Spearthrower wrote:
What's actually a problem is that your paper shows precisely the opposite, in fact, your paper manages to show one thing and argue the opposite.

If you haven't noticed this yet, you'll soon see by the number of citations you don't get.

LOL. I doubt you even understand what I am talking about. Look at Table 3. When there is complete linkage, ie. when the recombination rate =0, the fixation rate is actually slighly higher. Don't be such a moron as to tell me I don't understand my own data.

Atheistoclast wrote:

Spearthrower wrote:
What's actually a problem is that your paper shows precisely the opposite, in fact, your paper manages to show one thing and argue the opposite.

If you haven't noticed this yet, you'll soon see by the number of citations you don't get.

LOL. I doubt you even understand what I am talking about.

LOL - pathetic.

Atheistoclast wrote:Look at Table 3. When there is complete linkage, ie. when the recombination rate =0, the fixation rate is actually slighly higher. Don't be such a moron as to tell me I don't understand my own data.

I am not a moron, I can read... and I can see you playing the lesser spotted weasel frog's elbow tune too.

This is the paper you told us was going to make a big splash!

Well, I guess it's wet alright, so there's a basis for your claim, even if ridiculously overplayed as usual.


Incidentally, I can see one of my former tutors on the list of reviewers for the journal. That's going to make for an interesting chat over beers next time I go back to the UK.

Atheistoclast wrote:LOL. I doubt you even understand what I am talking about. Look at Table 3. When there is complete linkage, ie. when the recombination rate =0, the fixation rate is actually slighly higher. Don't be such a moron as to tell me I don't understand my own data.

Well, talking about that: If there are two genes with perfect linkage, then they can not have differing selection coefficients. Since the selection coefficient of a gene depends on the mean fitness of carriers vs. the mean fitness of the population any two genes with perfect linkage share the same set of carriers and thus have the same selection coefficient.

susu.exp wrote:

Atheistoclast wrote:LOL. I doubt you even understand what I am talking about. Look at Table 3. When there is complete linkage, ie. when the recombination rate =0, the fixation rate is actually slighly higher. Don't be such a moron as to tell me I don't understand my own data.

Well, talking about that: If there are two genes with perfect linkage, then they can not have differing selection coefficients. Since the selection coefficient of a gene depends on the mean fitness of carriers vs. the mean fitness of the population any two genes with perfect linkage share the same set of carriers and thus have the same selection coefficient.

Of course they can. Linkage just means that the sites (loci) cross over together during recombination. They can experience different mutations with different degrees of selection.

Spearthrower wrote:
This is the paper you told us was going to make a big splash!

Well, I guess it's wet alright, so there's a basis for your claim, even if ridiculously overplayed as usual.

Incidentally, I can see one of my former tutors on the list of reviewers for the journal. That's going to make for an interesting chat over beers next time I go back to the UK.

You just do that. But it's over, Spearthrower. The paradigm has shifted and the Earth has tilted. The theory of evolutionism is spinning out of control. Little by little the wheels are slowly falling off.

Atheistoclast wrote:Of course they can. Linkage just means that the sites (loci) cross over together during recombination. They can experience different mutations with different degrees of selection.

That´s incorrect. Linkage measures the degree to which the presence of one allele is correlated to the presence of another. Perfect linkage is identical to correlation coefficients of 1 or -1. Mutation is one of several processes that lead to changes in linkage and if the loci experience different mutations with different resultant fitness values in different individuals you don´t have perfect linkage. There´s a decay of linkage disequilibrium due to crossovers and this is what Haldanes c deals with. But there´s also a decay of LD due to other factors. If you have a model in which crossovers are the only relevant thing, then c=0 is equivalent to linkage staying stable. If you have other factors, it isn´t.

Atheistoclast wrote:

Spearthrower wrote:
This is the paper you told us was going to make a big splash!

Well, I guess it's wet alright, so there's a basis for your claim, even if ridiculously overplayed as usual.

Incidentally, I can see one of my former tutors on the list of reviewers for the journal. That's going to make for an interesting chat over beers next time I go back to the UK.

You just do that. But it's over, Spearthrower. The paradigm has shifted and the Earth has tilted. The theory of evolutionism is spinning out of control. Little by little the wheels are slowly falling off.

You and your delusional fantasies.

Sorry the real world doesn't conform to them!

Basically, it's: I haz published a paper, therefore I am rite about everyting I evar sed.

Jesus H. Christ on a fucking stick, Joe. You saying it doesn't make it so.

The_Metatron wrote:Jesus H. Christ on a fucking stick, Joe. You saying it doesn't make it so.

Let's be frank - if Joe claimed night was dark, I'd double-check.

Atheistoclast wrote:The theory of evolutionism is spinning out of control.

There's no such thing.

Evolution is an observable fact.
And I don't see how you have proven the theory that explains it here yet.

Thomas Eshuis wrote:

Atheistoclast wrote:The theory of evolutionism is spinning out of control.

There's no such thing.

Evolution is an observable fact.
And I don't see how you have proven the theory that explains it here yet.

Define evolution. If you mean changes in allele frequencies over time, not even the most ardent creationist will dispute this.

However, the evolutionary origination of eyes, limbs, hearts and so on is certainly NOT an observable fact.

I have shown how natural selection has an instinct to conserve at all times and that gene duplicates are not simply free to evolve.

susu.exp wrote:

Atheistoclast wrote:Of course they can. Linkage just means that the sites (loci) cross over together during recombination. They can experience different mutations with different degrees of selection.

That´s incorrect. Linkage measures the degree to which the presence of one allele is correlated to the presence of another. Perfect linkage is identical to correlation coefficients of 1 or -1. Mutation is one of several processes that lead to changes in linkage and if the loci experience different mutations with different resultant fitness values in different individuals you don´t have perfect linkage. There´s a decay of linkage disequilibrium due to crossovers and this is what Haldanes c deals with. But there´s also a decay of LD due to other factors. If you have a model in which crossovers are the only relevant thing, then c=0 is equivalent to linkage staying stable. If you have other factors, it isn´t.

You are confusing recombination with mutation. Two loci can be linked and have completely different types of mutation with entirely different selective effects.

Joe, it would be great if you could respond to my earlier post:

http://www.rationalskepticism.org/creat ... l#p1209147

Atheistoclast wrote:I have shown how natural selection has an instinct to conserve at all times and that gene duplicates are not simply free to evolve.

Where?

Made of Stars wrote:Joe, it would be great if you could respond to my earlier post:

http://www.rationalskepticism.org/creat ... l#p1209147

OK:

This sounds like a belief statement. Do you have any supporting evidence that bacterial genes that are shared by vertebrates have 'succumbed to (neutral) mutational pressures'?

Just compare a gene like transaldolase for bacteria and humans. You can easily see that the gene has evolved neutrally with some changes inevitably being made because of the constant mutation rate.

[quotep
What do you mean "go beyond this"? This is evolution in action. Can you not see that being able to access a new leaf-based diet could have a profound impact at an organismic and ultimately a population level?[/quote]

What I am saying is that an RNASE gene cannot evolve into anything other than an RNASE gene. Sure, RNASE1B is an interesting example of an adaptation facilitated by (degenerative) evolution, but it is just a variation on the same theme. For the broader theory to be true, duplicates have to be able to evolve distinctly new functionality. A modification of a modification isn't going to result in anything really novel.

Shrunk wrote:

Atheistoclast wrote:I have shown how natural selection has an instinct to conserve at all times and that gene duplicates are not simply free to evolve.

Where?

In Tables 3 and 4 of the paper. You might want to look at them.

Atheistoclast wrote:

Made of Stars wrote:This sounds like a belief statement. Do you have any supporting evidence that bacterial genes that are shared by vertebrates have 'succumbed to (neutral) mutational pressures'?

Just compare a gene like transaldolase for bacteria and humans. You can easily see that the gene has evolved neutrally with some changes inevitably being made because of the constant mutation rate.

How does this show how the gene has 'succumbed'.

Your writing here is laced with value statements that betray that you're just looking for facts to back up your position, rather than letting the facts take you where they lead. For example,

Atheistoclast wrote:

Made of Stars wrote:What do you mean "go beyond this"? This is evolution in action. Can you not see that being able to access a new leaf-based diet could have a profound impact at an organismic and ultimately a population level?

What I am saying is that an RNASE gene cannot evolve into anything other than an RNASE gene. Sure, RNASE1B is an interesting example of an adaptation facilitated by (degenerative) evolution, but it is just a variation on the same theme. For the broader theory to be true, duplicates have to be able to evolve distinctly new functionality. A modification of a modification isn't going to result in anything really novel.

What is 'degenerative' evolution? 'Degenerating' from what? A 'perfect creation'?

The mutation provided a 'distinctly new functionality' - in the example you cite, accessing a new diet. How is this 'degenerating'? You seem to be applying some sort of sliding scale where novel functionality is not novel enough unless the gene has a new name.

It's great to be skeptical, but you're not being skeptical, just looking for data points to support your presupposition.

Atheistoclast wrote:You are confusing recombination with mutation. Two loci can be linked and have completely different types of mutation with entirely different selective effects.

Nope. You are confusing linkage with not being seperated by crossing over events. That is a precondition for perfect linkage, but not in itself sufficient. The coefficient of linkage disequilibrium D is defined as
D:=pABpab-pAbpaB (for a 2 locus/2 allele each situation), where pxy is the frequency of xy individuals in the population.

Thomas Eshuis wrote:

Atheistoclast wrote:The theory of evolutionism is spinning out of control.

There's no such thing.

Evolution is an observable fact.
And I don't see how you have proven the theory that explains it here yet.

It's just Atheistoclast's pipe dream, a vain fantasy that not only is this upstart contradiction to his religious beliefs massively supported by evidence and widely accepted as the most useful model in biology, but also that he, the great Joe, will be the man to bring it down by any means.

You've not experienced the ravings we've had over the years from Joe to understand quite what it means to him. It's beyond obsession.

Atheistoclast wrote:

Thomas Eshuis wrote:

Atheistoclast wrote:The theory of evolutionism is spinning out of control.

There's no such thing.

Evolution is an observable fact.
And I don't see how you have proven the theory that explains it here yet.

Define evolution. If you mean changes in allele frequencies over time, not even the most ardent creationist will dispute this.

However, the evolutionary origination of eyes, limbs, hearts and so on is certainly NOT an observable fact.

I have shown how natural selection has an instinct to conserve at all times and that gene duplicates are not simply free to evolve.

Err, no you haven't.