vr_junkie writes:
quote:
What remains to be seen is: new, additional, and functional genetic information for new structures which were not already present.
I am open to this - but am very skeptical that it will be shown/discovered.
Then I suggest you do some research:
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.
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Rrhain
WWJD? JWRTFM!
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