Teaching evolution in the context of science

John, I would have hoped that the extensive posts I have made in this BBS on geology, paleontology, systematics, molecular biology and genome sciences were beginning to be seen as a rather systematic view of creation/flood with, yes, (i) gaps in my personal understandings in some areas and (ii) some gaps in answers by creationists, but otherwise rather neatly consistent.On this particular issue I see it as follows:Micro/macro evolution although used by both evolutionists and creationists are not a perfectly defined set of terms. However, a definition that might pass mainstream muster in various fields from paleotology to genome sciences might be one that is also compatible with creationism and the kind concept. It didn't have to turn out that way, but boy, it comes pretty close without working hard at all.So we simply see the created kinds as genomic stock, distinguishable primarily by ultimately cellular novelties that are nevertheless frequently evident anatomically. This discontinuity is manifest as novel gene families that bear no resemblance to other famiiles in the genome. Many of these gene families turn out to have new protein folds. Regardless of philosophical bias, it is harder to imagine between fold molecular evolution than within fold evolution. Within fold optimization is continuous at every point - exsiting function optimized by evoltuion. This is the evoltuion of an allele coding for a selectable trait. A new protein function on an existing fold requires a chance event to generate some novel, selectable funciton. Once this occurs there can be optimization up to a point dictated by the potential of that fold to allow that eg enzymatic activity. Even harder to imagine is going from one fold to another. It requires a chance event to generate something very different that is immediately useful. If it is not immediately useful then one may as well start from random DNA. Once the function is useble then optimization via natural selection can do its job. This is utterly standard of course but I have put it into the words of structural biology whihc is where the action actually occurs. The point is that in either getting a new funcition or a new fold you are not simply doing optimization. That is the discontinuity that differentiates micro/macro or existing gene/novel fold. In your scenario it could be the reason behind punctauted equilibriu although, for you, that probably requires even a bigger step - the tying together of multiple new pathways to get a new cellular/anatomical feature.Whatever the case the optimization of a gene (for disease resitance for example) is very different to generating a gene with a new funciton/fold. At the very least one is something we see real examples of in viruses and bacteria - the other has never yet been seen. So regardless of creation/evoltuion there is a discontinuity in expectations and reality. In our scheme it is simply becasue God created distinct genomes abut allowed them to optimze.

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

PercyI stand by "Microevolution is identified with allelic variation = same fold but with SNP(s)." How have I contradicted this elsewhere?Erwin does equate microevoltuion with allelic subsitution as stated by yourself but the key point is that moelcular biologists know that allelic subsituion will either be same fold or unfolded! It is irrelvant whether Erwin himself knows this or not. Alleles are either same fold or misfolded. Brown/blue eyes. Long/short nose. Sickle cell/healthy. I have made a statement that covers every allele ever studied by molecular methods. It is the bread and btter of structural biology. One might be able to demonstrate special artificial cases (such as the Nat Struc Biol paper recently) but that is not what generally distinguishes a allele.You just think Erwin is irrelevant becasue you don't know enough about the structural biology of proteins Percy. Alleles are fixed folds or unfolded faults!

SchrafEvery complex theory is difficult to falsify. It has been said about evolution itself. There are mainstream quotes that state that evolution could be compatible with anything!

JohnAre you aware that European artificial selection over about 200 years on the wild mustard led to cabbage, brocolli and cauliflower? That is the power/allelic variation within existing genes in the genomes.OK, our genomic stock could have been the horse family inlcuding donkeys, perhaps including the zebra. 2 or 3, maybe 1 big/small cat families etc.Cellular novelties? Origin of life issue of course invovles all systems. After that: Multicellularity. Respiratory proteins. Immune system proteins. Plant unique metabolic. Animal unique metabolic. Etc.The genomes document non-stop cellular nmovelty. A mammalian cell is very different to a prokaryotic cell.Gene families can be identified by sequence similarity. After 3D protein structure deterimnation, or fiunctional identification, many genes can go into existing fold families. Regardless there are tens of thousands of gene families and probably between 3,000 and 10,000 fold families.members of a gene family will always have the same fold. But some gene famiiles may share a fold with another gene family. Someteims considered divergent someteims convergetn by evolutionists.The potential of a fold is ultimately determined by it's ability to display sidechains (amino-acid (AA) chemical groups that vary from one AA type to antoher) in 3D. Each fold will hav a differnet repotoir of possibilities. It is not well understood by any means. But we all (TB puts his mainstream hat on) suspect that certain folds are better for some tasks than others but we also know that the same fodl can do multiple jobs. Evoltuionists predicted far, far more reuse of folds within bochemical enzymatic pathwyas tha nis observed in genomes.The discontinuity occurs as to whether it is an optimization issue (exisitng functional gene) or a discovey issue (new function needed). Regardless of bias these isseus differ in difficulty markedly and in time expected.Most (all?) studies deomnstrate that genuses, if not families, contain the same gene families. Obviously there are genes that are lost along the way which makes this issue not as easy as one would like. Mouse and man are only seperated by 300 gene families. Nevertheless it is a discontinuity.

PercyCystic fibrosis, as with almost any non-chromosomal disease one can think of is due to one or moreSNPS. I never said it had to be one SNP. http://www.aruplab.com/guides/clt/tests/clt_a169.htm

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The most common mutation is a deletion of phenylalanine at position 508 of the CFTR protein (F508del). This accounts for about 70% of CF alleles in European Caucasians and about 50% of individuals with CF have two copies of this gene mutation.

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The reason I and every strutural/molecular biologist knows this is the bread and butter of genetics is that genes are not fairy floss - they code for folded proteins. Your hemoglobin is the same fold as mine. When it ghoes wrong it is either the same fold with the wrong surface or unfolded (and perhaps forms fibrils).Allelic variation will be an SNP issue 99% of the time.Erwin talked about a discontinuity between allelic and large-scale!It is extremely clear from the abstract that he would associate microevoltuion with allelic subsitituion. He points out the discontinuity betwen allelic and large-scale and the paper is about the micro/macro difference! How else do you propose he support his the thesis stated in the title! I'll post segments from the paper to prove this but you are imagining that somehow the title will not be bourne out in the body of the article!

JohnMore precise? Creationist biologists recently stated that they expect the kinds to approximate the family level. When we've got more genomes we'll be able to say more.Are you doubting that there are thousands of cellular systems with associated novel gene families?I believe God separately created mammalian genomes.

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

JohnI think you need to check out your systematics - I am 99.99% sure we are not in the same (Linnean) family as chimps et al! I could do a Wilberforce but will refrain. You are confusing the chimp/human conection with a higher level of classification than family.Well, my point is that novel systems frequently use novel gene families with no hint as to where they came from.

PercyErwin shows that micro/macro is distinct via allelic/non-allelic. Standard struc biol tells us that this means existing/new gene family. You are wrong about me jumping to conclusions. I simply translated Erwin into the language of struc biol.Erwin is actaully stating the dead obvious.

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

JohnOK - you're right!As mentioned by the web site this is a 'recent' change in classificaiton. I wonder how recent. I have looked this up before and that's why I was so 'sure'.This is obviously one reason why creaitonists say the families approximate the kinds! The second reason is that everyone agrees that the classifcation scheme is not entirely objective. Once the genomes are in the system will tidy up I expect (although the issue of loss vs gain will always haunt both sides).

AndyaI'll sit it out until the genomes come in around 2005.Are you serious that sheep and bison are in the same family? I again doubt this but will not make a statement of 99.99% this time!

PercyWhy don't you tell us in what way Erwin's abstract supports the title?And what exactly do you debate? Do you disagree that alleles of a particular gene have the same fold? That's the whole point of the hunman genome and SNPs. We can all be largely descibed by the same human genome + a list of our personal SNPs. Otherwise the concept of The human genome would be silly.BTW - My thesis was passed without a single correction. Every scientists reads and interprets hundreds of abstracts a month. That is a fact. I have to tell my graduate students that frequently. You must read hundreds of abstracts and dozens of papers a month.

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[This message has been edited by Tranquility Base, 07-08-2002]

Joe, PercyIt's pretty unusual I'll admitt but it was an unusual situation - I completed the last 25% of my nuclear physics PhD (and all the write up) after 4 years of experience as a publishing RA in structural biology. I was pleasantly surprised to not have to rebind.

PercyWe'll just have to disagree about what Erwin could possibly mean about allelic substituion being discontinuous from large-scale evoltuion in a paper about macro not being just lots of micro!

JoeSorry - absolutely zero corrections! It was rather straight forward work - nothing startling or controversial. The referee's comments where not glowing - I just had learned to play the game of writing up. Becasue of the delay between the first 75% and the last 25% my thesis really was a rewrite of 3 published papers + the last bit of work.

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[This message has been edited by Tranquility Base, 07-08-2002]

OK, I'm glad we can agree on that part.What I've been trying to say is that I'm combining what Erwin's research on who knows what (pop genetics??, paleontology - we'll see) with standard structural biology knowledge.To a structural biologist saying that 'allelic variation' is not same fold is like saying that aeroplanes don't fly. I am not kidding.So, with that in mind, I still take what he is saying as indicating that there is a discontinuity between within protein fold variation (microevolution) and 'large scale' evolution. Via no great sleight of hand I suggest that large scale evolution frequently requires the origin of (i) new protein folds and/or (ii) genes with new functions and (iii) new networks of genes.So I disagree that Erwin is irrelvant. I simply took a concept he used and translated it into a the jargon of structural biology. The idea of alleles and folds are such that a non-strucutral biologists may never think of it that way and yet they are the same thing in this context. It is precisely the protein folding issue which (i) generates diseases from misfolded alleles and (ii) makes it difficult to go from fold to fold via multiple SNPs.The human genome simply has no examples where your gene (allele) for trait X has one fold and mine has another well defined fold. Hemoglobin is hemoglobin. Same for Leukemia Inhibitory Factor etc.