Darwin and Mendel

[Vaccine]

You are the one claiming that the observed processes of mutation can not produce those changes. You going to step up and prove it?

The burden of proof is on the people who say random mutations account for those 3 new genes. It's like you're asking for proof someone can't walk from California to Hawaii. While that may be logically possible it's not reasonably feasible. It may be logically possible random mutations caused the 3 new genes, but nobody has shown how it is reasonably feasible. It requires a great deal of faith to believe random mutations explain those new genes.
To me, an intentional directed cause is easier to believe than random mutations.

 

[Vaccine]

If genetics is a code, then so too is the rest of chemistry. The code for oxygen can be spelled like this

That code would be compiled and interpreted by a human. In other words it's a man-made code. The universal genetic code is encoded and decoded within a cell. It has syntax and grammar, comprised of codons, introns and exons. It is indeed a code. You don't find a code in nature and assume it happened by chance natural processes.

That's exactly what the pocket mouse example deals with. It is a change in a protein which changes the regulation of a gene.

The genetic basis of adaptive melanism in pocket mice

What does adaptation of an existing circuit have to do with the origin of gene regulatory circuits?

I guess it doesn't bother you that according to evolution mutations are supposed to be blind to need, but that paper shows otherwise.
It seems you've only complicated things by showing a built-in level of complexity not anticipated by Darwin's theory.

 

[USincognito]

Think about it, the Ark touches down about 4,000 years ago and from that barge emerged the common ancestors of all mammals, birds and reptiles. Now there are anywhere from 2 to 60 million species, depending on how you define species. Don't you think maybe they evolved?

Cool! Mark accepts that whales, dolphins, sea turtles, penguins. etc. evolved from terrestrial species. And in about 100-300 years no less.

 

[sfs]

Talk origins has a list of so-called "beneficial" mutations but beneficial and gain of function mutations are not the same thing.

I know. Since we were discussing beneficial mutations, not gain of function mutations, I'm not sure why you bring the latter up. How about we settle one question before we start on another. Do you agree that beneficial mutations have been observed or not?

Got any examples of mutations causing a completely new function that didn't exist before?

Yes, but first we'd better settle the question under debate.

I didn't see where he made that assumption:
"all nucleotide sites have selection coefficients within this range"

You mean this sentence: "If substitutions at 10% of all nucleotide sites have selection coefficients within this range"? Leaving out the "if" makes a bit of difference to the meaning of the sentence, no? He's saying that, if his model is correct, there's an issue that needs to be understood. I'm questioning his model. Clear?

As for where he makes that assumption, he makes it when he treats the deleterious mutation rate as being independent of the population's fitness. In a more realistic evolutionary model, populations do indeed arrive at a state where there are many very slightly deleterious mutations that can't be weeded out by selection: it happens when the population size has decreased. (Similarly, the number of mildly deleterious alleles decreases when population size increases.) After such a decrease (and all other things being equal), the number of deleterious alleles in the population will increase. As it does, however, the deleterious mutation rate drops, since there is a smaller target remaining unmutated, and the rate of compensating mutations increases.

I think other shortcomings to his analysis may be more serious, however. First, while he does allow for the possibility of soft selection (not in his model, but as a way of evading the problem seen in the model), his model of soft selection is more attractive mathematically than it is a good representation of common kinds of soft selection; specifically, it is not represent competition for resources or mates. More generally, I am quite dubious about making any kind of meaningful comparison between the fitness of populations millions of years apart. It's quite possible for a later population to have far more mildly deleterious alleles and still have greater absolute fitness (i.e. be able to sustain a larger population size) than an earlier ancestor, since the two populations are likely in different environments and may be filling quite different ecological niches.

I think it comes down to whether you believe beneficial mutations outnumber deleterious mutations or not. I think his model is correct because there are more deleterious mutations then beneficial mutations.

I'm quite certain that there are more deleterious mutations than beneficial ones. That has no bearing on my problems with the model. I'm quite doubtful that there are many more deleterious than beneficial mutations with selection coefficients (s) less than 10[sup]-7[/sup], and I think the number of compensatory mutations with s in the range of 10[sup]-5[/sup] - 10[sup]-7[/sup] is larger than he supposes.

Another example of using the micro- to infer the macro-. We can jump a foot so given enough time we can jump 30 foot. Those positive selections did not produce a new species so there was no violation of genetic homeostasis.

I said nothing at all about macroevolution. For me, genetic homeostasis simply means stabilizing selection. If you have some other process in mind, please spell it out.

 

[Loudmouth]

The burden of proof is on the people who say random mutations account for those 3 new genes.

We observe DNA recombination occuring through natural processes. Do we have to prove that every lightning strike is a natural occurence in order to disprove Zeus?

It's like you're asking for proof someone can't walk from California to Hawaii.

We observe gene duplication through natural processes.

It requires a great deal of faith to believe random mutations explain those new genes.

It's the same amount of faith needed that a new lightning bolt is the product of natural causes just like the ones that have been directly observed.

 

[Loudmouth]

That code would be compiled and interpreted by a human. In other words it's a man-made code.

So is ATCG.

The universal genetic code is encoded and decoded within a cell.

Yes, in the same way as the orbital code is encoded and decoded in molecules. It is no different.

It has syntax and grammar, comprised of codons, introns and exons. It is indeed a code.

DNA lacks abstraction, so it lacks syntax and grammar. Nice try though.

You don't find a code in nature and assume it happened by chance natural processes.

You don't assume that a code in nature is the creation of an intelligence, either. You need evidence. In the case of DNA, we have evidence that natural processes have produced the genomes we see today.

What does adaptation of an existing circuit have to do with the origin of gene regulatory circuits?

If the circuit existed before, then why weren't the mice black? Obviously, you need a new circuit.

I guess it doesn't bother you that according to evolution mutations are supposed to be blind to need, but that paper shows otherwise.

It shows no such thing.

 

[mark kennedy]

Cool! Mark accepts that whales, dolphins, sea turtles, penguins. etc. evolved from terrestrial species. And in about 100-300 years no less.

Sure, that one never really gave me any serious problems. The one thing that really had me puzzled when this first dawned on me was the logistics. I don't think there is a serious difference between Darwinism and Creationism, except for the time line and of course Darwinians reject God as even the designer, let alone creator.

Your leaving out a lot of head trip problems from the Creationist perspective and I have always been confused why it's the Creationists who argue against evolution, it really should be the other way around.

 

[mark kennedy]

How far do you think the Dunning-Kruger effect will get you?

Oh hi professor, glad to see your still milling around the place. So you still think I'm too ignorant to know how ignorant I am, that hurts. It would really be nice if every once in a while you would resort to some of the knowledge you have of how adaptation really works instead of treating all Bible believing Christians as if they were mentally ill.

All satire aside, what do you think turns arctic wildlife fur white?

 

[mark kennedy]

DNA lacks abstraction, so it lacks syntax and grammar. Nice try though.

Here's the syntax for protein coding genes. As much time as you spend arguing for and from science I wonder how you manage to miss the fundamentals so often and so badly.

CONSTANTS & EQUATIONS

Be seeing you....

 

[mark kennedy]

That has always been an argument for design for me, something in the genomic mechanisms was triggered by the arctic cold. It happened across too many species for it to be random, there must be an adaptive mechanism.

That's simply a story you made up -- it has no connection to the biological data. For example, as humans migrated away from the tropics, their skin got lighter in color. We know the change was the result of changes to their DNA, because we've looked at the DNA. We know that many of the changes are different in different populations (specifically, different in Europe than in East Asia). We know that each of these new genetic variants started as a single copy on a single chromosome -- in other words, as a mutation -- because all copies share an identical genetic background.

This isn't a mystery; it's bread and butter genetics.

Just made it up huh?

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)​

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. 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. 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. Your going to write that off as a random mutation with a beneficial effect? I'm a little fuzzy on the logic here, isn't there supposed to be a cause as well as an effect?

Grace and peace,
Mark

 

[Loudmouth]

Here's the syntax for protein coding genes.

That's not syntax. That is hydrogen bonding between mRNA and tRNA's. No syntax. No abstraction. Just chemistry.

 

[Loudmouth]

It seems rather odd that you are so sure about human brain evolution, even though you haven't a clue how it's possible,

It is the 40 million mutations that separate humans and chimps that make it possible.

 

[mark kennedy]

That's not syntax. That is hydrogen bonding between mRNA and tRNA's. No syntax. No abstraction. Just chemistry.

No that's the molecular structure of amino acids and again, with all your pseudo-scientific double talk you still can't get the basics straight.

 

[Loudmouth]

No that's the molecular structure of amino acids and again, with all your pseudo-scientific double talk you still can't get the basics straight.

What is the molecular structure? Show me.

Added by edit:

Can anyone see an A, U, G, or C in this picture? What about a "methionine" or a "Met"? I don't see them.

 

[mark kennedy]

It is the 40 million mutations that separate humans and chimps that make it possible.

You mean the 40 million differences including 40,000 differences in the protein coding sequences and 5 million of those differences come to 90 million base pairs and that's just the direct sequence comparison, some of them over a million base pairs in length of the 71% that diverge they average 2 base pairs per protein coding gene or one per lineage. .

I'll tell you what I think, I think your just contradicting creationists for the kudos, you obviously don't care enough about science to learn something about it. Just can't seem to understand something as basics straight can you?

It's called a frameshift and That is what usually results from a mutation in a protein coding gene.

Have a nice day
Mark

 

[Loudmouth]

You mean the 40 million differences including 40,000 differences in the protein coding sequences and 5 million of those differences come to 90 million base pairs and that's just the direct sequence comparison, some of them over a million base pairs in length of the 71% that diverge they average 2 base pairs per protein coding gene or one per lineage. .

Yep, those would be the ones.

I'll tell you what I think, I think your just contradicting creationists for the kudos, you obviously don't care enough about science to learn something about it. Just can't seem to understand something as basics straight can you?

What basics am I getting wrong?

Let's start with the basics of ERVs in the human and chimp genomes. How many ERV's are there in the human genome?

This is what usually happens with a mutation in a protein coding gene

What usually happens?

Added by edit: Since when do substitution mutations cause frame shifts?

 

[mark kennedy]

What is the molecular structure? Show me.

Added by edit:

Can anyone see an A, U, G, or C in this picture? What about a "methionine" or a "Met"? I don't see them.

Here it is again:

Its the Codon chart and amino acid symbols

Methionine (/mɛˈθaɪ.ɵniːn/ or /mɛˈθaɪ.ɵnɪn/; abbreviated as Met or M)[3] is an α-amino acid with the chemical formula HO2CCH(NH2)CH2CH2SCH3. This essential amino acid is classified as nonpolar. This amino-acid is coded by the initiation codon AUG which indicates mRNA's coding region where translation into protein begins.​

Methionine

Those are the codons LM, still can't get the basics straight, whats really sad is you probably don't know any better and the people who do never correct you no matter how wrong you are. Very sad indeed.

 

[mark kennedy]

Yep, those would be the ones.

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.

What basics am I getting wrong?

You haven't gotten one right yet.

Let's start with the basics of ERVs in the human and chimp genomes. How many ERV's are there in the human genome?

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.

What usually happens?

A frameshift

Added by edit: Since when do substitution mutations cause frame shifts?

I said mutations, period, nice try but the convoluted semantics shell game isn't going to change the basic errors in your posts. They used to be in every argument but apparently your now making them with virtually every statement. 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.

 

[Loudmouth]

Here it is again:

Its the Codon chart and amino acid symbols

Yes, those are man made symbols. They do not exist in the actual molecules.

Those are the codons LM, still can't get the basics straight, whats really sad is you probably don't know any better and the people who do never correct you no matter how wrong you are. Very sad indeed.

Where did I say they weren't codons?

What I said is that the real molecules are not made up of English characters as you are trying to pretend.

The reason that an AUG results in a methionine on the elongating protein is because of the chemistry between the molecules, not because of some language driven syntax. It is due to the chemical binding between the mRNA and tRNA.

 

[Loudmouth]

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.

Prove that they are devastating to the genome.

Yet another claim you can't back.

You haven't gotten one right yet.

Which ones have I got wrong?

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

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 am not seeing a number.

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

A frameshift

Added by edit: Since when do substitution mutations cause frame shifts?

[/QUOTE]

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

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.

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.