, academic and scientific cost. The issue isn't one of science vs religion but Darwinism derailing scientific progress which is has been famous for. The Nazis were much worse but definitely Darwinian:

Three generations of imbeciles are enough." This decision opened the floodgates for thousands to be coercively sterilized or otherwise persecuted as subhuman. Years later, the Nazis at the Nuremberg trials quoted Holmes's words in their own defense...In Mein Kampf, published in 1924, Hitler quoted American eugenic ideology and openly displayed a thorough knowledge of American eugenics. "There is today one state," wrote Hitler, "in which at least weak beginnings toward a better conception [of immigration] are noticeable. Of course, it is not our model German Republic, but the United States." HNN article​

Darwinism is inextricably linked to Eugenics, it has been prominent at every layer of it's development.

Have a nice day
Mark

 

[Split Rock]

The amino acid substitution is where this all started so you don't get to bury it in these tangents. We are talking about the color of mice in case you have forgotten and the amino acid change was sufficient to produce the change in color. Since that came up I've shown you again and again that changes in the amino acid sequence of protein coding genes are going to cause frameshifts the vast majority of the time. With that you have continually tried to derail the thread which would appear to be you only purpose in these discussions.

Which is based on the artificial substitution of an amino acid, now we are talking about what happens when the protein coding sequence is changed by a spontaneous mutation and the result is going to be a frameshift the vast majority of the time.

Mark, this is simply incorrect. The rate of substitutions is 10 times greater than the rate of indels. See for example Table 1 is this reference: Mutation rates of base substitutions, short indels and copy number variations : Genome-wide genetic changes during modern breeding of maize : Nature Genetics : Nature Publishing Group

Number of single-base mutations 179
Single-base substitution rate (per site per year) 2.02 × 10−8
Number of 1- to 10-bp indels 18
Mutation rate of 1- to 10-bp indels (per site per year) 2.03 × 10−9

I'm not the one conflating my terms, when the smoke clears you are going to be left with an inescapable fact. Mutations are a terrible explanation for the change of color in mice. Indeed, there are variant sequences but it's a lot like the Nylon eating bacteria the evolutionists on here used to love to bring up. When you track it down it's not a mutation at all, the genome was swapping out in tact reading frames.

If you change the reading frame by an indel it is a mutation. I do not understand your argument.

Unless or until you learn something about the difference between an adaptation and a mutation semantics is going to do nothing but expose the fallacious nature of your arguments.

Adaptions do not always require a new mutation, but are sometimes based on a new mutation. For example, one I often cite here is the single base substitution (proline to serine) based on a point mutation in the EPSP synthase gene that provided for resistance to glyphosate (Roundup) in goosegrass.
Glyphosate-Resistant Goosegrass. Identification of a Mutation in the Target Enzyme 5-Enolpyruvylshikimate-3-Phosphate Synthase

 

[mark kennedy]

Mark, this is simply incorrect. The rate of substitutions is 10 times greater than the rate of indels. See for example Table 1 is this reference: Mutation rates of base substitutions, short indels and copy number variations : Genome-wide genetic changes during modern breeding of maize : Nature Genetics : Nature Publishing Group

I have a better idea, lets try something relevant. How are you at doing the math? The burden of proof is on providing the directly observed and demonstrated mechanism for human evolution from that of apes. Evolutionists admit that they have no clue how and Darwin's natural selection was not a major contributor. So what was it then? In a word, it would have had to be mutations, primarily indels (aka length mutations). It is well known that length mutations have the lowest mutation rate at 2.3 x 10^-9. They are 10 times less common then single substitutions and yet they account for almost three times more divergence. This is the table based on 1.33% divergence:

Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8​

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8​

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1. (Estimate of the Mutation Rate per Nucleotide in Humans , Michael W. Nachmana and Susan L. Crowella Genetics, 297-304, September 2000)

Now, plug in 4%. With 5 million indels required for us to have a common ancestor with the Chimpanzee that means 1 indel permanently fixed in either genome per year for 5 million years.

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions (Initial Sequence of the Chimpanzee Genome)​

That's a mean average obviously but it leaves 90 million base pairs unaccounted for, some over a million base pairs in length. That is in addition to the three fold expansion of the human brain from that of apes.

Have a nice day
Mark

 

[Loudmouth]

The amino acid substitution is where this all started so you don't get to bury it in these tangents. We are talking about the color of mice in case you have forgotten and the amino acid change was sufficient to produce the change in color. Since that came up I've shown you again and again that changes in the amino acid sequence of protein coding genes are going to cause frameshifts the vast majority of the time.

Substitutions do not cause frameshifts. Ever. I showed you that the difference between the light and dark alleles was due to substitutions, not indels.

Which is based on the artificial substitution of an amino acid, now we are talking about what happens when the protein coding sequence is changed by a spontaneous mutation and the result is going to be a frameshift the vast majority of the time.

The mutation happened in a wild population. There is nothing artificial about. As shown above, the substitution rate is 10 times that of the indel rate which means that 90% of the time the result of a mutation will not be a frameshift.

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. Some are neutral, that is, they produce no effect strong enough to permit selection for or against (Rates of Spontaneous Mutation)​

How many mutations affect genes? That's what you keep ignoring. If only 2% of the genome is translated into protein, it would seem to me that 98% of mutations will not change the amino acid sequence of a protein.

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. Mutations​

You have two choices here, either accept this definition or provide another one. If you want to argue semantics then define your terms or quit correcting mine.

A mutation is a mutation. The fact of the matter is that offspring are born with new DNA sequences, with substitutions being 10 times more common than indels.

Mutations are a terrible explanation for the change of color in mice.

Why? How else do you get from the light allele to the dark allele?

When you track it down it's not a mutation at all, the genome was swapping out in tact reading frames.

There was nothing to swap out. The dark allele was not present in the population before the volcanic eruptions, as already discussed.

Unless or until you learn something about the difference between an adaptation and a mutation semantics is going to do nothing but expose the fallacious nature of your arguments.

I am showing you an adaptation that was caused by a mutation.

"Both alleles of the entire Mc1r gene (954 bp) were sequenced in the 69 mice in Fig. 1. Twenty-four single-nucleotide polymorphisms were observed: 15 were synonymous and 9 were nonsynonymous. Four of the nine amino acid polymorphisms were observed only in the dark mice from the Pinacate locality (Arg-18 → Cys, Arg-109 → Trp, Arg-160 → Trp, and Gln-233 → His). These four amino acid variants were present at high frequency (82%) among the Pinacate dark mice and were in complete linkage disequilibrium with one another. All other Mc1r amino acid polymorphisms were present at low frequencies and showed no association with mouse color. The distribution of Mc1r nucleotide variation among light and melanic mice from the Pinacate site is shown in Table 1. "
The genetic basis of adaptive melanism in pocket mice

 

[Loudmouth]

I have a better idea, lets try something relevant. How are you at doing the math? The burden of proof is on providing the directly observed and demonstrated mechanism for human evolution from that of apes.

We have directly observed the appearance of mutations in humans.

We have directly observed the effects of selection on humans.

Those are the two observed mechanisms.

So what was it then? In a word, it would have had to be mutations, primarily indels (aka length mutations). It is well known that length mutations have the lowest mutation rate at 2.3 x 10^-9. They are 10 times less common then single substitutions and yet they account for almost three times more divergence.

How strongly are they selected against within coding sequences?

What percentage of indels occur within genes?