What do Creationists Believe.

Probably I stand corrected about Crashfrog's use of the word 'god'. Perhaps he does use the term (on other posts) to correct a misnomer of his KJV 'God' vs. my 'god'.Sorry if presumptive offense was taken.

Andya, genetic variance vs. (raw) mutations has been taken up in heated debates elsewhere and won't be discussed here.As for the harsh depravity of human nature, I admit it is a difficult concept to swallow for all of us. Consider it merely dogmatic speculation on my part, based on perception of the observed data and the bible.But, I stated redemption/salvation as strongly as damnation. What about you? What do you state?

So far the arguments are leaning heavily in favor of the view that mutation can result in beneficial effects to an organism. Unless you have something to add? If so why don't you jump in to PhospholipidGen's topic "The Nature of Mutations". Without PPG to argue with we're talking to ourselves. Maybe you'd like to take up his banner?

Greetings Crashfrog.At present I don't have the unction/gunction to discuss beneficial mutations as viable. I don't believe we have enough genomic information to dogmatically state whether a mutation was pre-programmed to be tolerated by the gene or whether a real raw beneficial mutation actually took place in a life form (e.g. chromosomal doubling).Albeit I'll speak what some YECs and/or myself believe (to keep on the subject).Doubtless, many YECs accept raw beneficial mutations as a hypothetical or even a proven possibility based on the current data. But I dogmatically reject the possibility on EVERY level.Of course I do believe in the ToE as far as genetic variations are concerned (SANS any beneficial raw mutations).I realize that raw beneficial mutations per se are the only overcoming mechanism of any biological mega-ToE, thus I reject all mega-ToEs outright for that reason alone.'Hope this helps clarify my own dogmatic speculations concerning raw beneficial mutations vs genetic variation.

Philip writes:

quote:

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As a YEC (in orbital time), here's some of what I believe. Note, I reserve the right to change my speculations ad-hoc at anytime:

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7) Raw mutations (mutations outside mere genetic variation) can NEVER occur that are beneficial to any life form.

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8) Scientists have never witnessed nor ever will see a beneficial raw mutation.

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Then here's some information to allow you to change these in your ad hoc fashion: Remold SK, Lenski RE.
Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli.
Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11388-93.
PMID: 11572987 [PubMed - indexed for MEDLINE]"Beneficial mutations are generally thought to be rare but, surprisingly, at least three mutations (12%) significantly improved fitness in maltose, a resource novel to the progenitor." Elena SF, Ekunwe L, Hajela N, Oden SA, Lenski RE.
Distribution of fitness effects caused by random insertion mutations in Escherichia coli.
Genetica. 1998;102-103(1-6):349-58.
PMID: 9720287 [PubMed - indexed for MEDLINE]Imhof M, Schlotterer C.
Fitness effects of advantageous mutations in evolving Escherichia coli populations.
Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1113-7.
PMID: 11158603 [PubMed - indexed for MEDLINE]Rozen DE, de Visser JA, Gerrish PJ.
Fitness effects of fixed beneficial mutations in microbial populations.
Curr Biol. 2002 Jun 25;12(12):1040-5.
PMID: 12123580 [PubMed - indexed for MEDLINE]Okada H, Negoro S, Kimura H, Nakamura S.
Evolutionary adaptation of plasmid-encoded enzymes for degrading nylon oligomers.
Nature. 1983 Nov 10-16;306(5939):203-6.
PMID: 6646204 [PubMed - indexed for MEDLINE]Negoro S, Kakudo S, Urabe I, Okada H.
A new nylon oligomer degradation gene (nylC) on plasmid pOAD2 from a Flavobacterium sp.
J Bacteriol. 1992 Dec;174(24):7948-53.
PMID: 1459943 [PubMed - indexed for MEDLINE]Prijambada ID, Negoro S, Yomo T, Urabe I.
Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution.
Appl Environ Microbiol. 1995 May;61(5):2020-2.
PMID: 7646041 [PubMed - indexed for MEDLINE]What about this experiment you can do right now in your own bio lab?Take a single E. coli bacterium of type K. This means that it is susceptible to T4 phage. Let it reproduce until it forms a lawn. Then infect the lawn with T4 phage.What do you think will happen? That's right...plaques will start to form and the lawn will die since, after all, all the bacteria are descended from a single ancestor who was genetically susceptible to T4 phage.But what we actually see is that while the majority of the lawn dies, we see a colony or two surviving happily in the midst of all this virus. How can this be? Remember, all the bacteria in the lawn are descended from a single one that can't fend off T4. If these survivors were capable of fending it off because of some pre-existing genetic capability, then the entire lawn should be able to do so, too, since they all have the same genome.The only answer, of course, is that they don't have the same genome. These bacteria that are surviving are mutants. And, indeed, they are called K/4 because they can fend off T4 phage.But wait, we're not done. Take one of these K/4 bacteria and again, let it reproduce until it forms a lawn. Then, infect the lawn with T4 phage.What do you think will happen? Well, the lawn should survive without any trouble because the entire lawn is descended from a single bacterium that was immune to T4 phage.But what we actually see are plaques starting to form. How can this be? Remember, all the bacteria in the lawn are descended from a single one that is immune to T4. If that one could fend off T4, then the entire lawn should be able to do so, too, since they all have the same genome.But wait a second...did the bacteria evolve or did the phage? A little thought shows that it had to be the phage that generated a mutant, not the bacteria. That is, suppose there were a reversion mutation in one of the divisions of the bacteria to wild type. Well, that bacterium would be infected by T4 phage and die, but it would then open up space for the K/4 bacteria that is surrounding it to fill in. Thus, we'd never seen any plaques...as soon as a K-type bacteria died, it'd be replaced with K/4 bacteria which are immune.Thus, we necessarily conclude that the T4 phage is the organism that mutated. And, indeed, they are called T4h because of this mutation.So there you go: Beneficial mutations right before your eyes.------------------
Rrhain
WWJD? JWRTFM!

A very nice example. Not sure about the word necessarily.I assume you have glossed over a procedure for verifying that the K/4 bacteria did not die off as a result of some mutation unrelated to the phage, affecting them only after reproduction, or only when a quorum is reached? I'm no microbiologist, so these may be totally irrelevant questions. Could a control be exercised? Or is the conclusion inferred from repetitious experiments?In short, I agree that the conclusion you reach would be the prime candidate for an explanation, but is it the only one?