Definition of created kind!

I hope I can post in this thread even though my user name doesn't start with 'Z'.I definitely agree that the kind concept will become more clear as we get more genomes and that issues of 'loss' vs 'gain' are very improtant. In other recent threads I have shown refs that demonstrate that biochemical and cellular novelty is assocaited with the occurance of novel protein families.Creationists expect 'distinct' genomes diversified through microevolutionary processes.

ZAURUZ, in the thread below we talked about the assocaiton of novelty with protein fold families and I think we agreed that at least biochemical and cellular novelty is typically assocaited with new protein fold families: http://www.evcforum.net/cgi-bin/dm.cgi?action=page&f=5&t=35&p=6Here is one of the papers I came up with:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8706840&dopt=AbstractIn the pdf (if you have access to it) it says:

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"Using the presence of the protein families as taxonomic traits, and linking them to biochemical pathways . . ."

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and

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The mere presence or absence of a protein family can be indicative of the existence of an entire cellular process"

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I suspect that anatmical ovelty will typically be associated with new protein families too but that's just a guess.

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[This message has been edited by Tranquility Base, 06-24-2002]

All creationists who are actually practising biologists do not deny that mutations can lead to adaptive transformaitons. It is utterly undeniable. I have seen it with my own eyes. But it's always mutations to existing protein surfaces altering binding as you guys are discussing. There's no new cellular system developed.We need to discuss the origin of novel protein fold families, biochemical pathways, macromolecualr machines and systems. That is the issue. We don't even have to wait for all the genomes to be reeled into discuss that. We already know that novel protein fold families are correlated with cellular novelty. There is almost no mainstream literature on the origin of protein fold families (which may also be called gene families).The human/chimp discusion will have to await the chimp genome I'm afraid. For that we need to tune back here in around 2005 I think. And I think bonoboos just got the boot by the relevant genomic committee.

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[This message has been edited by Tranquility Base, 06-25-2002]

Johnyou are quite right that a protein could gradually morph from one fold to another via DNA changes. However in doing so it would spend most of its time unfolded and hence non-funcitonal in any sense. Hence it could not be open to acclerated adaptation by natural selection until it randomly drifted to something functional. So the point is going from fold to fold is something that is the same as going from random to non-random.I do draw the kind line on this sort of issue (and also micro and macro-evolution).Evoltuion is possible without a change in protein fold - it happens all the time. But all genomes above a certain level are differnetiatable by new gene families at some taxonmoic level. We suggest it will approximately be at the family level but we will see. Currently we can only say with surity that plants, yeast, worms, flies and man are distinguishable on the basis of gene family usage. We already understand why - distinct gene families are associated with the specific cellular processes (like the immune system, cell-cell interactions, metabolic pathways etc). If evoltuion occurred, in addition to resuing existing folds it systematically developed new folds at great uphill cost to achieve novelty.

SLPxHave a close look: almost all are about evolution within the gene or protein family. I have spent literally hours perusing the literature on these issues. I have found one or two papers only over the last few years.I read that JMB paper last week - it's simply about the distribtuion of fold families in sequenced genomes. Absolutely fascinating but completely consistent with literal creation.

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[This message has been edited by Tranquility Base, 06-27-2002]

SLPx, you never responded to (at least the second) of the quotes I dug out from the mainstream FEBBs Lett paper later:

quote:

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"Using the presence of the protein families as taxonomic traits, and linking them to biochemical pathways . . ."

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and

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The mere presence or absence of a protein family can be indicative of the existence of an entire cellular process"

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[This message has been edited by Tranquility Base, 06-27-2002]

Zhimbo99.999% of random protein sequence do not fold! The sequences that fold are either created or selected by evolution. Random protein sequences do not fold except by luck and no-one has ever randomly generated a protein sequence that has folded into a large protein fold. Some small folds have been generated by random means in the cases where all possibilities were exhaustively sampled (ie billions of possibilities).If you have one protein fold that is 'abbbab' for example (a = alpha helix, b=beta strand). It might fold into a four stranded beta sheet with two alpha helices. It is almost impossible to insert a third alpha helix into the middle of this sequence. If you inserted amino-acids that are likely to form an alpha helix (eg ALVSELVA) betwwen say the 'abb' and 'bab' parts you are almost 100% sure to get an unfolded protein. Proteins fold in a very, very cooperative manner. A single amino acid change can cause it to unravel. This is why one cannot go systematically from one fold to another. One could easily imagine going from a abbbab fold to a abbbaba fold on the other hand but the point is that the known protein folds do not fit a pattern lke this and we know probably 80% to 90% of the water soluble folds.

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[This message has been edited by Tranquility Base, 06-30-2002]

SLPxMy refed quote The mere presence or absence of a protein family can be indicative of the existence of an entire cellular process" shows what I claimed, that protein folds accompany cellular novelty - at least some of the time (if not most of the time). In other words if you pick almost any cellular cystem you will need new protein folds to constrcut them.Your study of globin genes is a study within a gene family - they are all homologs or orthologs of a single gene. These could have arisen by either creation or evolution.

SLPx - I said the human/chimp issue will have to await the chimp genome because it is only then that we will find to what extent we (humans) are diferentiated from chimps via(i) SNPs (single point mutations)
(ii) Regulatory sequences
(iii) Paralogs (extra new funtion copies of genes)
(iv) New gene families (protein folds)One non-creationist discussion I read recently points out that the 98% similarity experiments (determined by annealing rates) will definitely give an overestimate of similarity (because the non-similar parts wont combine!) and doesn't say much about the presence of new gene families. Human gene families that aren't in pan are known and extrapolation suggests about 30 novel gene families might be present in man. We will just have to see.

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[This message has been edited by Tranquility Base, 06-30-2002]

ZhimboProtein folding is something that happens almost automatically to a protein chain of amino-acids ('chaperones' help but don't change the final structure). Only a very small subset of protein sequences will fold to a compact specific structure with a defined shape and surface that can do a job. It is an optimized process because it has been demonstrated that if the sequence isn't carefully chosen a protein would take millions of years to fold to it's native functional state.If you constructed a random amino-acid sequence it will probably remain like a semi-extended string flopping around. A folded protein is quite rigid and most of the molecules in a population will have a near identical structure unlike a floppy chain.The point that your textbooks are yet to make is that the proteins we study most of he time are coded for in genomes and are foldable (ie they automatically find the right shape to do their job). A good textbook will somewhere point out that most random amino-acid chains will not have this property.And my point is that becasue protein structures are discontinuous in structure from one fold to another, and because protein folding is critically dependent on sequence, a protein typically will be unfolded (and hence non-functional) on the way to morphing into another protein fold via sequence changes. The point is that on the way to the new fold there is nothing good to select for so you are back to random sampling. The other point is that the protein families show no hint of their descendency from each other via their sequences.

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[This message has been edited by Tranquility Base, 07-02-2002]

ZhimboNot folded = "not folded to a single stable conformation" is a good summary.Protein fold families, among other things, do help define created kinds IMO, yes, and this is very well supported by studies of the association of fold families with cellular novelties. I also see it as a micro/macro-evolution differentiation which we equate to the kind distinguishment anyway.It is a difficulty for evolution becasue there doesn't seem to be anywhere near enought time for these families to evolve, let alone organise into pathways, systems and organs. But the only refs on that are creationist so you probably wont buy that. There is a surprising complete silence in the mainstream lit on the issue so I will take that as a sign that the creationists are, at the very least, not stretching the point.

SLPxI recently read about novel protein fmailies in man vs chimp. The researchers extrapolated to predict about 30 novel families but this could be a lower limit. DNA hybridization experiments that say we are 98% similar almost definetely will generate an underestimate. We'll soon see.

SLPxSNP may be defined that way but I am simply extending the term to refer to the way of comapring two near identical sequences regardless of where they came from. Just subsitute 'point substitution' for SNP.I agree about small changes in reg sequences and potential macroevolution.Selection will weed out non-folding proteins if your random protein also has a (new) function!I would generally see paralogous duplication as paralogous creation but I will concede that it is a potential mechanism of evolution. The rationale that duplication has not lead to novel gene families is that (a) there is not enough time and (b) there is very little, if any, sequence evidence that that has occurred.Something that rarely gets talked about is that it is not just the active sites of proteins which are conserved. For many homologous proteins, even though seprated by 100s of millions of years, the entire length of the sequences are similar even though only a handful of residues are really invovled in function. The rest are there no doubt for issues of folding. Since that is the case I would also expect different protein fold families to share sequence similarities across their lengths since we know that many protein families suppossedly evolved during the last 100 million years. This is rarely, if ever seen except where it is a funtional motif, yet we have non-functional folding motifs conserved across 100s of millions of years. This all fits our scenario superbly. The sequences, though related to each other, were sperately created and have drifted for only 10,000 years or so.The direct human-chimp sequence comparisons involve a priori similar genes of course. I do not debate at all that human and chimp genes are about 98% similar when comapred. Who knows howmany unique families there are. But I am prepared to concede that we are 98% similar regardless.Novel human genes?In this set of abstracts http://sayer.lab.nig.ac.jp/GEMINI/abstract.htmlit is stated that chorionic gonadotropin beta-chain is unique to anthropoid primates, that 300 human genes are not in mouse and that, by extrapolation, about 30 genes will differ between man and chimp. We'll see.

SLPxBecaue protein fold to fold evoltuion has a barrier, whether prohibitive or not, the existence of thousands of new folds throughout life is indicative of creation. Protein engineering and phage display comninatorial experiments demonstrate that life could easily get away with far fewer folds (although new folds undoubtdly give more diversity/specificity). Genomic studies has finally ruled out the most prevailing theory of biochemical pathway evoltuion now that we know that folds are rarely reused within pathways and very, very rarely consecutively. Evolution of a pathway by the consecutive reuse of the same fold by the duplication of an enzyme that already binds is exactly what one would expect evolution ot do. It does not. Reality requires a 'mosaic' evoltuion model.Examples of reuse of folds is not evidecne against creation. God reused folds when they fit the job. Your study of globin genes cleary indicates either reuse of folds by God or evolution. It does not distinguish between the two.

SLPxMy use of the term SNP for human-chimp relationships if anything favours evoltuion!! In your model how do you think point mutaitons got there between man and chimp? SNP by SNP! I used the term SNP becasue that is how I think about it and it is a trendy word. i will not use it anymore. You are inventing a new bias for me - no need - I am already biased enough thank-you! And how does this issue relate to homoplasy? Homoplasy for you is conincidence (or physi-chemio-bio predisposition), for us it is design.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.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.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.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.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).I am prepared to concede that genetically there are only 30 gene families between us and chimps. 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.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.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.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.