Posted on 03/28/2006 2:37:59 PM PST by Conservative Coulter Fan
"A new b-lactam-inducible penicillin-binding protein (PBP) that has extremely low affinity to penicillin and most other b-lactam antibiotics has been widely found in highly, b-lactam(methicillin)-resistant Staphylococcus aureus (MRSA). The gene for this protein was sequenced and the nucleotide sequence in its promoter and close upstream area was found to show close similarity with that of staphylococcal penicillinase, while the amino acid sequence over a wide range of the molecule was found to be similar to those of two PBPs of Escherichia coli, the shape-determining protein (PBP 2) and septum-forming one (PBP 3). Probably the MRSA PBP (Mr 76462) evolved by recombination of two genes: an inducible type I penicillinase gene and a PBP gene of a bacterium, causing the formation of a b-lactam-inducible MRSA PBP."
"Evolution of an inducible penicillin-target protein in methicillin-resistant Staphylococcus aureus by gene fusion." Song, M.; Wachi, M.; Doi, M.; Ishino, F.; Matsuhashi, M. FEBS Letters, 1987, 221, 167-171.
Maybe if you write them a letter they'll issue a correction even at this late date.
No, I'm saying they didn't. That old genes may have been acquired or reacquired through horizontal transfer. And that some gene variation is preprogrammed into bacterial DNA, but not at the level that would add information.
"MRSA is derived from a novel gene which originated in 1987 from splicing together a gene from S. aureus and E. coli. This novel gene has since undergone mutation to give several variants. "
Do you have a source for that. Because this article (dated 2001) from the CDC states that MSRA origins are unknown and suggests horizontal tranfer and mutations resulting in loss of function as the two most likely origins of MSRA.
http://www.cdc.gov/ncidod/eid/vol7no2/chambers.htm
"Origins of Community-Acquired MRSA The origins of these community-acquired strains are subject to debate. One possibility is that they are feral descendants of hospital isolates. If so, these isolates must have undergone considerable change because they possess distinctive PFGE patterns and have lost resistance to multiple antibiotics. Another possibility is that the community isolates arose as a consequence of horizontal transfer of the methicillin-resistance determinant into a formerly susceptible background. This possibility could also account for the unique PFGE patterns and lack of resistance to multiple drugs. In the case of penicillinase-mediated resistance, dissemination of strains from the hospital and horizontal transfer of the penicillinase gene into susceptible recipient strains were both likely to have contributed to emergence of penicillin-resistant strains in the community. Penicillinase typically is plasmid encoded and can be readily transferred by transduction or conjugation. These characteristics account for methicillin-susceptible, penicillinase-producing strains being genetically diverse and polyclonal. "
So this guy is basically accepts genetic mechanisms that allow bacteria to reproduce - ie descend. He also accepts genetic mechanisms that allow them to mutate - ie modification. But then he disagrees that there is any genetic mechanism for "descent with modification". Contradicts himself there.
Correct. And both have been observed occurring.
But we don't see spontaneous appearance of beneficial mutations
Sure we do.
except when the mutation results in a loss of functionality and that loss of functionality is somehow beneficial as in the case of sickle cell anemia.
False. Please stop posting your ignorant misinformation as if you had a clue what in the hell you were talking about.
Bacterial resistance has been offered as spontaneous appearance of beneficial mutations.
Because it is.
But this article examines that and rejects bacterial resistance as being the result of a beneficial mutation except for loss of functionality.
Because the author is a dishonest creationist, who falsely spins the science in service of his theological agenda instead of fairly assessing it.
False. There are countless examples of antibiotic resistance arising de novo in an isolated population in which it previously did not exist.
This is so common that it's a frequent experiment for beginning classes in biology -- which is probably why the anti-evolutionists are grossly ignorant of it, they don't seem to have bothered with even the most elementary education on the topic they attempt to pontificate upon.
And I'd rather know what I'm talking about than "argue" the subject on the level of a fourth-grader, as you have here.
The fit survive, the unfit die off..... regardless of what process produced the fitness.
No, I'm saying they didn't.
You say a lot of false things on this topic, due to your ignorance of it, and this is yet another example.
That old genes may have been acquired or reacquired through horizontal transfer.
Gosh, Mr. Wizard, then how do you explain antibiotic resistance arising in monocultures? Doh! Are you sure you have any clue what in the hell you're talking about? Oh, right, you're an anti-evolutionist -- the question is redundant.
And that some gene variation is preprogrammed into bacterial DNA, but not at the level that would add information.
ROFL! Yes, and the Easter Bunny brings the bacteria caramel eggs, too.
["MRSA is derived from a novel gene which originated in 1987 from splicing together a gene from S. aureus and E. coli. This novel gene has since undergone mutation to give several variants."]
Do you have a source for that.
Yes he does.
Because this article (dated 2001) from the CDC states that MSRA origins are unknown
No it doesn't. It says that the origins of community-acquired MSRA are "subject to debate". It's talking about some new strains of MSRA which are now being investigated, not the one he's talking about. Learn to read.
and suggests horizontal tranfer and mutations resulting in loss of function as the two most likely origins of MSRA.
Mutations, yes, "resulting in loss of function" no, you just made that up. Bad anti-evolutionist, no cookie for you.
ping.
Why is this Front Page News?
Glad somebody mentioned that. Aside from bacterial mutations which lose information, sickle-cell is the one other "beneficial mutation" we commonly hear about.
Sickle cell is supposed to confer some limited immunity to malaria but, when you think about it, shooting somebody through the head would prevent them from dying of malaria as well. You wouldn't call that "beneficial".
For addition of information and for evidence that MRSA comes from a novel gene splicing to produce a new gene, see my reply #21.
I guess Behe has company in tossing out a legitimate science degree and career.
2. Horizontal gene transfer occurs all the time among procaryotes in nature and even from procaryotes to eucaryotes. At least the author admits that there are mechanisms for new DNA acquisition (increase in DNA and information) that leads to increased selection for a "fitter" microbe. So many Creos argue that that cannot occur.
3. All the antibiotic resistant mutations noted in the paper and those mentioned as ignored (purposely or accidentally - ahayes) have arisen de novo in numbers of microorganisms without possible gene transfers, as Ichy has also noted.
Define "lose information" as you are using it in this context. Defend your use of this term by employing quantitative analysis. We'll wait.
sickle-cell is the one other "beneficial mutation" we commonly hear about.
And for good reason.
Sickle cell is supposed to confer some limited immunity to malaria but, when you think about it, shooting somebody through the head would prevent them from dying of malaria as well. You wouldn't call that "beneficial".
You're completely misunderstanding the sickle-cell example. The sickle-cell allele is entirely beneficial and not harmful when heterozygous. Try again.
But in response to the article's title question - there is no speciation here, so no classical Darwinian evolution. However, the process of acquiring new genetic information and producing a new phenotype is certainly a step in the evolutionary process.
There are easier and healthier ways to avoid malaria. DDT for one.
I notice Song is a lot less certain than you are. I always appreciate a scientist who allows for possibilities other than his own theory.
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