Definition of created kind!

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.

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Originally posted by Tranquility Base:
SLPx

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I 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.

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Ref please? I don't understand the sentence on 98% similarity. Could you rephrase?

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Originally posted by Tranquility Base:

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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.

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Ah, heck, give me a try. You're probably right, but I'd still like to see some information more detailed than is generally possible on a discussion board.------------------
"Colorless green ideas sleep furiously." - Chomsky

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Originally posted by Tranquility Base:
SLPx

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SNP may be defined that way

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Of course it is, because that is what it is - a single nucleotide polymorphism.

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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.

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Oh, so you mean you are making up your own definition to suit your needs? You see, what you are really referring to is homoplasy, and believe it or not, we stupid evolutionists have taken that into consideration.

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I agree about small changes in reg sequences and potential macroevolution.

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Selection will weed out non-folding proteins if your random protein also has a (new) function!

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I think I am a bit confused by your use of the term 'fold' - are you saying that only some proteins exhibit secondary and tertiary structure? I suppose I should have asked for a clarification earlier.

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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.

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But I suppose thgere is sequence evidence of a loss of the unnecessary genes from the original kinds?

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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.

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I think I weill need some documentation on this. I know, for example, that cytochrome c's differ by as much as 50% in their AA sequence, so forgive me iof I do not take you at your word.

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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.

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Hmmm.... So this 10,000 year drift (we will ignore the wholsale slaughter of innocents by Yahweh and the ensuing bottlenecks and such) can explain the 50% divergence in cytochrome c?

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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.

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Novel human genes?

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In this set of abstracts

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http://sayer.lab.nig.ac.jp/GEMINI/abstract.html

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it 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.

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Allow me to remove the ambiguities and implicit spin:Evolutionarily significant genetic differences between Homo and Pan (i.e.,
those contributing to phenotypic differences) can potentially be of several
forms, given our knowledge of comparative data from other species. These
can range in type from single nucleotide changes in coding or regulatory
regions to the acquisition of novel expressed genes. Although changes in
regulatory evolution are considered to be the primary means by which new
phenotypes are created (Carroll, Grenier, and Weatherbee, 2001), the
acquisition of novel genes is also likely to play a role in Homo-Pan
differences. Given that the human genome has 300 genes which the mouse
genome lacks, this is a net additive gain of 4-5 novel genes per million
years, assuming a 65 million year old common primate-rodent ancestor. If
novel genes were acquired at roughly a constant rate (4-5 genes per million
years per lineage), then we would expect to see approximately 27-28 novel
genes unique to humans since the 6 million year divergence from Pan (and
similarly, the same number of novel genes unique to Pan).30 genes is small potatoes. Where is the 'novel gene familiaes' you mentioned before? Novel protein families? Novel protein fold families? Or was that all just hyperbole?

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.

So bo, whould you sleep on the idea in particular that I am a creationist or would you rather be bold enough to asser that generally I am? I have no fancy comptuer behind this mark so feel free to answer it. Another question remarked will not do here.

There is actually in the new reality of the new biology in the if a new evolution is appearing more, plese talk a bit U

Adaptive transformations may also be reached WITHOUT mutations, in theory, and this is not only my idea, the evolutionist Gottlieb also thinks so.

Very interesting, these are not "doubts" but affirmations. I do predict there will be time that secular education will get scietific support either from Islam or Christian Scientists. This is no doubt now in my mind. What the news head-line will be I can not say.

TB, I know hardly any one in C/E wants or relishes a toungue lashing of mine and I am not in a place to put that in your direction nor is it my desire but this is something that I had written up in high school that got me into to all kinds of ontological water at Cornell because on trying to get what if ever andy truth out of Sheldrake's morphic resonance in effect I found Maxwell vortex by imagining that a denatured protein could fold by influence of gravity waves which I never bothered to calculate the probability from a dissipative system but such non-equilibrium conditions may be available to if not contain the thought you "open" epistemologically (in the context of actual protein pathway kinematcs) at least the intent which is to permit behavior to be available for study before all genetic change such offering as we(if others here choose to) extend the scholarship in and close off the ability to talk out of a tradition of one-gene one enzyme for some actual physiogical gentics. I know I did not complete the last sentence. I left it C/E pending.

It could go this way if ion chanells are topological inversion positions relative to bioentropism or absolute space of centrome chromosome "splitting" for the lipid/water immiscible eddies of golgi etc. Dont understand? Sorry that is a description.

If gravity wave resonance exists it would be "unfolded" relative to the effect of mass on the formation of the wave or soliton that would be able to be used in caluculations of protein folding if true and then shown to how it works thermodynamically.

They may not, but they may be in rest of any given bioentropism in the alternative

We would then be discussing straight physical chemistry and not adaptive transformations etc.