Posted on 09/27/2001 2:04:57 PM PDT by BikinLiLo
Veronica Miller of Goethe University in Germany experimented by ceasing all antiviral
drug treatments to a patient. Then the few surviving original (‘wild’) types easily
out-competed the vast numbers of resistant forms. She said this was a risk, because the
wild types were also more dangerous, more efficient. The superior efficiency and
reproductive success of the wild type implies that the others have acquired resistance
due to a loss of information somewhere. This should not be surprising, because the same
is true of many examples of antibiotic resistance in bacteria. E.g. the bacterium has an
enzyme that usually has a useful purpose, but it also turns an antibiotic into a poison. So
a mutation disabling this enzyme would render the antibiotic harmless. But this
bacterium is still disabled, because the useful process the enzyme usually enables is now
hindered, so it would be unable to compete in the wild with non-resistant ones. The
information loss in both HIV and the bacterium is the opposite of what evolution
requires. AiG has already explained antibiotic resistance in Superbugs: Not super after
all, and answers the question Has AIDS evolved?
As usual, the opponents of intelligent design/evolution take a well known scientific fact and distort it by leaving out information. It is true that if you take a bacterium and expose it to antibiotics, there will be some cells in the population that have mutated to become antibiotic resistant. Antibiotics target essential physiological processes (e.g. cell wall synthesis, transcription, translation) and mutations in the target genes that encode the proteins involved in these processes will be at a disadvantage when there is no antibiotic in the environment. There are two classical examples of this: resistance to penicillin and resistance to streptomycin. Both can arise from mutations in genes that encode proteins in cell wall synthesis (ampC) and ribosome function (rpsL). In the case of rpsL, mutations in that gene conferring streptomycin resistance decrease the elongation rate of translation.
However, if one examines streptomycin resistant bacteria isolated from clinical settings, few, if any, have rpsL mutations. Where does resistance come from then? The answer is that these strains have acquired antibiotic resistance by the addition of a different gene. Quite often this gene is part of a transposable element (transposon). A transposon is a segement of DNA that can catalyze the transfer of itself from one place in a chromosome or plasmid to another site, either in the same DNA molecule or a different DNA molecule. The acqusition of such a transposon encoding antibiotic resistance does not impose any selective disadvantage to the resident cell, but it does confer a strong selective advantage to the cell in the presence of an antibiotic. Since there are many plasmids and viruses that can move themselves between different bacteria, all a transposon needs to do to spread itself is to transpose onto one of these plasmids and either reside there or transpose into the chromosome.
How could these transposons arise(evolve)? One scenario (among many) comes from the observation that many transposons carrying antibiotic resistance are what are called composite transposons. These are composed of a gene for antibiotic resistance that is bracketed by two insertion elements. Insertion elements are transposable elements that carry only the gene required for their transposition. The transposition process involves recognition of the ends of the insertion sequence. When two insertion sequences bracket a gene, the gene can be transposed by recognition of the ends of the two transposons bracketing the gene. Once this occurs, then further mutations within the gene in the composite transposon can create an enzyme that will confer ever greater resistance to the antibiotic. In this process, there is no loss of information and there is a gain in information. Gene duplication is a common mechanism that allows an increase in information and evolution of different functions in the two different genes.
I could point out other similar errors in this post from AiG, but time I only have a limited life span.
P.S. Whereas the genes that confer resistance to streptomycin are aminoglycoside-modifying enzymes and are not derived from the ribosomal protein gene, genes conferring penicillin resistance are clearly derived from cell wall biosynthetic genes.
Shhhhhhh!!!!!
"Blank Out!
I personally watched the documentry, I think it was very well done, and I think creationists were treated in a respectful manner
This entire creation science hoax, is based upon a stupid book a huckster wrote 40 years ago, you clowns just stack bullshit on bullshit and will shovel over cash to any fraudster who you cross,
From idiots in Peru selling rocks with pictures of dinosaurs to idiots like Hammy who go around ranting for $30,000 a day
ABSOLUTLY NOTHING IN THE THEYOR OF EVOLUTION CONTRADICTS GENESIS,
You were not around to witness creation, the writers of the bible were not around to witness creation, NO ONE WILL EVER KNOW EXACTLY HOW CREATION TOOK PLACE,
GET A LIFE,
What has happened--Marx-Darwin-Liberals--to our culture!
The Bible says love-Truth builds---Man's knowledge destroys(Anti-thiesm/evolution)...do you go along with that?
Are you living in a monastery-convent--missle silo??
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