Darwin and Mendel

[mark kennedy]

Prove that they are devastating to the genome.

One can be devastating but a million...this is just sad.

Yet another claim you can't back.

You can dish out the false corrections but you can't admit your own mistakes no matter how many you make.

Which ones have I got wrong?

I don't think you got one right yet.

How many ERV's are there in the human genome? I bet I have that one right.

Bet you never found a single documented case where a human genome suffered an ERV invasion.

How many ERV's are there in the human genome?

By my count, none.

My question still stands. Since when do substitution mutations cause frame shifts?

Didn't say they did, as usual you think twisting the wording around is the same thing as an actual argument.

Even by your own admission, substitution mutations outnumber indels by a factor of 6 to 1. Substitution mutations do not cause a frame shift. Therefore, most mutations do not result in a frame shift. You are absolutely wrong about that one.

Never said a substitution did, I said a mutation. Wrong again! Your batting a thousand today slugger.

Add to the fact that indels of 3 bases or multiples of 3 will only add or subtract amino acids while keeping the reading frame intact, so not all indels will result in a frame shift mutation.

Yea but what are the odds? That's the whole thing about natural selection, if it's beneficial sure it can become fixed but how does it get there in the first place?

Funny, the Evolutionists are steadily clearing out of the Origins theology forums but you remain. Didn't you hear, the culture wars are over LM.

Have a nice day
Mark

 

[Loudmouth]

One can be devastating but a million...this is just sad.

Prove it.

You can dish out the false corrections but you can't admit your own mistakes no matter how many you make.

What mistakes?

I don't think you got one right yet.

Show me one.

Bet you never found a single documented case where a human genome suffered an ERV invasion.

Of course not, you can't ben invaded by an endogenous retrovirus. It's already there.

I can give you a bunch of examples of retroviruses inserting into the host genome.

By my count, none.

That's another one you have wrong. The human genome paper lists over 200,000 ERV's in the human genome.

Didn't say they did, as usual you think twisting the wording around is the same thing as an actual argument.

That is exactly what you said. You said that most mutations cause frame shifts. Most mutations are substitutions. Therefore, you implied that substitutions cause frame shifts.

Yea but what are the odds? That's the whole thing about natural selection, if it's beneficial sure it can become fixed but how does it get there in the first place?

Have you been asleep at the wheel? THROUGH MUTATIONS!!!

Funny, the Evolutionists are steadily clearing out of the Origins theology forums but you remain. Didn't you hear, the culture wars are over LM.

Have a nice day
Mark

You still can't understand the basics. You still argue that most mutations cause frame shifts, when they don't. You claim that 200,000 ERV's would devastate the genome, which you have never shown. Do you really think that molecules are made up of real letters?

I could go on and on.

 

[USincognito]

...the white fur of arctic wildlife. Something common toall arctic wildlife adapted them to the colder climate...

 

[USincognito]

They are protein coding genes that have been disabled by mutations like the pseudo genes you guys want to pass off as some kind of proof for universal common descent.

I don't see an answer to the question. How many ERVs are in the human genome?

I sometimes wonder if your not doing it on purpose because I don't see how you could be that wrong, so many times in a row, unless it were.

Dunning-Kruger.

 

[USincognito]

Bet you never found a single documented case where a human genome suffered an ERV invasion.

This sentence doesn't make any sense.

By my count, none.

Yep. Dunning-Kruger.

203 x 1000 = 203,000. Your count is a bit off.

 

[sfs]

Oh whatever, those are differences, calling them mutations doesn't account for them it just assumes a natural process that is devastating to genomes, especially protein coding genes.

Mutations are just changes to DNA, many of which are not devastating at all. Each human carries several tens of thousands of such differences in protein-coding genes, such that they change the amino-acid produced. You really think all 30 or 40 thousand are devastating?

 

[sfs]

Just made it up huh?

Yup, you just made it up. Your claim has no basis in genetics or biology, no factual support and no connection to reality. It's a fantasy you made up out of whole cloth. Clear?

Antarctic notothenioid fishes and several northern cods are phylogenetically distant (in different orders and superorders), yet produce near-identical antifreeze glycoproteins (AFGPs) to survive in their respective freezing environments. AFGPs in both fishes are made as a family of discretely sized polymers composed of a simple glycotripeptide monomeric repeat. (Convergent evolution of antifreeze glycoproteins in Antarctic notothenioid fish and Arctic cod, PNAS 1997)​

"Despite these apparent similarities, detailed analyses of the AFGP gene sequences and substructures provide strong evidence that AFGPs in these two polar fishes in fact evolved independently." Do you read the abstracts you're quoting from? And what does this have to do with fur color in the arctic?

It seems rather odd that you are so sure about human brain evolution, even though you haven't a clue how it's possible, but seem at a loss for explaining the white fur of arctic wildlife. Something common to all arctic wildlife adapted them to the colder climate and it wasn't random DNA copy errors.

Of course it was random DNA copy errors. We know the kinds of changes that have to happen to DNA for skin or fur to change to white, and those changes are easily produced by random copy errors. It often takes just a single substitution to change the color; single substitutions like that happen by chance all the time. The only reason for thinking otherwise is that you don't want it to be true.

Surely you have a better explanation then that, an entire gene is produced from simple repeats and your not a little bit curious how this was facilitated.

You mean the kind of simple repeats that litter most genomes? These couldn't become functional genes because . . . why, exactly?

It didn't just happen to a couple of random fish, two populations at either pole evolved the same gene, or at least it did the same thing.

Other antifreeze proteins have been evolved independently at least four times.

Your going to write that off as a random mutation with a beneficial effect?

Yes. Of course, yes. 150 years of evolutionary biology isn't going to be thrown out just because you ask in a disbelieving tone, you know. How about offering some evidence random mutation couldn't have done it?

I'm a little fuzzy on the logic here, isn't there supposed to be a cause as well as an effect?

I'll grant you the fuzziness, but don't know what you're looking for. The mechanism(s) of evolution are well known and well established.

 

[sfs]

So Mark, were the examples we gave you beneficial mutations or not?

 

[mark kennedy]

So Mark, were the examples we gave you beneficial mutations or not?

That's what this is all about isn't it, random mutations. I've seen plenty of beneficial effects from mutations, they are anecdotal. Why is it so objectionable to you that there might be an actual mechanism that can build a protein coding gene in the ancestors of the cod fish. What is so appalling about a distinctive adaptive trait across broad taxonomic categories as a place to search for molecular mechanisms involved in adaptive evolution?

Nothing, absolutely nothing. Just like you encourage LM to make nearly constant errors that you pat him on the back for, your interest is not in promoting the life sciences and making a substantive argument for evolution. All your doing here is bashing a Biblical worldview.

I'll just keep checking back from time to time, who knows, maybe you guys will snap out of it at some point but I won't hold my breath and I'm certainly not chasing the drivel in circles.

 

[whitebeaches]

Mod Hat On​

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Mod Hat Off​

 

[sfs]

So Mark, were those beneficial mutations or not?

 

[mark kennedy]

Bumping a thread I liked, wondering if there is any interest.

 

[sfs]

Bumping a thread I liked, wondering if there is any interest.

Does this mean you're going to answer the question?

 

[mark kennedy]

Does this mean you're going to answer the question?

Hi Steve, maybe you could refresh my memory, are what mutations beneficial?

 

[sfs]

Hi Steve, maybe you could refresh my memory, are what mutations beneficial?

You can refresh your own memory quite easily: read the thread you want to reopen. Then answer the question.

 

[mark kennedy]

You can refresh your own memory quite easily: read the thread you want to reopen. Then answer the question.

I did, it didn't make any sense. What mutations are you talking about?

 

[mark kennedy]

I can only assume these are the supposed 'beneficial mutations' you wanted me to address.

Yup, you just made it up. Your claim has no basis in genetics or biology, no factual support and no connection to reality. It's a fantasy you made up out of whole cloth. Clear?

No, we are anything but clear. You are not applying this statement to anything relevant or tangible. I have never argued that there was no such thing as a beneficial effect from a mutation, your begging the question. I'm saying that mutations are not the cause of adaptive evolution the vast majority of the time. What is puzzling is I think you know that.

"Despite these apparent similarities, detailed analyses of the AFGP gene sequences and substructures provide strong evidence that AFGPs in these two polar fishes in fact evolved independently." Do you read the abstracts you're quoting from? And what does this have to do with fur color in the arctic?

Your not the only scientist I have interacted with and a research scientist I encountered elsewhere was telling me how this protein was simple repeats even though it was a brand new gene introduced to the cod genome. I find that so much more fascinating then equivocating mutations with adaptations.

Of course it was random DNA copy errors. We know the kinds of changes that have to happen to DNA for skin or fur to change to white, and those changes are easily produced by random copy errors. It often takes just a single substitution to change the color; single substitutions like that happen by chance all the time. The only reason for thinking otherwise is that you don't want it to be true.

I don't happen to care if it's true or not, I just know adaptive evolution is not the same thing as genetic mutation.

You mean the kind of simple repeats that litter most genomes? These couldn't become functional genes because . . . why, exactly?

Because they don't, the vast majority of the time. It's fascinating that you don't have the slightest interest in this. A brand new gene, a protein coding gene that adds a vital adaptive trait to arctic cods in two populations, independently and you don't pause to ask whether there might be a molecular mechanism involved.

Other antifreeze proteins have been evolved independently at least four times.

I can only assume you could care less what caused them as well.

Yes. Of course, yes. 150 years of evolutionary biology isn't going to be thrown out just because you ask in a disbelieving tone, you know. How about offering some evidence random mutation couldn't have done it?

I'm anything but disbelieving although I like to watch you squirm when the facts challenge your Darwinian assumptions.

I'll grant you the fuzziness, but don't know what you're looking for. The mechanism(s) of evolution are well known and well established.

We are in perfect agreement with that point, it's just your equivocation of random mutations with molecular mechanisms that has to be continually sorted out.

Have a nice day
Mark

 

[Loudmouth]

I'm saying that mutations are not the cause of adaptive evolution the vast majority of the time.

Why not?

Even the different alleles that Mendel studied in pea plants were produced by mutations. That's how you get more than one allele, through mutations.

Your not the only scientist I have interacted with and a research scientist I encountered elsewhere was telling me how this protein was simple repeats even though it was a brand new gene introduced to the cod genome. I find that so much more fascinating then equivocating mutations with adaptations.

We can discuss the mutations in pocket mouse Mc1r gene if you want:

The genetic basis of adaptive melanism in pocket mice

Mutations gave rise to a dark fur color that was adaptive for dark basalt rocks. Even more interesting, two different populations of dark mouse evolved dark fur through different mutations. It happened at least twice.

I don't happen to care if it's true or not, I just know adaptive evolution is not the same thing as genetic mutation.

Genetic mutation is how you get a change in phenotype.

 

[mark kennedy]

Why not?

Even the different alleles that Mendel studied in pea plants were produced by mutations. That's how you get more than one allele, through mutations.

No they were not, they were 7 traits with genes that were either on different chromosomes or far enough apart that they could cross over. As long as you have done this you never learned basic biology.

We can discuss the mutations in pocket mouse Mc1r gene if you want:

The genetic basis of adaptive melanism in pocket mice

Interesting investigation of 4 mutant alleles but nothing conclusive as far as I can tell. You want to get into something substantive try answering a very simple question, Grizzly Bears and Polar Bears are closely related, they can even interbreed. So why is the Polar Bear white and the Grizzly Bear dark. Not the effect, of course there is an advantage to being white in the snow. What is the molecular basis?

Mutations gave rise to a dark fur color that was adaptive for dark basalt rocks. Even more interesting, two different populations of dark mouse evolved dark fur through different mutations. It happened at least twice.

Not really seeing the significance here:

Two different models for Mc1r evolution: (i) a single amino acid difference is responsible for the observed phenotypic differences, and the other amino acid variants have hitchhiked with the selected site, or (ii) two or more amino acid variants (acting additively or epistatically) are required to produce the observed phenotypic differences.​

What I'm getting is the first model that require a single amino acid substitution that is sufficient in lab mice to produce the color change. That doesn't tell me how the substitution happened in the wild mice. What is more that is not how a genetic mutation happens the vast majority of the time, most often when there is a change in the amino acid sequence it usually results in a frameshift:

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

How does the amino acid substitution happen?

Genetic mutation is how you get a change in phenotype.

You are discussing the effect as if it were a viable cause, that's called begging the question. What is the cause?

Have a nice day
Mark

 

[Loudmouth]

No they were not, they were 7 traits with genes that were either on different chromosomes or far enough apart that they could cross over. As long as you have done this you never learned basic biology.

If you have two alleles for a gene, this means that the alleles have different DNA sequences. Guess what produces differences in DNA sequence? Mutations.

Interesting investigation of 4 mutant alleles but nothing conclusive as far as I can tell.

It is very conclusive. Please address it.

The genetic basis of adaptive melanism in pocket mice

Not really seeing the significance here:

Two different models for Mc1r evolution: (i) a single amino acid difference is responsible for the observed phenotypic differences, and the other amino acid variants have hitchhiked with the selected site, or (ii) two or more amino acid variants (acting additively or epistatically) are required to produce the observed phenotypic differences.​

You don't see the significance of mutations producing a beneficial phenotype? Really?

What I'm getting is the first model that require a single amino acid substitution that is sufficient in lab mice to produce the color change. That doesn't tell me how the substitution happened in the wild mice.

The mechanisms of mutagenesis are well understood. Are you denying that mutations occur?

What is more that is not how a genetic mutation happens the vast majority of the time, most often when there is a change in the amino acid sequence it usually results in a frameshift:

That is false. Substitutions are more common than indels. We have shown you this many many times. It also doesn't change the fact that I just showed you that they are substitution mutations. You are trying to deny the facts.

How does the amino acid substitution happen?

A non-synonymous substitution mutation.