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Punctuated Equilibria theories


bumab
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___Well, I just read the first five pages of posts, then skipped to the end to post. The problem I have is the use of terms "random" & "likely" which pepper this discussion. In view of chaos theory, these references are meaningless. Posts use "random" to mean no recognizable pattern, & in fact there is pattern to everything recognized or not.

___Any argument stilted up on probability is fundamentally faulted.

___PE is a fascinating topic & as someone pointed out early on in this thread, the jury is still out. Still out. ;)

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...Allopatric speciation explains how those mutations stick around (i.e. are not dilluted out of the gene pool), but not how those mutations come to be....
Well, the core thesis of allopatric speciation is that the liklihood of expression of recessive alleles rises in a small popualtion. This is just the arithmetic.

 

The open issue is what the recessive alleles actually do. You hypothezied that they increased the rate of mutation. I hypothesizxed that they initiation expression of new features of the genome that were not previously expressed in genes, i.e., that the recessive alleles generate new genes based on existing "metagenetic" information.

 

But I still think that gradualism via mutation if more like hope than science.

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___Well, I just read the first five pages of posts, then skipped to the end to post.
I would like to reference my post #44 in response to the point following.
...Any argument stilted up on probability is fundamentally faulted....
I agree that probabilistic arguments are not proofs, but they certainly can be used to draw inferences.

 

I think the evidence in support of mutation-based Gradualism is specious. The rare cases where Gradualism looks likely do not suggest and particular mechanism.

 

The mechanism underlying PE is certainly conjecture, but I see no reason to look for two mechanisms when one might suffice. I suspect that whatever the biochemical mechanism is that reflects itself in PE is the same one that occasionally shows up as Gradualism.

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I would like to reference my post #44 in response to the point following.I agree that probabilistic arguments are not proofs, but they certainly can be used to draw inferences.

 

___I beg to differ & say they are misused to draw false inferences. Again, all of probability is based on 1 assumption, ie. equal likelyhood, or fairness. Chaos theory (& quantum mechanics for that matter) show there is no such equality, therefore all of probability theory is wrong. Flat wrong. Is it used extensively? Yes. Is in encouched in the robes of authority ? Yes. Is it right? No. It is wrong.

 

__Now where does the logic take you when you begin with a false proposition, no matter how long the argument to follow? That's right. ;)

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...I beg to differ & say they are misused to draw false inferences...
Sure. But you acknowledge the inference, and then use experimental design to support the inference.

 

Chaos theory does not preclude probabilistic analysis. It can sometimes preclude prediction of outcome or cloud identification of causality.

 

One shouldn't throw out all mathematical analyses because chaos obscures a portion of them. Heavens, where would relativity, quantum mkechanics or string theory be without math?

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Like Bumab said, go away for a few days... Finally caught up, and Bio, I now understand where you're coming from and why you believe what you believe. You need a major refresher course on applied probability: your mathematics in post #44 is worthy of Demski! You're doing probability without any application of Baysian Prior Probabilities, and assuming that mutations are entirely random. Actually *because* of the fact that you note that you need many hundred neucleotide pairs to make up a useful exon in a gene, its unlikely that this works if the creation of these sequences is *entirely* random, but its *not*! Random genetic sequences will mutate, existing replication mechanisms will in many cases get rid of bad ones, but many are left and *because* of the selective process that *leaves* many mutations around, the "random" process will *highly* favor sequences that may prove viable. In addition, we're finding that the replication process of RNA in itself includes introns (unused junk sequences) in the replication process and there are other introns that work to increase their numbers, hidden, but contributing to the foreward movement of the evolution of the genes. (See "The Alternative Genome" in the April 2005 SciAm for some of this (not related to Evolution))

 

Moreover, you seem to be really stuck on the notion that any change to these junk sequences that is incremental *must* be "Gradualist dogma". The notion that the changes build up in non-coding sequences--corrected all the while by the existing mechanisms to make them potentially viable--that are switch to active exons seems to be abhorent to you, but I really don't understand why. It *does* explain major, rapid changes, and under stress *many* different newly expressed genes could be tried in an explosive frenzy, and in a harsh environment, only some will survive. You haven't really explained why this scenario is so hard to accept.

 

Bottom line: if you got away from the fallacy of the mutations working on *purely random* mechanisms, you'd see that its possible to create viable new genes--not just random mutations of sub-sequences of neucleotides--much more easily than your fallacious math would indicate. And if you could get away from your "if its at all gradual its dogma and must be rejected" dogma (!) it might be easier to see some alternatives, rather than insist that your rather unlikely theory (everything was all precoded in the beginning), is the *only* logical conclusion.

 

Honestly Bio, I think you're being a bit more heretical than you need to be, but I know you have fun doing it! ;)

 

What-Me-Dogmatic?

Buffy

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...You need a major refresher course on applied probability: your mathematics in post #44 is worthy of Demski! You're doing probability without any application of Baysian Prior Probabilities, and assuming that mutations are entirely random.
First, thanks for comparing me to Dembski. He is a mathemetition: I certainly am not. The misapplication of Bayes in the context of intracellular biocmemical mechanics is probably the best example of hope over reason. Sure, you could find some theoretical cases where incremental permutations (either of nucleotides or of proteins) are incrementally valued (and hence "perferred" ) but the vast, vast majority of cases are clearly not in this category. Ergo, the majority of phenotypical improvement would have to be incurred by a random process if it was based on mutation. That is, of course, unless the "mutation" was previously specified in the nucleotide sequence as "more likely". I think you agree with that much. My point is that the plethora of incremental improvements are not only more likely, they are MUCH more likely. If they are much more likely, why not acknowledge that the parent species code has a propensity for the daughter species code? That is all I did. It is actually the obvious conclusion, given our current state of biochemical knowledge.
...Random genetic sequences will mutate, existing replication mechanisms will in many cases get rid of bad ones, but many are left and *because* of the selective process that *leaves* many mutations around, the "random" process will *highly* favor sequences that may prove viable.
Did you read your own text here? You are identifying a "selective" process that retains sequences that will "prove viable" in the future. Where did that information in the retention mechanism come from? You are agreeing it was already in the parent species genetic code.
In addition, we're finding that the replication process of RNA in itself includes introns (unused junk sequences) in the replication process and there are other introns that work to increase their numbers, hidden, but contributing to the foreward movement of the evolution of the genes.
Yet another example of violent agreement. Where do you suppose the biochemical service that drove introns to create more introns was specified?
...you seem to be really stuck on the notion that any change to these junk sequences that is incremental *must* be "Gradualist dogma". The notion that the changes build up in non-coding sequences--corrected all the while by the existing mechanisms to make them potentially viable--that are switch to active exons seems to be abhorent to you, but I really don't understand why.
There is nothing abhorrent about it. It is only that the evidence for incrementalism-via-mutation is completely absent. You keep referencing something about randomness, and then offer that the outputs are "corrected to make them potentially viable". If you just take out any reference to random mutation, then we agree. Do keep in mind that the evidence for random mutation in this context is essentially zero. Why bother to contend that an unnecessary mechanism is present if there is no data to support it?
It *does* explain major, rapid changes, and under stress *many* different newly expressed genes could be tried in an explosive frenzy, and in a harsh environment, only some will survive. You haven't really explained why this scenario is so hard to accept.
Have I explained it now? You have acknowledged that there are a number of genetically defined mechanisms that generate new, previously unavailable codon sequences. Why would you hypothesize an intermediate "random mutation" step if there is little evidence for it?

 

Everything you offered here supports that the daughter species code was substantially driven by preexisting genetic code in the parent species. Nothing you have offered here suggests any value in some sort of intermediate mutation step. Why contend that the mutated intermediate ever happened?

...if you got away from the fallacy of the mutations working on *purely random* mechanisms, you'd see that its possible to create viable new genes--not just random mutations of sub-sequences of neucleotides--much more easily than your fallacious math would indicate.
...and if you just dropped the notion that mutations were required to give the genetic mechanism something to "steer", you would be further ahead.
...rather than insist that your rather unlikely theory (everything was all precoded in the beginning), is the *only* logical conclusion.
I don't thik I said it was the "only" logical conclusion. I said it was the simplest one. In your examples, how many species-generations back did the genetic service to "select" for "potentially viable" genes exist? Or did this mechanism "mutate" into existence too? How about the intron multiplication mechanism? Wouldn't this have had to have been in the prokaryote in order for the fraction of non-coding DNA to have risen from less than 10% in the prokaryote to about 98% in humans?

 

Why are you hung up on the occurrence of mutations in speciation?

 

...And I am have a lot of fun with this.

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Ergo, the majority of phenotypical improvement would have to be incurred by a random process if it was based on mutation.

 

I think the point was in the coding genome, mutations are usually deleterous, thus suppressing change. But in the introns, mutations can proceed apace since there's no outward effect. Thus, they can accumulate and be expressed en mass at some time in the future. The mechanism for this expression, however, is unknown. That's gradualism, and your math doesn't apply.

 

 

My point is that the plethora of incremental improvements are not only more likely, they are MUCH more likely.

 

Why assume they are improvements? Randomly, improvements would persist, negitive mutations would not. After an extinction event, far more will be viable (improvements). Why go beyond this random model?

 

You keep referencing something about randomness, and then offer that the outputs are "corrected to make them potentially viable". If you just take out any reference to random mutation, then we agree.

 

It's an arugment over mechanism. Burden of proof is on Bio, since gradual change in the genome is an established fact. That's how we date species, for goodness sake.

 

Everything you offered here supports that the doughter species code was substantially driven by preexisting genetic code in the parent species. Nothing you have offered here suggests any value in some sort of intermediate mutation step. Why contend that the mutated intermediate ever happened?

 

I'm confused how you made this conclusion. Mutations are the only established way to change the genome, and they do. You've postulated that there is some other mechanism, based on parental coding. That's an alternative explanation, not a criticsm of the older model.

 

Perhaps I'm still confused on a possible mechanism for your theory, Bio.

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...But in the introns, mutations can proceed apace since there's no outward effect. Thus, they can accumulate and be expressed en mass at some time in the future. The mechanism for this expression, however, is unknown. That's gradualism, and your math doesn't apply.
Sure the math applies. If the introns (or more correctly, the codon sequence with the intron and the future exon) are essentially random, there would need to be a mechanism to steer the intron/exon sequence toward viability. That cannot be mutation and natural selection, since there is no phenotypical expression to "naturally" select for a viable alternative. Ergo, the "selection" is part of the genome.
Why assume they are improvements? Randomly, improvements would persist, negitive mutations would not.
"Improvements" only persist in the mutation model if there is some pressure for retention based on expressed phenotype. In our examples, there is no phenotypical expression to act as a basis for natural selection. Both of you (Buff, Bumab) are hypothesizing EXACTLY the same mechanism that I am , execpt you keep insisting that mutations create the fodder upon which a genetically determined selection mechanism can act. I am merely suggesting that there is ABSOLUTELY NO EVIDENCE for a mutation-based activity to provide the fodder.
It's an arugment over mechanism. Burden of proof is on Bio, since gradual change in the genome is an established fact. That's how we date species, for goodness sake.
I should openly acknowledge here that I need to increase specificty of my argument. The issue is not with Gradualism per se, but Gradualism based on serial mutation. My suggestion is that serial mutation is not the mechanism. I suggest that Gradualism is based on pre-existing genomic direction. Both of you have agreed that there are biochemical services that select for downstream genes that are more likely to be viable. If those selection processes predate phenotypic expression, there would be no opportunity for any flavor of natural selection to assist. Ergo, the Parent species genes estblished the likely outcomes for the daughter species genes. Where is there any evidence for mediation via mutation? Anyone?
...Mutations are the only established way to change the genome, and they do. You've postulated that there is some other mechanism, based on parental coding. That's an alternative explanation, not a criticsm of the older model....
My point is that mutations are not established as the mechanism, they are postulated. The more we uncover complex biochemical services that "steer" code toward viability, the more we should ask the question whether mutations play any material role at all. Remember, we are not discussing whether mutations occur. We are asking whether they play a role in speciation. To my knowledge, there is absolutle no data to support that mutations play a role, and there is a lot to suggest that they are completely unnecessary.

 

It is just that the implications of the obvious conclusion are troublesome to some.

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The more we uncover complex biochemical services that "steer" code toward viability, the more we should ask the question whether mutations play any material role at all.

 

But change does occur. That CHANGE is usually considered from mutation. Whether it's steered randomly or not is the question. I think we were all talking past one another!

 

 

Remember, we are not discussion whether mutations occure. We are asking whether they play a role in speciation. To my knowledge, there is absolutle no data to support that mutations play a role, and there is a lot to suggest that they are is completely unnecessary.

 

Partially. There is evidence that mutation as a simple process cannot equate to the PE we see in the fossil record. That could mean two things: There is another mechanism- your way, or mutation rates increase suddenly and dramatically- my way.

 

You keep saying mutations can't cause cumulative, effective change. Then what can? It's all encoded ahead of time, so there's no real change overall. Then a simple test would be looking for genes for wings in our introns. If there isn't any, then two things could have happened- they were never there, or they changed. Either one invalidates your idea, right?

 

I'm still conviced a more likely explanation for PE is a genetic code that increases the rate and severity of mutations after a cataclysm. There's no direction here, it's still a fundamentally random process (although there are some mutations that are more likely then others). Regardless, it requires no information loading.

 

It is just that the implications of the obvious conclusion are troublesome to some.

 

True. Doesn't bother me, but it's not the inevitable conclusion yet.

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Bio, you are arguing again that changes must be "preferred" in order to survive. As Bumab points out and as I think I was saying too, changes *do not* have to be selected for immediately, rather as I understand it the mechanisms for self correction *remove* the dangerous changes but *leave* the good or *indifferent* changes. This process does in fact make the probability computations that you and Dembski use completely irrelevant (and I don't think being compared to Dembski should be considered a compliment! ;) ). And its the *indifferent* changes, driven by mutation, that cause morphological changes over time. They are changes to existing code that is already "correct", and it has no correlation to "random changes to random sequences that improbably come together." Why you don't see this is lost on me, and in my book if you understand that you've put the cart before the horse on the issue in the first two sentances of this post, then you can't help but come around to the notion that random mutations can and do move things forward, and this is a much simpler explanation than "every animal that has ever existed or will exist was precoded in the first prokaryote." ;)

 

Cheers,

Buffy

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But change does occur. That CHANGE is usually considered from mutation.
I agree that they are "usually considered" to be from mutation. That is the problem.
... mutation as a simple process cannot equate to the PE we see in the fossil record. That could mean two things: There is another mechanism- your way, or mutation rates increase suddenly and dramatically- my way.
I have no problem with your hypothetical increase in mutation rate, but I don't think it addresses the mathematical burden. In our intron/exon discussion above, the "randomly mutated" intron/exon base sequence is still reengineered to steer toward viability in order to hasten change. If we have a steering mechanism to identify the target gene, why would we reasonably assume that it is working on a randomly mutated source sequence? Is there any evidence for that? Isn't it simpler (in the Ockham's razor sense) to assume that the engineering of the target gene is based on preexisting code rather than on mutation?
You keep saying mutations can't cause cumulative, effective change. Then what can? It's all encoded ahead of time, so there's no real change overall. Then a simple test would be looking for genes for wings in our introns. If there isn't any, then two things could have happened- they were never there, or they changed. Either one invalidates your idea, right?
What would you look for in the wings of the introns that we have not already found? We have found :

  1. Introns that act as a gene that codes for proteins other than the "main" protein of the gene (e.g., "nested" genes}
  2. Introns that assist in chromosome crossover, apparently even "ectopic" crossover that results in new and deleted genes
  3. Introns that are both included and not included in the mRNA transcription, hence result in alternative splicing of the mRNA, ergo multiple proteins fromt the same gene
  4. Introns that assist in "frame shifting", again resulting in an alternative live functional protein from the same gene (and what are the odds of that?)

What else could we find to add to the case that the non-protein coding portions of DNA are inextricably linked to current cell function and to creation of genotypical variety?

I'm still conviced a more likely explanation for PE is a genetic code that increases the rate and severity of mutations after a cataclysm. There's no direction here, it's still a fundamentally random process (although there are some mutations that are more likely then others). Regardless, it requires no information loading.
It is true that the mutative model gets around the information load issue. It is just that the evidence does not support it, and the weight of information load in steadily increasing every year anyway. I am just extrapolating based on what we have demonstrated over the last 50 years since Watson and Crick described DNA. Every time we find out more, it gets more complicated.

 

We have hundreds of examples of mutations causing genetic dysfunction. We have no examples of mutations causing genetic function. Maybe we ought to stop looking assuming mutations had a place in it?

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Bio, you are arguing again that changes must be "preferred" in order to survive. As Bumab points out and as I think I was saying too, changes *do not* have to be selected for immediately, rather as I understand it the mechanisms for self correction *remove* the dangerous changes but *leave* the good or *indifferent* changes. This process does in fact make the probability computations that you and Dembski use completely irrelevant
Oh come on. Given that you are now wandering into wild postulation, exactly how do the "mechanisms for self correction" identify which changes are going to be "dangerous" when there is no possibly way to know what the phenotypic expression will be?

 

Wouldn't that make the VAST majority of the code non-functional? Aren't you saying that the "mechanism for self correction" knows about danger and value in advance? Based on what? If you say that the genetic propensity was prespecified, you are now agreeing with me.

 

Tell me how the Dembski math does not apply here? What number of base sequences would be found to be "not dangerous"? If you contend that the number of potentially-useful proto-genes is anything more that one millionth of one percent of the code in higher phyla, this is again the triumph of hope over reason.

 

It certainly does not explain the fact that even in humans 2% of the code actually transcribes into proteins, and more of the non-coding portions are found to be required every year.

 

Buff- This position is nonsensical.

... And its the *indifferent* changes, driven by mutation, that cause morphological changes over time. ...
Then suggest why non functional DNA not 99.99999999 % of our genome. It is less than 98%. Not counting the ever increasing intron/functional but non-coding DNA load. OK make it 95%. Let's be gracious. You are saying that the "mechanisms for self correction" can get the accurate retention of proto-genetic DNA down to odds of less than one in twenty?? Those "self correction" mechanisms must be awfully accurate. Maybe that's because they (and their target genetic specification) were part of the genome.

 

SUGGEST SOME OTHER MECHANISM FOR THIS!!!!

Why you don't see this is lost on me, and in my book if you understand that you've put the cart before the horse on the issue in the first two sentances of this post, then you can't help but come around to the notion that random mutations can and do move things forward...
Last time. There is not a shred of evidence that this is true. And there is a cascade of evidence that genetic change come through genetically defined mechanisms.
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Oh come on. Given that you are now wandering into wild postulation, exactly how do the "mechanisms for self correction" identify which changes are going to be "dangerous" when there is no possibly way to know what the phenotypic expression will be?
Now you're saying that these mechanisms don't exist? You said they do above. There's lots of documentation that the mechanisms for removal of mutations exist. If you're going to argue, at least don't contradict yourself! ;)
Wouldn't that make the VAST majority of the code non-functional? Aren't you saying that the "mechanism for self correction" knows about danger and value in advance?
Actually, the vast majority of code *is* non-functional! But you're contradicting yourself, and putting words in my mouth (and your's too, because you agreed that there are self-correction mechanisms earlier! really! you did!). This self correction does not have to "know" about danger, in fact it may not be dangerous at all, its just that over time the RNA and proteins have been selected that will zap a certain sequence.

 

Again, the main problem with your argument is that you insist that this selection process is inclusive rather than exclusive: if you simply see that yes its unlikely that this self correction process doesn't protect "good" but rather just gets rid of "selected bad", all of a sudden lots of mutations escape being excised, giving themselves opportunity to be expressed.

Tell me how the Dembski math does not apply here? What number of base sequences would be found to be "not dangerous"? If you contend that the number of potentially-useful proto-genes is anything more that one millionth of one percent of the code in higher phyla, this is again the triumph of hope over reason.
First its not that they are "found not dangerous", they are not *known* to be dangerous: the self correction mechanisms have been selected over time because they *do* get rid of proven bad stuff (proven by selection!). Secondly, this whole quote proves you have no idea of why any mechanism that selects has a dramatic impact on probabilities. It turns unbelieveably remote possibilities in to near-certainties. You really need to read up on this. Further, you are stuck on this notion that "whole sequences are constructed randomly" when you should know that that is not what's in those introns: they are in most cases not just random sequences of neucleotides, they are in most cases copies of sequences that at one time were exons themselves, and a single change to one neucleotide pair in that sequence could make it useless or useful and ready to be expressed. If its useful, the organism that has it will survive, otherwise it won't.
Then suggest why non functional DNA not 99.99999999 % of our genome. It is less than 98%. .... Those "self correction" mechanisms must be awfully accurate. Maybe that's because they (and their target genetic specification) were part of the genome.
Well, again, your math here is meaningless. All that has to happen is that the mechanisms get rid of a lot of stuff, but either of those numbers indicates there's a huge playground to work in. So what? And these correction mechanisms have evolved over time because they're selected for by protecting organisms and allowing them to succeed, which I guess to you is much more logical in saying they were programmed in from the very beginning....You wanna try to figure the odds that all this stuff was *bam* programmed perfectly in the first prokaryote? :)
Last time. There is not a shred of evidence that this is true. And there is a cascade of evidence that genetic change come through genetically defined mechanisms.
Again you keep tripping over this absolutist position that any sort of one at a time change must be in conflict with PE. Again we agree that there are genetically defined mechanisms that control change, and the only difference here is that you insist that these changes were all programmed in in the beginning and that mutational changes have had no effect ever, and you insist that there's a large body of evidence that proves it which unfortunately I can't find... hmmmm...

 

Cheers,

Buffy

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I apologize for my last post above. I re-read it, and it sounded a little harsh. Apologies again.
No problem! I didn't get to be the Slayer without having a pretty tough hide! :)

 

Cheers,

Buffy

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There's lots of documentation that the mechanisms for removal of mutations exist. If you're going to argue, at least don't contradict yourself!
Sorry for my lack of clarity. I certainly agree that genes are self correcting and self policing.
Actually, the vast majority of code *is* non-functional!
Not nearly enough. And every year we find out that more of the stuff that we though was "junk" isn't junk at all. But even if 95% is non-functional, there is no explanation for the incredible efficiency of removal of code from the primary DNA sequence.
...This self correction does not have to "know" about danger, in fact it may not be dangerous at all, its just that over time the RNA and proteins have been selected that will zap a certain sequence.
Really. Which sequences? Where is that information stored?
...if you simply see that yes its unlikely that this self correction process doesn't protect "good" but rather just gets rid of "selected bad", all of a sudden lots of mutations escape being excised, giving themselves opportunity to be expressed.
Again, that "selected bad" is an awfully large information file to get the efficieney of retention up to being useful 5% of the time. Where is that information stored?
...this whole quote proves you have no idea of why any mechanism that selects has a dramatic impact on probabilities. It turns unbelieveably remote possibilities in to near-certainties. You really need to read up on this.
This is mathematical sleight of hand. If you are suggesting that all previously recognized "bad sequences" are stored, remembered and then deselected, where is that information stored?
Further, you are stuck on this notion that "whole sequences are constructed randomly" when you should know that that is not what's in those introns: they are in most cases not just random sequences of neucleotides, they are in most cases copies of sequences that at one time were exons themselves, and a single change to one neucleotide pair in that sequence could make it useless or useful and ready to be expressed.
Well, are you saying with that "bad" sequences (in all of phylogeny?) are stored, recognized and rejected? Or that unexpressed codon sequences can be recognized before their phenotypic expression for rejection? I don't think it is my math that is bad here.
If its useful, the organism that has it will survive, otherwise it won't.
You are still dodging the math. Either we stored all previous errors in the phylogeny in the higher phylum code (which would take up some significant portion of the 95% of "junk") or we can predict bad stuff berfore it is expressed phenotypically. How? The quantity or previously rejected "errors" would have to dwarf the existing funcitional code by at least a factor of 10^1,000 (conservatively). That is a lot of recognition. Where is that stored?
Well, again, your math here is meaningless. All that has to happen is that the mechanisms get rid of a lot of stuff, but either of those numbers indicates there's a huge playground to work in.
Buff- This math is real. It seems to me that you wave your wand and say it is not a problem.
...these correction mechanisms have evolved over time because they're selected for by protecting organisms and allowing them to succeed, which I guess to you is much more logical in saying they were programmed in from the very beginning...
This is now a circular argument. You are saying that the selection mechanisms themselves were selected, but they require a learning capability to store previous adverse selections to make them functional. That is a pretty high bar for a system to be selected. When did this biochemical service arrive on the scene? The first prokaryote?
....You wanna try to figure the odds that all this stuff was *bam* programmed perfectly in the first prokaryote?
Buff, I was not trying to answer that problem. It is what it is. The issue I am addressing is the problem of a viable mechanism for PE. If the "simplest" solution for PE makes abiogenesis more complicated, so be it. But the evidence for mutation-based speciation is absent. The evidence for programmed speciation is inferential but strong, and it gets stronger every year.
...you insist that these changes were all programmed in in the beginning...
Technically no. I am suggesting that the specific propensity for the characteristics of the daughter species is contained in the genome of the parent species. The unfortunate logical corollary is that all phyla were coded a long way back. If you can think of some other mechanism, let me know.
... and that mutational changes have had no effect ever, and you insist that there's a large body of evidence that proves it which unfortunately I can't find...
Now you are being absolutist. What I said was that mutation had an insigificant effect on speciation. I don't really care if it EVER happened, because it is not the primary mechanism. You cannot prove a negative in the scientific method. No one can prove it never happened. But I noticed that you have not produced evidence that it did.

 

And there are numerous demonstrable mechanisms for viable genetic alteration that are not based on mutation.

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