Annoying creationists

[Ivor the Engineer]

Are you saying he leaves no room for the co-evolution of social memes? That would seem rather one-sided. Or is he simply saying that our social behavior is ultimately a product of our genes, in that our brains are genetically determined?

~~ Paul

I haven't got the book in front of me now, but he talks about our sexual impulses 'misfiring' when, for example, we (want to) have sex but are using contraception.

I can think of plenty of reasons and ways to have sex that have nothing to do with procreation. While our basic drive and reward systems are genetically determined, what we do to satisfy or activate them evolve separately.

As I understand Dawkins' definition of mimes he gives in the book they are limited to ‘digital’ rather than ‘analogue’ information. The example he provides is a sequence of people teaching the next to fold paper into a certain shape rather than, say, passing on a meaningless message to each other. Perhaps the results of these experiments are more indicative of how our memories ‘work’ than what types of behavior can evolve?

I shall continue reading tonight.

 

[John Hewitt]

This is a silly reply to a perfectly sensible point. Repetitive silliness is not humour and is unlikely impress sensible observers.

As I said, RNA is a chemically labile molecule - it degrades very easily, which is what makes it quite suitable as a messenger RNA. The same property would make it unsuitable as the coding molecule for a replicator.

No RNA molecule has ever been detected that is capable of replicating itself and, as has been discussed at some length, one would not expect such a molecule to emerge by chance - not in this universe at least.

Moreover, making RNA requires precursors - these are chemically complex, energetically activated nucleotides that are not to be expected in primordial environments. Even if such precursors did appear, they would diffuse away in ubounded environments.

There are observers who subscribe to the "RNA world" theory, but that theory is entirely inadequate.

 

[kleinman]

Annoying Creationists

I provided you [Kleinman] with evidence of the development of the insulin superfamily. You now try to evade this evidence by falling back on... abiogenesis

Oscillating goal posts. Nice!

The difference is I see the point Dr Richard is trying to make, he doesn’t see the point I’m making. I acknowledge that there are similarities in genes between different species but Dr Richard is not explaining how these genes arose originally or how these genes transform from one species to the next.

"It is not enough to observe similarities between genetic structures. You must demonstrate how these structures could have arisen initially and how they can transform from one to another. You have done neither"

I say: it is not enough to notice similarities between physics and astronomy. You must demonstrate how these structures could have arisen initially and how they can transform from one to another. You are a loser, Archimedes, Newton, Einstein, Feynman, and you always will be.

If you are going to hold to the position that the theory of evolution is driven by mutation and natural selection, you must demonstrate how this happens. Dr Schneider’s ev computer simulation attempts to do this but reveals that when realistic genome lengths and mutation rates are used in this model, the process is too slow to support your theory.

you don’t have the selection mechanism to transform one gene to another.

Greater leniency is "shown" towards changing the base in the third position of the codon than the other two, as this generally does not change the amino acid coded for. However, occasionally the amino acid will be changed, which may or may not force a conformation change on the protein. If this occurs, I'd wager stabilisation of the protein in this new conformation could very well be considered a valid "selection mechanism" for changing one gene into another by using for example only random point mutation.

Unless the base change is beneficial or detrimental, natural selection can not act upon this mutation.

Feel free to choose any base sequence for the gene you want and then explain the selection mechanism that would evolve that gene from the beginning. If you choose the insulin gene, then let it be the antecedent gene that you propose that gives rise to the insulin gene.

No, Kleinman, you are having some trouble understanding the concept.

You asked how "insulin" could have evolved from the "beginning".

In order to answer your question, I need to know what you mean by "insulin" and "beginning". Why is this so hard for you?

Since you are proposing that insulin is part of a family of molecules that goes back to Zebra fish, explain where the gene/molecule that appeared in the Zebra fish originated, then once you explain that explain where the pre-Zebra fish gene/molecule originated and so on until you arrive at the first gene that coded for this insulin type molecule. Then explain how this first gene that coded for this insulin type molecule evolved and what was the selection process that allowed this. In addition, explain the selection process that occurred as this gene evolved from species to species.

When you do this, you have established the accounting rules that allow you to describe step by step how this family of molecules evolved. Without describing the selection process, you are only noting similarities in molecules which is not sufficient to prove you theory.

Let’s keep the definition for “gene” as general as possible and say that it is a sequence of bases that performs some useful function for the creature. It may be coding for a polypeptide but let it include other possible beneficial function for the creature.

For someone presumably interested in evolutionary debate, the work of Richard Dawkins seems to have strangely passed you by.

Try again for your definition of gene.

Richard Dawkins’ work has not completely passed me by, I have co-opted one of his sayings for this debate.

Life isn't like that. Evolution has no long term goals.

With respects to a definition for “gene”, would the concept of one gene-one polypeptide satisfy you? I happen to prefer a more general definition that any beneficial sequence of bases be used in the concept of mutation and selection since ev models binding sites which is conceivably beneficial to a creature.

The evolution of a gene from the beginning can not be subject to selection until it performs some useful function for the creature.

Wrong, see above

How far above do I have to look? I don’t recall you or any other evolutionarian describing how selection can act unless there is some beneficial or detrimental property to act upon. And that prevents a gene evolving from the beginning with a selection process. Only when the newly evolving gene performs some function can selection act upon that gene. Until then, the frequency of that sequence of bases in the population is not increased.

There is another issue which ev is harbinger of mathematical bad news for evolutionarians. This issue was touched on earlier but now that we are talking about selection processes in more detail, it is worthwhile to address this issue again.

Ev has two error conditions that are being select for. One error is not recognizing a binding site where one should exist (the binding site region) and the other error is recognizing a binding site where one should not exist (the non-binding site region). With short length genomes, errors in the binding site region dominate the selection process and rapid convergence can be obtained. As the genome is lengthened, more potential errors can occur in the non-binding site region and slows the evolution process until finally the genome is lengthened sufficiently that non-binding site region errors dominate the selection process and no convergence can be attained.

What this is indicating that if you have more than a single selection condition, one may interfere with the other. If you have multiple genes evolving, each is responding to their selection pressure (whatever that may be), each is interfering with others preventing any from evolving.

As an example of this concept, let’s consider Dr Richard’s case of the evolution of the insulin family of proteins. At the same time, the globin family of proteins is evolving in the same creatures. What may be an advantageous selection for the insulin family may
in turn be a disadvantageous selection for the globin family of proteins and visa versa. Consider the complications that would arise if you have multiple different families of proteins evolving simultaneously in the same creatures. Each would be interfering with the evolution of the others.

Ev demonstrates this effect mathematically with its two selection conditions. Introducing more selection conditions would only slow this profoundly slow evolutionary process more so.

Again, I thank Dr Schneider and Paul for their good work on the ev computer model.

 

[Paul C. Anagnostopoulos]

As the genome is lengthened, more potential errors can occur in the non-binding site region and slows the evolution process until finally the genome is lengthened sufficiently that non-binding site region errors dominate the selection process and no convergence can be attained.

No convergence? What property causes the information gain to slow down, but then suddenly disappear? (I presume you are not talking about the Rcapacity problem.)

What this is indicating that if you have more than a single selection condition, one may interfere with the other. If you have multiple genes evolving, each is responding to their selection pressure (whatever that may be), each is interfering with others preventing any from evolving.

Why would they necessarily prevent each other from evolving?

Ev demonstrates this effect mathematically with its two selection conditions. Introducing more selection conditions would only slow this profoundly slow evolutionary process more so.

I'd say Unnamed introduced a selection condition and it sped things up. How did you reach this conclusion?

You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.

~~ Paul

 

[Kotatsu]

I acknowledge that there are similarities in genes between different species but Dr Richard is not explaining how these genes arose originally or how these genes transform from one species to the next.

Fortunately for your education, several other people --- including myself --- have already explained this to you. It can occur by random point mutation, insertions, deletions, polyploidization and several other mechanisms, mentionings of which can be found scattered throughout the thread.

Fortunately for your continued mental well-being, you are not required to read and comprehend everything people say, and can easily continue to switch to innocent-ignorance mode whenever a new person enters the thread.

Unless the base change is beneficial or detrimental, natural selection can not act upon this mutation.

Which, while probably true, is beside the point, as your contention was that "we" don't have a selection mechanism with which to transform one gene to another.

I clearly stated that I was talking about a case where a random point mutation in the third codon position caused a change in the amino acid sequence, which in turn caused a conformational change in the resulting protein, which then may have to be stabilised in this new configuration by "allowing" other acids to change. Even if this should prove to be unlikely, it is still a valid selection process with which one gene could be transformed into another.

All cases in which any of the steps which leads to my last point --- that stabilisation of the protein in the new configuration becomes necessary --- are invalid are irrelevant to the point, namely that when all steps are present and stabilisation of the protein does become necessary, a known selective mechanism to transform one gene into another exists.

 

[Kotatsu]

What this is indicating that if you have more than a single selection condition, one may interfere with the other. If you have multiple genes evolving, each is responding to their selection pressure (whatever that may be), each is interfering with others preventing any from evolving.
As an example of this concept, let’s consider Dr Richard’s case of the evolution of the insulin family of proteins. At the same time, the globin family of proteins is evolving in the same creatures. What may be an advantageous selection for the insulin family may in turn be a disadvantageous selection for the globin family of proteins and visa versa. Consider the complications that would arise if you have multiple different families of proteins evolving simultaneously in the same creatures. Each would be interfering with the evolution of the others.

Dear mother of the Empire! Are you allowed to vote?

 

[Dr Adequate]

This is a silly reply to a perfectly sensible point.

No that was me laughing my ass off at someone who claimed that RNA wasn't "suitable material for a replicator".

No RNA molecule has ever been detected that is capable of replicating itself ...

But this is untrue. There are RNA viruses, there is, dammit, Spiegelman's bucket o' chemicals, which we've just been discussing. "Labile" or not, RNA self-replicates given the right environment.

 

[Dr Adequate]

The difference is I see the point Dr Richard is trying to make, he doesn’t see the point I’m making. I acknowledge that there are similarities in genes between different species but Dr Richard is not explaining how these genes arose originally or how these genes transform from one species to the next.

If you are going to hold to the position that the theory of evolution is driven by mutation and natural selection, you must demonstrate how this happens. Dr Schneider’s ev computer simulation attempts to do this but reveals that when realistic genome lengths and mutation rates are used in this model, the process is too slow to support your theory.

Unless the base change is beneficial or detrimental, natural selection can not act upon this mutation.

Since you are proposing that insulin is part of a family of molecules that goes back to Zebra fish, explain where the gene/molecule that appeared in the Zebra fish originated, then once you explain that explain where the pre-Zebra fish gene/molecule originated and so on until you arrive at the first gene that coded for this insulin type molecule. Then explain how this first gene that coded for this insulin type molecule evolved and what was the selection process that allowed this. In addition, explain the selection process that occurred as this gene evolved from species to species.

When you do this, you have established the accounting rules that allow you to describe step by step how this family of molecules evolved. Without describing the selection process, you are only noting similarities in molecules which is not sufficient to prove you theory.

Richard Dawkins’ work has not completely passed me by, I have co-opted one of his sayings for this debate.

With respects to a definition for “gene”, would the concept of one gene-one polypeptide satisfy you? I happen to prefer a more general definition that any beneficial sequence of bases be used in the concept of mutation and selection since ev models binding sites which is conceivably beneficial to a creature.

How far above do I have to look? I don’t recall you or any other evolutionarian describing how selection can act unless there is some beneficial or detrimental property to act upon. And that prevents a gene evolving from the beginning with a selection process. Only when the newly evolving gene performs some function can selection act upon that gene. Until then, the frequency of that sequence of bases in the population is not increased.

There is another issue which ev is harbinger of mathematical bad news for evolutionarians. This issue was touched on earlier but now that we are talking about selection processes in more detail, it is worthwhile to address this issue again.

Ev has two error conditions that are being select for. One error is not recognizing a binding site where one should exist (the binding site region) and the other error is recognizing a binding site where one should not exist (the non-binding site region). With short length genomes, errors in the binding site region dominate the selection process and rapid convergence can be obtained. As the genome is lengthened, more potential errors can occur in the non-binding site region and slows the evolution process until finally the genome is lengthened sufficiently that non-binding site region errors dominate the selection process and no convergence can be attained.

What this is indicating that if you have more than a single selection condition, one may interfere with the other. If you have multiple genes evolving, each is responding to their selection pressure (whatever that may be), each is interfering with others preventing any from evolving.

As an example of this concept, let’s consider Dr Richard’s case of the evolution of the insulin family of proteins. At the same time, the globin family of proteins is evolving in the same creatures. What may be an advantageous selection for the insulin family may
in turn be a disadvantageous selection for the globin family of proteins and visa versa. Consider the complications that would arise if you have multiple different families of proteins evolving simultaneously in the same creatures. Each would be interfering with the evolution of the others.

Ev demonstrates this effect mathematically with its two selection conditions. Introducing more selection conditions would only slow this profoundly slow evolutionary process more so.

Again, I thank Dr Schneider and Paul for their good work on the ev computer model.

Same old lies. See my sig.

 

[kleinman]

Annoying Creationists

As the genome is lengthened, more potential errors can occur in the non-binding site region and slows the evolution process until finally the genome is lengthened sufficiently that non-binding site region errors dominate the selection process and no convergence can be attained.

No convergence? What property causes the information gain to slow down, but then suddenly disappear? (I presume you are not talking about the Rcapacity problem.)

I’m glad you asked. The property that causes the information gain to slow down in ev are the errors in the non-binding site region. Don’t you recall what happens if you ignore the errors in the non-binding site region? I’ll remind you. When you ignore the errors in the non-binding site region and maintain a mutation rate fixed to a number of bases, you uncouple the convergence from the length of the genome. You called this the Rcapacity problem but this is what is happening that slows down and ultimately prevents convergence in ev as you lengthen the genome. Why do you think the Rcapacity problem disappeared with Unnamed’s selection process?

What this is indicating that if you have more than a single selection condition, one may interfere with the other. If you have multiple genes evolving, each is responding to their selection pressure (whatever that may be), each is interfering with others preventing any from evolving.

Why would they necessarily prevent each other from evolving?

Two selection conditions can either slow or prevent evolution if the two selection conditions are not working in harmony. One selection condition can cancel out the effect of the other selection condition. This is exactly what you are seeing in ev. The selection condition that requires no binding sites in the non-binding site region interferes with selection condition that requires you have binding sites in the binding site region. As long as the non-binding site region remains small or the errors in this region are ignored as Unnamed did, you have only the one selection condition, that is you require binding sites in the binding site region and you can attain convergence. If you can imagine some selection condition that allows the morphing of one gene to another, you would have all genes on the genome subject to similar selection conditions. Once you explain what these selection processes are, then you have to explain how all these selection conditions can work without interfering with each other as the two conditions in ev interfere.

Ev demonstrates this effect mathematically with its two selection conditions. Introducing more selection conditions would only slow this profoundly slow evolutionary process more so.

I'd say Unnamed introduced a selection condition and it sped things up. How did you reach this conclusion?

You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.

Unnamed uses the value computed in the weight matrix directly which biased the selection process to the binding site region.

The millions of selection pressures (which you have yet to describe mathematically) can only operate when a creature has something to select for or against. A partially completed gene offers nothing to select for. The transformation of genes from one to another as described by Dr Richard requires that a series of beneficial mutations subject to selection occur without interference from other selection pressures. Even Dr Schneider’s stylized model of random point mutations and natural selection demonstrates why you can’t transform genes because of conflicting selection conditions.

What you can have with mutation and selection are microevolutionary processes such as small changes in genes in microbes that bring about antibiotic resistance or small changes in proteins such as Hemoglobin S which gives benefit to those who live in malaria endemic areas.

Here is a little experiment you can try with ev. Instead of evolving a single set of binding sites, evolve two sets of binding sites with different weight matrices for each. Each set of binding sites will have their own regions on the genome. What do you think will happen to the evolutionary process? You will have three selection conditions, errors in the non-binding site region, errors in the first binding site region and errors in the second binding site region. It would be interesting to see what happens if you ignore errors in the non-binding site region and see what happens when considering only the errors in the two binding site regions.

Unless the base change is beneficial or detrimental, natural selection can not act upon this mutation.

Which, while probably true, is beside the point, as your contention was that "we" don't have a selection mechanism with which to transform one gene to another.

Since your theory of evolution is based on mutation and selection, there is no other point to be made until you describe what the selection mechanism is. A slogan does not constitute a scientific proof.

 

[Dr Adequate]

I’m glad you asked. The property that causes the information gain to slow down in ev are the errors in the non-binding site region. Don’t you recall what happens if you ignore the errors in the non-binding site region? I’ll remind you. When you ignore the errors in the non-binding site region and maintain a mutation rate fixed to a number of bases, you uncouple the convergence from the length of the genome. You called this the Rcapacity problem but this is what is happening that slows down and ultimately prevents convergence in ev as you lengthen the genome. Why do you think the Rcapacity problem disappeared with Unnamed’s selection process?

Two selection conditions can either slow or prevent evolution if the two selection conditions are not working in harmony. One selection condition can cancel out the effect of the other selection condition. This is exactly what you are seeing in ev. The selection condition that requires no binding sites in the non-binding site region interferes with selection condition that requires you have binding sites in the binding site region. As long as the non-binding site region remains small or the errors in this region are ignored as Unnamed did, you have only the one selection condition, that is you require binding sites in the binding site region and you can attain convergence. If you can imagine some selection condition that allows the morphing of one gene to another, you would have all genes on the genome subject to similar selection conditions. Once you explain what these selection processes are, then you have to explain how all these selection conditions can work without interfering with each other as the two conditions in ev interfere.

Unnamed uses the value computed in the weight matrix directly which biased the selection process to the binding site region.

The millions of selection pressures (which you have yet to describe mathematically) can only operate when a creature has something to select for or against. A partially completed gene offers nothing to select for. The transformation of genes from one to another as described by Dr Richard requires that a series of beneficial mutations subject to selection occur without interference from other selection pressures. Even Dr Schneider’s stylized model of random point mutations and natural selection demonstrates why you can’t transform genes because of conflicting selection conditions.

What you can have with mutation and selection are microevolutionary processes such as small changes in genes in microbes that bring about antibiotic resistance or small changes in proteins such as Hemoglobin S which gives benefit to those who live in malaria endemic areas.

Here is a little experiment you can try with ev. Instead of evolving a single set of binding sites, evolve two sets of binding sites with different weight matrices for each. Each set of binding sites will have their own regions on the genome. What do you think will happen to the evolutionary process? You will have three selection conditions, errors in the non-binding site region, errors in the first binding site region and errors in the second binding site region. It would be interesting to see what happens if you ignore errors in the non-binding site region and see what happens when considering only the errors in the two binding site regions.

Since your theory of evolution is based on mutation and selection, there is no other point to be made until you describe what the selection mechanism is. A slogan does not constitute a scientific proof.

It must take you hours to write this trash.

And you still can't get round the facts in my sig.

You poor little man.

 

[The Atheist]

I found the juxtaposition of posts #2362 and #2363 by The Atheist rather amusing.

~~ Paul

Hey, I didn't say there was anything wrong with ad hominem attacks. I wouldn't, would I?

 

[Mercutio]

There go those damned goalposts again

A simple kick, an extra point
Is all, and then we may annoint
The victor in this war of words
Twixt idiots and science nerds

In order for the team to win
The gene producing insulin
Must split the uprights, straight and true,
That's all that Kleinman asks of you.

But wait! The crossbar's much too near
A child could make that kick from here
Precursers shown are not enough--
We need to make the task more tough

And so, I send my best regards
And move the goalposts ten more yards.

The protein superfamily
For insulin in you and me
Is found in other mammals, too
(And rats and mice--why, they have two!)

We'll trace it further, if you wish
To proteins found in zebra fish
(What's cool, you'll see upon reflection--
It fits with natural selection!)

Wait! You'll make that kick with ease
And so, if you'll indulge me, please,
To make the kick that has you winning
Trace the gene to its beginning!

With due respect, and beaming smile,
I'll move the goalposts half a mile.

The crossbar now is but a speck
From here--but maybe...what the heck--
I'll try it, under one condition:
Before I kick--your definition?

Could you define your terms, I mean?
Define "beginning", also "gene"
Your definitions seem to change
If you could narrow down the range--

Wait! The start I want is this--
The gene's abiogenesis!
Or if I think I still might hang
Then trace it back to the Big Bang!

And all the time that I've been talking
Those goalposts, they have kept on walking.

To satisfy my little query
Don't attempt to feed me theory
But, from time itself, condense
The binding, legal evidence.

If insulin evolved, why then
You ought to know precisely when.
Before the gene was well-dispersed
There must be someone who was first.

I want his name (and, you've surmised,
I want it duly notarized!)
If you cannot do that, you fail
And by default, I will prevail!

If lunacy you must defend
The moving goalpost is your friend.

 

[kjkent1]

I’m glad you asked. The property that causes the information gain to slow down in ev are the errors in the non-binding site region. Don’t you recall what happens if you ignore the errors in the non-binding site region? I’ll remind you. When you ignore the errors in the non-binding site region and maintain a mutation rate fixed to a number of bases, you uncouple the convergence from the length of the genome. You called this the Rcapacity problem but this is what is happening that slows down and ultimately prevents convergence in ev as you lengthen the genome. Why do you think the Rcapacity problem disappeared with Unnamed’s selection process?

Two selection conditions can either slow or prevent evolution if the two selection conditions are not working in harmony. One selection condition can cancel out the effect of the other selection condition. This is exactly what you are seeing in ev. The selection condition that requires no binding sites in the non-binding site region interferes with selection condition that requires you have binding sites in the binding site region. As long as the non-binding site region remains small or the errors in this region are ignored as Unnamed did, you have only the one selection condition, that is you require binding sites in the binding site region and you can attain convergence. If you can imagine some selection condition that allows the morphing of one gene to another, you would have all genes on the genome subject to similar selection conditions. Once you explain what these selection processes are, then you have to explain how all these selection conditions can work without interfering with each other as the two conditions in ev interfere.

Unnamed uses the value computed in the weight matrix directly which biased the selection process to the binding site region.

The millions of selection pressures (which you have yet to describe mathematically) can only operate when a creature has something to select for or against. A partially completed gene offers nothing to select for. The transformation of genes from one to another as described by Dr Richard requires that a series of beneficial mutations subject to selection occur without interference from other selection pressures. Even Dr Schneider’s stylized model of random point mutations and natural selection demonstrates why you can’t transform genes because of conflicting selection conditions.

What you can have with mutation and selection are microevolutionary processes such as small changes in genes in microbes that bring about antibiotic resistance or small changes in proteins such as Hemoglobin S which gives benefit to those who live in malaria endemic areas.

Here is a little experiment you can try with ev. Instead of evolving a single set of binding sites, evolve two sets of binding sites with different weight matrices for each. Each set of binding sites will have their own regions on the genome. What do you think will happen to the evolutionary process? You will have three selection conditions, errors in the non-binding site region, errors in the first binding site region and errors in the second binding site region. It would be interesting to see what happens if you ignore errors in the non-binding site region and see what happens when considering only the errors in the two binding site regions.

Since your theory of evolution is based on mutation and selection, there is no other point to be made until you describe what the selection mechanism is. A slogan does not constitute a scientific proof.

Obviously from the above comments, you've determined not to concede any of the prior points, and instead you want to argue all three issue simultaneously, i.e.: (1) ev's performance, (2) development of any new gene and (3) development of the first organism (abiogenesis).

Concerning ev, I think your logic is incorrect. ev slows down using its original selection process, not because the genome is lengthened, but rather because the selection process treats mutations in the non-binding site region as equally non-beneficial to the organism as are mutations which occur in the binding site region. Thus, ev prematurely kills off organisms which in reality would not be less fit (or unfit) as the result of a mutation occurring in a junk-DNA location.

This isn't to suggest that a mutation in the non-binding site region couldn't activate what was just previously a random string of meaningless information, and damage/kill the organism, but no one here has yet quantified the relative benefit/detriment of mutations in the binding site vs. the non-binding site region.

Unnamed's selection mechanism treats random mutations in the non-binding site region as irrelevant to survival, which clearly speeds up evolution. Schneider's original selection mechanism treats random mutations in the non-binding site region as equally relevant to those in the binding site region, which clearly slows evolution.

Neither selection mechanism is substantially realistic, in my opinion, but, it seems to me that Unnamed's mechanism is more realistic than Schneider's original, because if a portion of the gene is junk, it's irrelevant to the organism before a random mutation occurs, and it's reasonable to view it as more often than not irrelevant to the organism after the mutation. This is probably one of the ways that junk DNA regions are formed: as the result of neutral mutations.

I don't think you've carried your burden of proof here, Alan. You need to either describe a realistic selection mechanism, or concede that ev demonstrates a reasonable model of RMNS.

 

[kleinman]

Annoying Creationists

In your dreams you see goal posts moving,
while when awake you see your logic losing.

No selection process to save your theory,
only mathematics that makes you teary.

Change the subject, whine and complain,
because ev’s sending your theory down in flames.

 

[Mercutio]

In your dreams you see goal posts moving,
while when awake you see your logic losing.

No selection process to save your theory,
only mathematics that makes you teary.

Change the subject, whine and complain,
because ev’s sending your theory down in flames.

I see you rhyme as well as you argue.

Well, slightly better. You got one out of three, anyway.

 

[kjkent1]

If here we are by random chance,
then Shakespeare's thoughts are quantum dance.

But, if Bard's words be by design,
then life's a fantasy sublime.

 

[The Atheist]

Haha, it's the inadequate doctor! I was wondering when you'd join the fray. C'mon in and have a seat.

Dear The Atheist,

Would you please get religion. I don't care which one, except not Buddhism, 'cos there are atheist Buddhists. Something theistic.

Scientology maybe? Actually, they may suit you better than me - they have some strange ideas about people with excessively high intellect that I think might strike a chord with you.

Your choice, but I recommend fundamentalist Christianity, you appear to have all the the necessary mental equipment for it.

As do you, by the looks of your posts. I guess we all have that deep down somewhere. Fortunately, I've past that stage. Have you? I'd certainly class people who spend time writing their own version of the bible to be more than a little suspect. Are you a little bit lost? Lacking something in your life? (Other than a personality and a woman, that is.)

But please stop being an atheist. I feel no need of your company.

Fortunately, there is little chance of either of those coming to pass. I don't hang out with overblown intellectuals who suffer from their own inadequacy to the extent that it keeps them awake at night, but I could make an exception. Interesting that despite not needing my company you've chosen to address a post to me. I wonder what you really think. Do you even know yourself?

PS: Like other posters here, I too am beginning to wonder whether you can really be an atheist. But if you are, please stop.

No.

Statements like that do please me no end. I really enjoy the fact that I piss off atheists more than christians. I'm loving the fact that I've been classed as a christian apologist and have at least two genuine geniuses doubting my atheism in the past week. I guess you all get PMS at the same time.

Now you can crawl back into your study and write another poem or two to console yourself with the realisation that ignorant, violent scum are just as likely to be atheists as christians.

Disrespectfully.

The Atheist.

P.S. On a lighter note, you clearly don't have any idea what I'm up to here. Maybe next time, you might consider asking what I'm doing rather than jumping in half-cocked.

P.P.S. If you want to go down the abusive track, I need somthing really clever and vitriolic to add to my sig, so see what you can do.

 

[John Hewitt]

No that was me laughing my ass off at someone who claimed that RNA wasn't "suitable material for a replicator".

No, it was you pretending to a case you cannot make

But this is untrue. There are RNA viruses, there is, dammit, Spiegelman's bucket o' chemicals, which we've just been discussing. "Labile" or not, RNA self-replicates given the right environment.

How many times does the same thing need saying.

RNA does not copy itself. Qbeta is an RNA phage that codes for an enzyme - Qbeta replicase. When that phahge infects a cell, the cell, using its own protein synthetic apparatus, makes that enzyme from the phage RNA acting as a messenger. The RNA is then copied by the enzyme, again making use of the cell's metabolism to provide ribonucleotides. Spiegelman, or whoever, can smash open those cells and chemically isolate that enzyme from infected cells. They can also replace the cell's metabolism with activated ribonucleotides and put the mixture into a test tube. The result is not RNA replicating itself, it is RNA being replicated by an enzyme and the whole thing depends on cells that made the enzyme and quite probably many of the ribonucleotides. Nobody has yet found a piece of RNA that, even under laboratory conditions, can replicate itself without a cell's involvement.
The RNA world theory posits that some piece of RNA can do this lot, not in a laboratory but in a primordial ocean. You believe that if you like but at least try to understand the ideas in which you currently have such blind faith.

 

[fls]

P.S. On a lighter note, you clearly don't have any idea what I'm up to here. Maybe next time, you might consider asking what I'm doing rather than jumping in half-cocked.

Performance art?

Linda

 

[Dr Richard]

In your dreams you see goal posts moving

Wow, Kleinman, I was, perhaps foolishly, prepared to have a discussion with you.

You have repeatedly failed to answer the simplest of questions.

You asked how "insulin" (amongst other genes) could have evolved; I cited you a paper (which you did not even bother to read) that demonstrated this to a point at which I would consider the gene in question not to be "insulin".

This was not enough for you, and I asked you define "insulin". You have repeatedly declined to do so, and moved goalposts so fast I must admit I've given up trying to keep track of them.

It has I feel been worth it however; you claim to have read Dawkin's work, and yet can come out with howlers such as:

With respects to a definition for “gene”, would the concept of one gene-one polypeptide satisfy you? I happen to prefer a more general definition that any beneficial sequence of bases be used in the concept of mutation and selection

My bolding.

Does anything in Dawkin's book "The Selfish Gene" give you any clue as to what is wrong in your assertion? Did you catch the bit where he argues that genes are NOT of necessity beneficial to the creature? That they are... erm... selfish?

(Hint - clue is in the title)

I apologise for trying to have a reasoned discussion with you.

As you have yet to give a reasoned response to Dr Adequate's post, I feel that this thread has obviosly moved into Christophera territory and any further discussion is sadly pointless.