Mutations & structural modifications ...

It seems that there is a creationist perspective that says
that mutations cannot cause non-fatal major changes to
structure.What about polydactylly (sp?) ?

You mean, being born with more than 10 fingers or toes?The weird thing is, I've heard that the gene for this is dominant, so I'm not sure why it hasn't spread further through the population...I understand it's a pretty common thing among Pennsylvania Amish, though... I guess they do just fine with it. I have no idea if the extra fingers or toes actually work.

Crashfrog- diminance or recessiveness has nothing to do with the spreading of genes, only with their phenotypic expression. salty

That's not quite what I meant.What I meant was, what prevents the gene from spreading? Because if the gene were evenly distributed throughout the population, we should see a lot more extra fingers (because it's a dominant gene).I didn't mean to imply that the gene's dominance would MAKE it spread, but my miswordings obviously implied that. My apologies.So, is it just a recent gene? Or only found in the Amish (who don't typically marry non-Amish, I imagine) and thus doesn't spread to America at large?

Yes that's what I meant.It seems to me to be quite a significant structural difference
to me, and no-one has anything more than aesthetic problems
with it.I'd wondered about the way dominant/recessive traits appear in
unusual frequencies too.Blue eyes are apparently the most common in Europe, and yet
blue-eyedness is recessive ... and there is no lack of brown
or whathaveyou eyed europeans.

I think crashfrog is aware of that, in any case
the question raised was concerning a mutation that
has caused a non-fatal structural alteration.I presume that this is originally forged in a mutation
event of some kind.

There are a number of distinct mutations in a variety of genes which can give rise to polydactyly. While some may be dominant this is by no means the case for all polydactyly mutations. Even within the Amish populations there are at leasr two distinct loci associated with polydactyly, that for McKusick-Kaufmann syndrome and that for Ellis-van Creveld syndrome and a spectrum of severity linked to different mutations at these loci.SeeBiesecker LG.
Polydactyly: how many disorders and how many genes?
Am J Med Genet. 2002 Oct 15;112(3):279-83. Review.Stone DL, Slavotinek A, Bouffard GG, Banerjee-Basu S, Baxevanis AD, Barr M, Biesecker LG.
Mutation of a gene encoding a putative chaperonin causes McKusick-Kaufman syndrome.
Nat Genet. 2000 May;25(1):79-82.Ruiz-Perez VL, Ide SE, Strom TM, Lorenz B, Wilson D, Woods K, King L, Francomano C, Freisinger P,Spranger S, Marino B, Dallapiccola B, Wright M, Meitinger T, Polymeropoulos MH, Goodship J. utations in a new gene in Ellis-van Creveld syndrome and Weyers acrodental dysostosis.
Nat Genet. 2000 Mar;24(3):283-6[This message has been edited by Wounded King, 04-24-2003]

Not to intrude, but on the other side of the spectrum there are specific Hox gene mutations involved in syndactyly...it is of interest that the pathways disrupted (and hence the mutant phenotype) are conserved between human and mouse.Goodman FR, Bacchelli C, Brady AF, Brueton LA, Fryns JP, Mortlock DP, Innis JW, Holmes LB, Donnenfeld AE, Feingold M, Beemer FA, Hennekam RC, Scambler PJ.
Novel HOXA13 mutations and the phenotypic spectrum of hand-foot-genital syndrome.
Am J Hum Genet. 2000 Jul;67(1):197-202.Post LC, Margulies EH, Kuo A, Innis JW.
Severe limb defects in Hypodactyly mice result from the expression of a novel, mutant HOXA13 protein.
Dev Biol. 2000 Jan 15;217(2):290-300.Post LC, Innis JW.
Infertility in adult hypodactyly mice is associated with hypoplasia of distal reproductive structures.
Biol Reprod. 1999 Dec;61(6):1402-8.Post LC, Innis JW. Related Articles, Links
Altered Hox expression and increased cell death distinguish Hypodactyly from Hoxa13 null mice.
Int J Dev Biol. 1999 Jul;43(4):287-94.Innis JW, Mortlock DP.
Limb development: molecular dysmorphology is at hand!
Clin Genet. 1998 May;53(5):337-48. Review.Mortlock DP, Innis JW. Related Articles, Links
Mutation of HOXA13 in hand-foot-genital syndrome.
Nat Genet. 1997 Feb;15(2):179-80.Mortlock DP, Post LC, Innis JW.
The molecular basis of hypodactyly (Hd): a deletion in Hoxa 13 leads to arrest of digital arch formation.
Nat Genet. 1996 Jul;13(3):284-9.

...which is partly why I raised it.Single mutations in a number of different genes
(in separate individuals) can cause the same
or similar phenotypic effect.This is medically researched and documented formally.This has two major implications (for me):1. Structurally altering, non-fatal mutations are possible.2. Convergent evolution is possible.

This emphasises the importance of distinguishing between the convergent evolution of proteins/ DNA and convergent evolution of a specific structural feature.Both polygeny and the hierarchical nature of so many signalling pathways means it should come as no surprise that there are many syndromes which have a number of different causes.Simply looking at the early drosophila genetic screens shows tons of this sort of thing, leading to lots of different names describing the same sort of phenotype, i.e. snake, tube and pipe or hedgehog and echidna.[This message has been edited by Wounded King, 04-28-2003]

Perhaps it is suggestive of the lack of a common
designer too.Why re-use some things, but re-do others when the
outputs (i.e. the end results) bear so much resemblance to
one another that they can only be differentiated by
genomic investigation.

We could go back and forth about what constitutes evidence for design, and what doesn't, but when it all comes down to it you can't draw a justified metapysical hypothesis from physical evidence.

It's treu that what constitutes design is,
at present, ill-defined at best. That's generally
why ID is considered to be flawed, after all.Reasoning about 'what might indicate a common
designer' is different to reasoning about whether there
is any designer, though.By-and-large I can tell which students have written a
C-program without looking at the name on the cover sheet
by the style of the program. The same students even make
the same mistakes, quite often, in different assignments
(much to my frustration )

By-and-large I can tell which students have written a
C-program without looking at the name on the cover sheet
by the style of the program. The same students even make
the same mistakes, quite often, in different assignments
(much to my frustration )I'm assuming here that you are making an argument about the feasibility of determining a creator based on empirical evidence. I'm not totally positive that this is your argument, or if there is an argument at all. Please correct me if I'm wrong.The problem with this argument is that when you look at the code with the presupisition that it has been created, you can determine its creator. This doesn't have much bearing to the biological evidence that we've found. When you say evolution brought forth what we see today, then I can agree with you. However, when you state because organisms have evolved, there was no creator you are making a statement that is not logically cohesive. This is the same as a Biblical Literlist's opinion that evolution didn't happen because they believe in God. These arenas are mutually exclusive.Furthermore, when you make a statement saying because the Big Bang Happened, there is no God, I'll just disagree with you saying that it was God's method of creation. You can't prove or disprove either of our opinions with science. Both theories are untestable, and therefore beyond the realm of science.The only thing I can hope to accomplish is to show that it is equally reasonable to talk about the Origins of the Earth in terms of God, and in terms of a naturalistic worldview. I think I summed up this arguement pretty well in one of the passages from a paper on Origins that I wrote:

quote:

---

First of all, before we progress, we must prove the reasonability of evaluating evolution from a Christian point of view to my atheistic and humanistic colleagues. The argument is simple:
1) If God exists, his existence is necessary
2) If God does not exist, his existence is impossible
3) Either God exists or he does not exist
4) God’s existence is either necessary or impossible
5) God’s existence is possible (not impossible)
6) Thus, God’s existence is necessary
While you might object to premise #5, you can’t deny that the possibility of God’s existence is a faith claim. Therefore, it is just as every much a faith claim to say there is no God as it is to say there is a God. It follows that it is just as rational to talk about the origins of life in terms of God, as it is apart from God.

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For anyone that seems to recognize those primises, they are Norman Malcom's contemporary version of the Ontological Argument.------------------
"Science without religion is lame; religion without science is blind." - Albert Einstein

The problem with even this form of the Ontological argument is that it boils down to saying "I assume that God exists". Well why not say that instead of dressing it up in the sophistry of the Ontological argument ?