Punctuated Equilibria theories

[Biochemist]

...You are arguing massive changes (which I don't disagree on), but that these are entirely "new genes" when parent dna which no longer exists might well show some significant shifting and multiple branches. A key part of your argument seems to be that the sequence is:

 

 

1. Environmental Stress occurs
   
2. A SINGLE set of APROPRIATE genetic changes are caused that respond to the stress
   
3. A SINGLE new daughter species results
   

Evidence of this sequence could erroneously be inferred by comparing the dna of a current living example parent species to a currently living dauthghter species.

Hmmm. If only we had ONE definitive example of a species creating another species. Or even better, an example of a species launching a new phylum. What, exactly would you look for in the parent? If the daughter species is morphologically different, how would you identify the parent? We use taxonomy to identify relationships. That is how we got in this mess. THERE ARE NO IDENTIFIABLE TAXONOMIC PARENTS.

 

Do keep in mind that the problem of lack of serial mutation is not limited to the launch of phyla. It goes all the way down to orders. All 32 animal orders appear abruptly, with no readily recognizable precursor. If my hypothesis is born out, a single parent species would have to be the progenitor of MULTIPLE PHENOTYPICALLY DISSIMILAR daughter species. It would be the only way to reconcile the process with the fossil record.

...It also implies that the dna changes are completely pre-programmed to take the effects based on specific stresses--which is a significant increase in the level of complexity in the programming your model requires in those cells!

Maybe. But I am just trying to accept the fossil record at face value, and then extrapolate and integrate a known set of complex biochemical services demonstrable in the cell. My main point is simple: mutations do nothing to address this problem.

This is distinctly different from the model that I'm describing (which by the way, Gould appears to agree with):

1. Environmental Stress occurs
   
2. A LARGE NUMBER of DIFFERENT genetic changes are caused that respond to the stress
   
3. MANY changes in morphology result in MANY new daughter species, and under the stressful environmental conditions, only a few survive.
   
4. Environmental stresses can clearly span many generations, resulting in successive rounds of these changes, multiplying the number of changes that are expressed over the stress period
   

This introduces randomness as well, which I know you abhor, but we'll come back to that.

I have no problem with the "large number" element in your position. My issue is that your argument is somehow aided by including some sort of mediation via mutation. The math is weak, the affirmative evidence is nonexistent, and there is significant counterevidence. And do remember that Gould was not a biochemist or mathemetician. He was a paleontologist. Most of my biochemical arguments did not exist until after 1978, six years after Gould first advocated PE.

...the sequence of events due to environmental stress I just described provide a significant mechanism for feedback.

Buff, Buff, Buff. Are you going to suggest that we launched, maybe, millions of phyla 530 million years ago, and that only 100 made the fossil record, and that 30 survived to the present? Where did all of THOSE new genes come from? This compounds your cases. It doesn't help it. The body plans of the 100-ish new Cambrian phyla were all completely new. The phenotypical expression did not prexist. You are suggesting that somehow these genes were "tried out" in different previous unrelated phenotypes? How were they tried out? By selecting for unrelated functional benefits?

The only thing that makes your view reasonable and the other "unlikely" is that you do not allow for the likelyhood that a single stress will result in many morphological branches that are tested severely under the stressed environment. Not believing that such multiple branches would occur simulaneously--indeed that only one new branch occurs--defies logic, but its the only situation in which your math starts to work.

I have absolutlely no idea where you got this assumption. I presumed absolutely nothing about the number of morphological branches. Clearly branching had to occur (unless God or aliens stuck in new species de novo) to go from fewer species to more species. And that last part- you are picking on MY math???? Yours is the model with the math problem.

..These genes in fact seem to be extremely sensitive to such small changes!

Yes, and mutations are almost always deleterious or lethal. Reconcile those two ideas won't you? Successful small change=dramatic step forward; Random small change=damage. Maybe the former small change example was part of the phylogenetic plan and the latter was not?

Moreover, due to their status as "functional" there's no reason to think that they would be excised!

You are now fully circuitous. It was randomly generated (at least partially), yet idenitifed as "functional" only because it was retained? What about the other 10^1000 introns that would have to have been "in process" to identify whether they were functional? Where are they????

...It is only your insistence that "any mutation argument requires that all construction of genes be random" that creates any inconsistency, and that's your issue, which you still have yet to explain....

I made no such argument. I would be open to any credible argument that gets the odds of a viable mutation down to, say, one in a billion.

You keep saying this without explanation, but the surrounding arguments you make keep pointing to you believing that the words "mutation drives speciation" insists that unless its *all* mutation--without any role of the other mechanisms--then its in agreement with your argument that mutation plays *NO ROLE WHATSOEVER*.

Evidence, evidence, evidence. There is no evidence for mutation in speciation, and there is significant counterevidence. YOU ARE THE ONE responsible to create/find evidence. There is already a lot of counterevidence.

There is obviously no middle ground for you, which to me makes no logical sense.

I allowed that mutations COULD cause species, although the odds are small. The issue we are debating is the CORE mechanism for speciation to account for PE. Mutation is HIGLY UNLIKELY to have anything to do with this. Nothing you have offered changes any of this.

...The copying/steering mechanisms are designed to preserve the existing version--that's why they go for so long *without* changing over time--and so stuff has to get thrown out constantly.

Another empirical leap. It would be MORE REASONABLE to assume that the genetic code is fundamentally about as stable as the species is. You are assuming that stuff is routinely rejected because you are assuming serial mutation. You are building non-evidenciary assumption based upon non-evidenciary assumption.

This is probably the explanation for why there are so many identical copies of functional genes in the introns: its a survival mechanism when stuff gets excised when the dna strands get too big. It takes evolution to grow them!

Please tune your language here. This is ALL evolution. It takes a well specificed biochemical mechanism to create introns (demonstrated). It takes a well specified biochemical mechanism to exise the intron-encoded mRNA from the immature mRNA (demonstrated). The quantity/fraction of introns rises with hygher phylogeny (demonstrated). Introns have very specific insertions points by species (demonstrated). Point to the random or mutative evidence in this?

But lets cut to the chase:I'm only a millimeter from your position in your mind because of this continued insistence that "any mutation=completely random formation". That's your issue, not mine. I have consistently said throughout this thread that there are mechanisms for steering and reuse of functional genes. Now its fine that you believe that mutation has no effect, but you still have to deal with why they have no effect when you admit that they occur. You have avoided this so far by continuing to insist that any inclusion of mutations in the process requires completely random formation of elements, and I keep telling you it does not. ...

Buff, you are circumlocuting again. I said that we are close because you have imputed a highly specified, complex biochemical mechanism to "steer" mutation. You have offered no evidence that mutation is required EVEN IN YOUR MODEL. That is why I thought we were not far apart.

 

(I want you to notice that I did not insert any obvious letcherous inuendo when we discussed being a millimeter apart.)

There is another interesting problem in your formulation that has occurred to me, that you'll need to explain: given that your model posits only single changes and they are all pre-programmed, then that pre-programming would have to know in advance the environmental changes that would occur in the future earth, and know when to express them.

Maybe. But there are a relatively small number of major environmental stresses. The factors are mostly temperature and amount of oxygen.

...But lets take a look at the second issue, where we really diverge:Now, we both agree that there are two elements to the mechanism of change:

1. There are useful functional genes in the junk
   
2. There are steering mechanisms (a combination of the proteins, RNA, etc that do the copying)
   

You are insisting that

1. all of the information is pre-coded
   
2. the steering mechanism is more complicated than the data
   
3. the steering mechanism had to be part of the original programming
   

All of which I disagree with, and this is based on my own work with neural networks which have many of the same principles involved. First: in neural networks, the rules for steering can start out unbelievably simple. They can include mechanisms for feedback that not only affect the system being built but also *alter the feedback systems themselves*! All of this is unbelievably simple to code initially, and it becomes unbelieveably complex over time, *both* in the system and the meta-system (the steering mechanism). Most importantly one of the most important steps in making neural networks work is that they have a built-in mutation mechanism that says "well, we've always done this thing this way, lets flip a coin and try it a different way". This is the only way to find optimal solutions when there are isolated sub-optimal solutions.

1) I addressed your erroneous assumption about single branching above

2) I understand your point about neural networks, but the infrastructure on which you build a neural network is highly, highly specified. If we agreed that we had that much advance specification back to the prokaryote, we are back on the same page again, and only millimeters apart again.

As I say, this is unbelievably simple to code, BUT the only way you get to more complex systems is by *throwing in a random change*!!!!

Tell me EXACTLY HOW you SPECIFY the boundary of what factor(s) are random. Does the random factor including turning off power to the computer? Does it include adding new verbs into the programming language? Does it include subtracting old verbs? Does it include changing the binary-readable code? Does it include deleting, copying and editing any character or portion of a character in the existing operating executables? If it didn't then it WAS NOT RANDOM. It was a tighly constrained subroutine in which a relatively small number of options were presented, many of which were likely to be feasible.

This is the source of my argument that the explanation I have does indeed provide a much simpler solution. Yours requires an unexplainable appearance of a highly complex system...where as mine ends up not requiring much complexity for abiogenisis (which you may find philosophically troubling...sorry!).

I still don't know what your are talking about. You can dislike my hypothesis, but you have not disproved any of it. What did you disprove? Please make that one a separate post.

 

...And abiogenesis was inexplicable anyway. Neither of us improved the odds for that.

One last point: "Usually" does not equal always. So what if the bad ones are weeded out? If anything, this is proof that much of the change caused by mutations is not morphological, but rather microevolves species to better survive over time. There's lots of evidence that mutations provide the ability for those that have evolved protection mechanisms to survive.

Really? Offer some evidence. While you are there, look for evidence of species microevolution (that is, a species from a species). Even those are extraordinarily rare. And all animal orders start suddenly and then carry forward until today (or extinction). Gradual speciation BY ANY MODEL is very hard to argue as a general mechanism for speciation. And it is most difficult to arge it for PE.

Is the fact that genetic resistance to desease in certain racial groups--provably caused by mutation--still not relevant to speciation?

Read this text, Buff. How in the world did you leap to mutation as causality for genetic resistance? Are you talking E Coli plasmids? Take 30 minutes to write down all of the biochemical infrastructure that has to be in place for plasmids to successfully pass. Now remind yourself that this is a prokaryote. Then talk about mutative causality. When you talk about higher phylogeny (like racial differences), the arguments are even weaker.

Given PE says speciation is a rare event, this point does not prove that they {mutations} have no role.

Sure, but read the very same information the other direction. PE also says that MOST speciation is in puncuated phases. It makes the mathematical likelihood of speciation by mutation EVER to be far smaller. I think the mathematics for mutative speciation is unreasonable over 4 billion years. It is far worse over 40 million. This doesn't "prove" anything. But it sure would suggest you look in different places.

[Biochemist]

...all these pages you're pointing to--while yes, hosted on a UC Santa Barbara system--are all related to arguments for Intelligent Design, and the quotes and pictures shown are entirely out of context...

Hmmm. If you can't refute the facts, attack the source. In this case, the source is Darwin and Gould. Have at it.

[Biochemist]

...I like the accidental - and I guess by that I mean the random - approach better and what survives to see tomorrow becomes the fodder for the next event.

 

It seems a better design. ...

You are in the majority, certainly. I just wish that someone, someplace would build a mathmatical argument that actually addresses how one functional enzyme system could arrive in the 500 million years before the first prokaryote. Or how a new, fully functional morphology with no phenotypical precursor, based presumably on at least one new fully functional gene can ROUTINELY show up in the fossil record.

 

Ain't been done. Ain't likely to happen.

[Buffy]

Hmmm. If only we had ONE definitive example of a species creating another species. Or even better, an example of a species launching a new phylum.

Well look, PE only says changes occur rapidly, at stress points, separated by lengthy periods of stability. If the speciation occurs rapidly, theres no evidence of intermediate stages because they don't last long, giving them no opportunity statistically to survive in the fossil record. Moreover, they'd all look like they appeared simultaneously anyway as multiple species.

 

Now I've become convinced that this creationist-style "we don't see any intermediate species" is the only proof that you're refering to in your statement that "mutation has no role in speciation" because you insist that the intermediate stages must appear if mutation has a role. If pointing to the fossil record is your *only* evidence on this point, then you're arguing against mutation in PE by arguing against the traditional gradualism model of monotonically progressive change. This is akin to arguing against Relativity by saying that Newton was wrong. Unless you can come up with some other evidence--which I keep asking for but you don't point to--there doesn't seem to be any point to trying to argue with you on this. You simply can't accept that "mutation" in *any* form must mean traditional gradualism. But then, its clear to me you have no understanding of how randomness can be fundamental to complex systems:

My issue is that your argument is somehow aided by including some sort of mediation via mutation....you are circumlocuting again. I said that we are close because you have imputed a highly specified, complex biochemical mechanism to "steer" mutation. You have offered no evidence that mutation is required EVEN IN YOUR MODEL.

Well you're not reading it then. The way that neural networks work is that they *depend* on mutation. That is why they *don't* need front loading of massive amounts of information: they can make it up as they go along. Feedback and adustment of the rules based on results means that although randomness has a *major* role, pure combinatorial probability *PLAYS NO ROLE*. You obviously don't get this. Its the source of your insistance that I'm a wrong, but its obviously an area that you have no knowledge of, and I do suggest you look into it.

 

You do later try to sweep this issue under the rug by saying:

...I understand your point about neural networks, but the infrastructure on which you build a neural network is highly, highly specified. If we agreed that we had that much advance specification back to the prokaryote, we are back on the same page again, and only millimeters apart again.

Firstly, the infrastructure may be specified, but on the other hand, we get results after just a few *hundred* iterations, and the smarter the system gets, the more it does. Second if you take the initial system and replicate it and alter it only to have a different goal to seek, it evolves much faster than the original system: it learns from the previous attempts. You don't get this, so you don't understand that my model of what's in a prokaryote is a simple system with little data that evolves. Yours is this unbelievably complicated system that must have all knowledge built into it because it cannot take advantage of the goal-seeking optimization that randomness provides.

Tell me EXACTLY HOW you SPECIFY the boundary of what factor(s) are random. Does the random factor including turning off power to the computer? Does it include adding new verbs into the programming language? Does it include subtracting old verbs?...If it didn't then it WAS NOT RANDOM.

You're simply not reading what I wrote: YES feedback into the *rules themselves* is *essential* to make these things move forward! They most certainly can affect all kinds of things in the system, although some of you examples here are exactly the kinds of things that the rules would proscribe, whether it was a neural net or a strand of DNA. You don't understand how these neural nets work, so be careful about dismissing them. You are continuing to see mutation as this awful demon, when in fact it can work what appears to be magic, *IF* it is applied by a *system.* I know this is inconvenient for your theory, but you can't simply dismiss it. We do know these systems work, and they are in fact based on the same model as evolution.

 

Just one further bit on your Luddite-like fear of randomness:

..These genes in fact seem to be extremely sensitive to such small changes!

Yes, and mutations are almost always deleterious or lethal. Reconcile those two ideas won't you? Successful small change=dramatic step forward; Random small change=damage. Maybe the former small change example was part of the phylogenetic plan and the latter was not?

First you kindly use the words "almost always", but then you imply that "successful" and "random" are logical antonyms. You really gotta get over this, guy: small changes make things happen. Insisting that they *always* be preprogrammed or they are de facto "damaging" is simply not logical.

 

Again, if your only proof is based on "if its at all random then there has to be traditional gradualism and its likelyhood therefore must be based on combinatorial probability" then you're still not showing that "randomness has no effect on speciation."

 

Cheers,

Buffy

[Buffy]

Hmmm. If you can't refute the facts, attack the source. In this case, the source is Darwin and Gould. Have at it.

Darwin and Gould and others are *very* conveniently quoted out of context on this site. This is intermixed with the usual ID blather by Behe and advertisements for his books. The graph you point out, which does nothing more than say "see lots happened all of a sudden at this line!" where the line in question spans probably a million or so years! So what? This is just PE saying "lots of things happen quickly" and it does nothing to disclaim your points about mutation. Sorry!

 

I'm not refuting the facts because its been done elsewhere, so why should I waste my time? For the discerning reader, this is a code warning to put the arguments presented on these pages in context: they are not science....

 

Cheers,

Buffy

[Biochemist]

...they are not science....

Oh yes, that again. The line in those charts was probably more like 30-40 million years than 1 million. Funny, the point still stands. 100 (or so) animal phyla pop up without explanation in 30 million years about 500 million years ago, and none have popped up in the intervening period. Mutation? Must have stopped a while ago. Bad mood or something.

 

Speaking of non-science, have you uncovered ANY affirmative evidence that mutations contribute to speciation?

[Biochemist]

...Now I've become convinced that this creationist-style "we don't see any intermediate species" is the only proof that you're refering to in your statement that "mutation has no role in speciation" because you insist that the intermediate stages must appear if mutation has a role. ...

Buff-

 

I am disappointed and giving up.

 

1) I have listed a number of demonstrated biochemical mechanisms that are elements in expanding or modifying the genome. The evidence for their mutagenicity is absent.

2) I have refrenced the undisputed incongruity in the fossil record, a long list of issues that is widely recognized; Most importantly a sudden occurrence of all major phyhla and even all animal orders; Also the lack of taxonomic parent for any initial anuimal phylum or order representative

3) I have raised legitimate questions about the likelihood of mutations ever creating positive outcomes, given the current state of biochemical knowledge

4) You have acknowledged the majority of my argument, in that you agree there are intracellular biochemical tools that "assist" in steering speciation, even in the absence of any expression of phenotype

5) You have offered no justification for including mutation in your schema, as it is not even necessary in your model

6) I have requested affirmative evidence for mutation in speciation (of coure, there is none)

 

If you solution is to label me a "creationist", have at it. I did not see any reference to that in my posts.

[Buffy]

The line in those charts was probably more like 30-40 million years than 1 million. Funny, the point still stands. 100 (or so) animal phyla pop up without explanation in 30 million years about 500 million years ago, and none have popped up in the intervening period. Mutation? Must have stopped a while ago. Bad mood or something.

Good! More time to do some rapid evolution!

 

You know, the biggest die-off ever happened at that boundary, we think due to an asteroid impact. The next largests ones were at 250mya and 60mya before and after the dino-era. If you want to argue that these more recent events produced no phylla, fine, I think theres enough change to show significant morphological change. Nonetheless, I thought we agreed that the bigger the evolutionary shock, the bigger the changes, thus the bigger the pool of introns that gets turned on, and I argue get morphed in all those trials. 30 million years? That's *plenty* of time!

Speaking of non-science, have you uncovered ANY affirmative evidence that mutations contribute to speciation?

Your nattering about affirmative evidence of speciation is specious: we've been agreeing here that speciation is a rare event, its hard to catch evidence of it with the associated dna to observe, and we've only recently begun to have the tools to do so. Now it took me all of 5 minutes to find this explanation: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mga.section.1242 which you will claim is inadequate because it does not show absolute proof, but it does explain a mechanism from an expert (rather than amateur lil' ol' me!). This same NIH database had a good 100 papers on the topic including this one (which is a bit harder to read than that other link): Quantum speciation in Aegilops: molecular cytogenetic evidence from rDNA cluster variability in natural populations. which says tantalizingly:

"Comparative molecular cytogenetic analysis based on the intrapopulation variability of rRNA-encoding DNA (rDNA) chromosomal patterns of individual Ae. speltoides geno-types revealed an ongoing dynamic process of permanent chromosomal rearrangements. Chromosomal mutations can arise de novo and can be eliminated. Analysis of the progeny of the investigated genotypes testifies that inheritance of de novo rDNA sites happens frequently. Heterologous recombination and/or transposable elements-mediated rDNA transfer seem to be the mechanisms for observed chromosomal repatterning. Consequently, several modified genomic forms, intermediate between Ae. speltoides and Ae. sharonensis, permanently arise in the studied wild population of Ae. speltoides, which make it possible to recognize Ae. sharonensis as a derivative species of Ae. speltoides, as well as to propose rapidness and canalization of quantum speciation in Sitopsis species."

What'a ya think? Huh?

 

Oh yes, that again.

"Your mother was a creationist and your father smelled of ID-berries! I Evolve in your general direction! Now go away before I taunt you again!" :)

 

Cheers,

Buffy

[Buffy]

I am disappointed and giving up.

<crowd>Awwwww....</crowd>

1) I have listed a number of demonstrated biochemical mechanisms that are elements in expanding or modifying the genome. The evidence for their mutagenicity is absent.

Yes, and they are mostly things we agree on, but the issue of mutation is the one you're hung up on, and if you feel I'm being unfair to you, you dismiss my discussion of how mutation can indeed work out of hand without responding to it, and indeed, not even indicating that you feel its worth bothering to read or understand at all. I could take that badly too!

2) I have refrenced the undisputed incongruity in the fossil record, a long list of issues that is widely recognized; Most importantly a sudden occurrence of all major phyhla and even all animal orders; Also the lack of taxonomic parent for any initial anuimal phylum or order representative

I agree with all this evidence. I agree with PE. I simply say that there are viable mechanisms that do not require massive front-loading. Evidence of PE is not proof that mutation has no effect. This argument is unconvincing. (And is used by the way, yes, pretty much exclusively from the creationist/ID crowd, which is why it came up, see below).

3) I have raised legitimate questions about the likelihood of mutations ever creating positive outcomes, given the current state of biochemical knowledge

And I think your conclusion is premature. At the same time that you're haughtily and dismissively saying that I'm out to lunch because I haven't shown proof of speciation that involves mutation, you have shown no proof that it does not, in spite of the fact that you admit that mutation does cause changes. I personally do not find this logical, and I've been asking why you believe this.

4) You have acknowledged the majority of my argument, in that you agree there are intracellular biochemical tools that "assist" in steering speciation, even in the absence of any expression of phenotype

Yep! The only issue is the front-loading of all information versus mutation assisting evolutionary development. So this issue is not a problem!

5) You have offered no justification for including mutation in your schema, as it is not even necessary in your model

Well, actually I just did in the previous post above since I bothered to look. But your statement that it is "not even necessary in your model" indicates that you have not really been reading or understanding my discussion of neural networks: to avoid front loading, experimentation via mutation is an *essential* element. It is *not* the only element. It works in conjunction with the existing rules and data to form new rules and new data, but you can't do it without the mutation/flipping of a coin/whatever you want to choose as a random element. I can prove to you if you wish that programmatic random numbers are wholly inadequate for performing this step, so if you're arguing that your pre-programming does this (and you have not yet), then I can prove that it won't work numerically. It would be horridly off topic though!

6) I have requested affirmative evidence for mutation in speciation (of coure, there is none)

As I just said, I just did. It was not hard to find, but again, since speciation and phylla changes are rare events, and we're just scratching the surface of analysis of the mechanism (as you point out yourself!) its not surprising that there's not a mountain of proof yet, but there is some and it seems to be growing from what I see....

If you solution is to label me a "creationist", have at it. I did not see any reference to that in my posts.

No, you've studiously avoided the term, but your arguments seem to exactly parallel the creationist/ID arguments in the ways that I have explicitly described and you have not refuted, however I apologize for calling a spade a shovel.

 

You shouldn't give up while you're ahead of course! It gives people the incorrect impression that you're wrong and you're not willing to admit it! We know you're right, we just want an explanation! (no smilies!) Honest, given that I'm a programmer and Linda is a determinist and Bumab and I both agree on the gal-who-pushed-the-button, we'd all *love* for this to be true! But your arguments have not held up in my book, and Bumab has been complaining too. That should tell you something other than "we hate you because you're beautiful." Puuuleeeze!

 

Cheers,

Buffy

[Biochemist]

...Now it took me all of 5 minutes to find this explanation: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mga.section.1242 which you will claim is inadequate because it does not show absolute proof, but it does explain a mechanism from an expert (rather than amateur lil' ol' me!). This same NIH database had a good 100 papers on the topic including this one (which is a bit harder to read than that other link): Quantum speciation in Aegilops: molecular cytogenetic evidence from rDNA cluster variability in natural populations. which says tantalizingly...

I read your first link in its entirety, and just your excerpt from your second. I admit I am at a little bit of a loss to see your point. I would suggest that you go back and re-read your first link and imagine all of the very same evidence under a presumption that speciation is programmed versus a series of accidental events. There is nothing in the treatise that argues for mutation, other than the explicit assumptions of mutation as stated by the author. It would be easier to suggest that the dramatic flexibility of Drosophilia is engineered rather than random benefit. Ditto for the higher phyla.

[Biochemist]

...You're simply not reading what I wrote: YES feedback into the *rules themselves* is *essential* to make these things move forward! They most certainly can affect all kinds of things in the system, although some of you examples here are exactly the kinds of things that the rules would proscribe, whether it was a neural net or a strand of DNA. You don't understand how these neural nets work, so be careful about dismissing them. You are continuing to see mutation as this awful demon, when in fact it can work what appears to be magic, *IF* it is applied by a *system.* I know this is inconvenient for your theory, but you can't simply dismiss it. We do know these systems work, and they are in fact based on the same model as evolution....

I am pretty sure that you skipped over what I wrote. I was (of course) not talking about feedback into the rule set. I was talking about constraining the "mutations" to a very narrow domain. You did not let the "mutations" change anyting but the rule set. No change to operating environment (hardware, OS, language, verb structure, etc) AND YOU GAVE THE SYSTEM A TARGET.

 

You really think this is applicable to speciation by mutation? Where do you suppose chordates got their target?

[Biochemist]

... your arguments seem to exactly parallel the creationist/ID arguments in the ways that I have explicitly described and you have not refuted...

It is not really my problem that you maintain a bias (clearly) that avoids any curcumstance that seems to advantage folks with a theistic worldview. I was talking biochemistry in this discussion. I think my hypothesis fits empirical facts better than a mutation based approach. Your main complaints were:

 

1) I have not proved mutations DO NOT cause speciation (which would, I think, be impossible under the scientific method) and

 

2) You preceive some risk that my hypothesis makes abiogenesis look more like a theistic solution.

 

Neither of those are valid scientific arguments. They just reflect your bias.

[paultrr]

There are two types of Speciation. Speciation occurs when two subsets of a formerly interbreeding population become reproductively isolated and it occurs in what's termed sympatric speciation when two lineages of a formerly interbreeding population diverge to the point of reproductive isolation while still residing in the same locale. This was first demonstrated to occur by Guy Bush working on the Apple maggot fly Rhagoletis pomenella.

 

For past evidence one must look for both. And it might be mentioned that the above case shows it can happen even today. The theoretically preeminent species definition has been the biological species concept (BSC). This concept defines a species as a reproductive community. In the above case, and several others one has two distinct species drived out of a common background. Du Rietz in 1930 first defined this as:

 

"... the smallest natural populations permanently separated from each other by a distinct discontinuity in the series of biotypes."

 

Barriers to interbreeding are implicit in this definition and generally depend upon the idea of no interbreading being possible.

 

Chromosomes 1, 4, 5, 9,12, 15, 16, 17 and 18 in humans have inversions of major tracts of code compared with homologous chromosomes in chimpanzees, and human chromosome 2 results from the end to end fusion of two acrocentric chromosomes that remain separate in all the other great apes. Chromosomal rearrangements occur when substantial tracts of DNA are inverted or repositioned on the chromosome. This generally results itself in interbreading being impossible or not leading to offspring that can bread. But it is also only part of the picture that has tended to evolve when it comes to human's diverging from out of the ape line. In short there are other factors involved.

[paultrr]

 

2) You preceive some risk that my hypothesis makes abiogenesis look more like a theistic solution.

 

The motivation is well proven behind that in the origins of that type of alternative. Which does tend to make us suspecious. However, I'd also say that not everyone out there that holds to such a view also holds to the idea of a real devine being in the classical definition of such.

 

The problem is generally most of those who first proposed this alternative held to some theistic worldview. It arose as an alternative in light of there being no evidence for the young earth alternative at all. Those of the theistic views where faced with a crisis who's only solution was to adapt or perish. The adapation chosen was the alternative that somehow God, using a long timeline, partial evolution within a species, and other factors had managed to create a world that by left behind evidence appears as if natural process developed everything we have, yet, had those large gaps in the evidence that argues for a creative process simular to Genesis where each species had a distinct special origin. In some ways this whole line is very much akin to the older God of the Gaps theistic evolution approach where you have species divergence as the result of devine intervention. Problem is that approach lacks as much evidence as they tend to claim we lack. If anything it overlooks a lot of modern findings and totally ignors some modern examples of natural occuring seperation into distinct species.

 

What almost to a tee believers want is a direct evidence of something that's say half ape and half man or rather half dog and half cat. On the first by genetic/historical evidence we do have some examples. On the second, to my knowledge there is none. The problem is there are aspects of our origin we still do not fully understand. Some of these aspects are conditions in the local area we first evolved in, what produced the genetic inversions in our genes, etc, etc. However, the other side on this cannot supply decent answers to all this either, except perhaps invoking the God of the Gaps as a solution. Sorry to term it that way. But that's the origin of the idea you tend to hold to. That's why you find that preceived idea in the first place. You also might say that those who are religious tend to distrust us evolutionists because we totally discount the theistic idea. Yet, all these general arguments here rather point to the fact that such is not always the case across the board.

[paultrr]

One thing you have to consider is how can you present you're ideas devoid of the theistic aspect in the first place if you want to avoid this.

[bumab]

......and Bumab and I both agree on the gal-who-pushed-the-button, we'd all *love* for this to be true!

 

Well, I don't know about that :), but as far as this goes, sure.

 

Ya go away for a couple days, and miss miles of posts...

[bumab]

It is not really my problem that you maintain a bias (clearly) that avoids any curcumstance that seems to advantage folks with a theistic worldview.

 

Good Lord, everybodies gettin' hot under the collar.

 

Personally, I don't see any theistic bent to Bio's points. Sure, they are mirrored by Behe and many ID folk who clearly have a bias, but guilt by association has never been fair. I think your theory, Bio, is consistent with the facts and possible. It's no harder to believe then all the stuff about the origins of the universe, inflation, etc etc. that has been theorized to agree with the known facts.

 

My problem with your theory (again) is it's proposing an entirely new mechanism (which you have not supplied) to take care of a "problem" (rapid speciation) that can be taken care of through traditional means (mutation). Rapid speciation (over 10 million years or so) of many phyla would automatically create gaps in the fossil record, since such a short time span could easy skip around in the record. It's just not very long. So right off the bat, the time frame precludes (most likely) a good transitional fossil. Thus, it's not a gap in the theory at all, and you can't use it as such.

 

Secondly, you've not presented any evidence for your idea. None- it's all problems with the old idea. If you could present some data about the possible future forms of shrimp based on their DNA, great. If we could find dino DNA and look for bird genes, great. But nothings been found yet.

 

Third, there are other theories. A genetic predisposition to rapid genetic change (good and bad) to increase the palatte on which natural selection can act after a major enivironmental change is certainly more believable then a super-prokaryote, and the mechanism is known and has been described.

 

I'm still interested in your ideas, Bio, but you've not addressed the main concerns yet- evidence and mechanism.