Definition of created kind!

Evolutionists believe that new proteins after new proteins make it more complex. These mutations are thought be be good all the way up to the new systems, besides other individuals, who have bad mutations spoiling it all. And thats where we have to hit them.
I didnt mean that you were WRONG with the protein foldings. I was interested in it. But first I thought that unfolded proteins might do kind of the same things as a folded protein. For example regulate a system a little. But now I just learned that they aggregate!!We could combine this to: "How many new folded proteins (not new foldings) can accumulate until its lethal to have any new folded protein". If an unfolded one appear, or if any negative mutation appear, then the organism die. And different foldings as well as different embryology is thus a sign of different created kinds.

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Originally posted by Tranquility Base:

Can you briefly and clearly explain your point about 'binding sites of proteins and sugars in combination with different ion-concentration'.

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I meant that a protein could be active or inactive whether its bound to an ion or not. I the muscle-cell: When a Ca-ion hit Troponin, troponin change it form so tropomyosin draw back and expose actin binding sites to myosin heads.

Ok, take your time!

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Originally posted by Tranquility Base:
SLPx

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And how does this issue relate to homoplasy? Homoplasy for you is conincidence (or physi-chemio-bio predisposition), for us it is design.

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Apparently you do not deal with sequence data. An example of Homoplasy in sequence data might be something like a human and a rabbit 'sharing' a unique mutation that neither share with any other taxon. Looking at the entire alignment of, say, 10,000 bps, such synapomorphies might number half a dozen. But the synapomorphies between, say, rhesus monkey and human number in the hundreds. Therefore, the alleged synapomorphy between human and rabbit would be an example of homoplasy.
Is that design? If so, why on earth would it be?

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Only very few random protein sequnces have stable folds with appreicable secondary structure content. Most of the coding genome of course codes for folded proteins.

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I find thathard to believe, frankly. It could be true, of course, it just seems fantastic.

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In mainstream analyses of genomes of closely related bacteria potential gains in one species are often interpreted as losses in the other species. Presumably in some cases there is pseudo-gene evidence for this. A real comparative genomics person would know the answer of the top of their head. I'm moving into this area but am concentrating on structural aspects.

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Of the top of my head ubiquitin is a remarkably conserved protein going a long way back. I plan to come up with documentaiton of this. I have read mainstream comments of surprise on the extent of concervation. I of course am not surprised.

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I am not either. I see no reason to be surprised that certain proteins (via their gene) exhibit a great deal of conservation, just as I am not surprised that some proteins - metabolically important ones, like cytochrome c, for example - vary considerably in their structure yet still perfrom the 'necessary' function.

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The 50% conservation of cytomchrome C is still rather surprising since there is usually zero sequence relationship between folds which are younger than cytochrome C. Active sites usually only involve 3 or 4 residues that must be absolutely conserved. I will document this gradually. To do it propoerly is real work and I have a day time job but I will do it.

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Really? What about the globins? Of course, it really shouldn't that surprising at all. Proteins like cytochrome c are necessary - or close to it - for energy production. Organisms with defective cytocrome cs will not likely survive to pass on their malady. No surprise.

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The 10,000 year drift would explain the small drifts but the sequences are also related via the heirarchy of life (proportional to useage rather than time in our sceanrio) and is hence a designed difference. 10,000 years would be long enough to explain large drifts evident in closely related rapidly reproducing organisms (bacteria etc).

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If you say so...

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I am prepared to concede that genetically there are only 30 gene families between us and chimps.

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But the abstracts you provided mentioned "30 genes", NOT 30 gene families. Were you hiding some?

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Given that there are no sequence hints as to the origin of protein folds it is hard to avoid the implication that these new families came out of thin air.

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Hmmm... It seems to me that protein folds are a byproduct of the coding sequence of the gene that encodes them, no?

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To many without knwoledge of structural biology and protein engineering a new gene family is 'dime a dozen', just a sequence of letters. To me it is an optimized machine different to all of the other machines in the genome.

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And that gives you. above all others, special insight into this matter such that you can see the fingerprints of the Hebrew tribal deity, right?

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More generally I am prepared to concede that macroevolutionary nearby organisms are separated by millions of point mutations, dozens of chromosomal rearrangements and about 20 novel gene families. The hardest part to explain for you guys is the 20 novel gene families.

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And yet you have failed to produce the documentation for these 'protein families' that you are hanging your hat on.
For Fred Williams, it is Haldane's model. For Gish it is the fossil record. For you, it is 'protein fold families' (or is it now gene families'?). A bunch of hedgehogs...

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Why we got latte-drinking primates sitting at computers out of all of this is also a problem but with evoltuion anything is possible of course when you know the answer beforehand.

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Or when some magical superbeing simply wills it to be so, no questions asked, no answers forthcoming...

I'm going to need another day off. Thanks. I just realized the scientific backing of Bush's environemtal policy is up the creek. My Church acquaintences had already told me so but I tried as hard as possible to not believe them. This is no longer possible. It is not a good day because this was a Maxwell footnote and not even one of Croizat, so every one is really affected not merely drinking the stewed GOuld juice.

Tranquility base!If you want to, you can go to my msn-group and post this definition of created kinds there, since you are most familiar with it. Let the discussion topic name be "Protein folding".Otherwise I will summarize what youve written here and put it there. http://groups.msn.com/Createdkinds

SLPxI see your homoplasy from sequence data. Obviously such examples are simply prononunced to be chance simlarities (eg your human vs rabit one). I can gaurentee you that almost no one in our department would call it 'homoplasy' but of course that is what it is - I agree. 6 out of 10,000 sounds like something one would expect from chance to me (without doing the stats). Sounds like drift - shouldn't surprise either of us should it?My statement about random protein sequences is almost undoubtedly true. It is of course hard to nail down - it is a (mainstream) expectation. It is difficult to nail down because there is no common assay for 'folded'. Having said that someone could do a study on random sequences and study compactness using ultracentifugation sedimentation or even size exclusion?? It would be an interesting basic science study but hard to get grant money for. But compact and folded are not the same thing either but compactenss would be a first screen.Of course if you pick a particular 3D fold there wold be billions of sequences that would arrive at that fold - but for a 100 residue protein there are of course 20^100 potential sequences.It is hard to imagine that the entire sequence of ubiquitin is required for function and I'm quite sure this hasn't been shown. We'll see. Whatever happens I don't expect it to be an evoltuon killer - just not quite expected by evolution.Of course the function of cytochrome c must be retained. My suprise comes as a structural biologist and having worked in an institute which intensely studied viral proteins. The sequences change incredibly and are still functional. But, I'm not trying to shoehorn the data - cytochrome c probably fits both models.My main point is that given the amount of conservation evident within gene families I would expect recent new folds to retain sequence similarities to the genes they were duplicated from if that's where they came from. I think it really does seem that folds come from truly junk DNA in your scenario.That abstract is talking about 30 distinct (no seq similarity/homology) genes. The majority of human genes are their own family! They give you one or two paralog hits in the genome and that is it!You stated 'It seems to me that protein folds are a byproduct of the coding sequence of the gene that encodes them, no'. Protein folds are ditated obviously by sequence but not in any dead obvious way. Hydrophobic residues tend to be in the core etc, yes. What is your point exactly? There is no simple way to design at the DNA nucleotide level to get folds without thinking in 3D. Folds really are 3D things that requie a finely tuned prtoein (and hence DNA) seqeunce. Protein folds are not just a unique set of random letters. You can trust me on that.It is clear that genes families (identified via no other sequence hits in the genome) require explanation!

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[This message has been edited by Tranquility Base, 07-14-2002]

ZAURUZ, I might head over there eventually but I'm too busy at the moment so post away and send a link here if you like. A key point for accuarcy is that gene families (distinct by seqeunce similarity) are a subset of protein fold famlies (distinct by 3D strcuture) but that there are probably about 2000 fold families and 15,000 gene families in the human genome. The fold families would be a better definition of created kinds becasue evoltuion from fold to fold is harder. Having said that, but even the distinctness of gene famlies themselves (especaially evoltuiuonarily recent ones) is somehting to characterise a kind by.

Indeed, I would say like-wise, there NEVER was a common notion for folding yet the language led me as a young biologist that this seeming commonality existed. It did not. It is part and parcel of the science. But that chance and not some form of selection must be the a posteriori soulution is far from certain in my mind. I know that selection is over rated but I have not been convinced in some alternative that "developmental constraints" should replace the scholarship in the area of asserting adaptations are concerned first and then foremost with forms of gene frequency variations. If proteins are such it would not be FOX's proto-cells but the thought would extend beyond this to TB's notion of a barrier and drift but that seems to me best if is developed a priori. I have not done my homework in this thread so that is as far as I assert and go today. To do so I have conceptually seperated at least in my own 'visualization' "randomness" from "chance" for any so-called co-action where I tend to think rather too subjectively that chance occurs WITHIN a level of organization and randomness between any such levels that compete for potential selection. What is acutal out of this, remains the dillema. By sequestering chance this way conceptually I avoid much of the C/E polemic or rethoric in the topic.

SLPxOne more point about homoplasy. I'm unaware of the precise definition but it seems to me that talking about homoplasy with 6 out of 10,000 bases is a bit idffernet to the homoplasy evident between a duck and a platypus! The bill of these animals is clearly functional. The 6 out of 10,000 nucleotides example can surely be demonstrated to be drift! Even in your model the bill is clearly selceted due to function. It is unlcear if the sharted rabbit/human nucleotides are simliarly selected or just drift.I can imagine more genuine genetic homoplasy and I cite my example of convergent flight specific use of developmental genes thread for that (and its associated controversy).

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[This message has been edited by Tranquility Base, 07-14-2002]