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Response to PBS series Evolution
Answers In Genesis ^ | 9/01 | Jonathan Sarfati

Posted on 09/27/2001 2:04:57 PM PDT by BikinLiLo

#4
This program aims to show that biological forces rather than the environmental ones drive evolution most strongly. But real evolution requires changes that increase genetic information, while non-information-increasing changes are part of the creation model. None of the examples presented in Episode 4 prove that information has increased, so provide no support of evolution over creation.


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To: f.Christian
Boom going... BUST!!
41 posted on 09/28/2001 1:34:22 PM PDT by f.Christian
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Comment #42 Removed by Moderator

To: netman
First, we see the equivocation—HIV producing HIV is supposed to show that particles
          could turn into people. Second, in Episode 4, it’s made clear that the related
          phenomenon of antibiotic resistance in bacteria took the medical community by
          surprise—this means that it wasn’t a prediction of evolution, except after the fact. Third,
          they fail to demonstrate that new information is involved, and the next segment shows
          that the opposite is true:

          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.

43 posted on 09/28/2001 2:46:45 PM PDT by ecoli
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To: Central Scrutiniser
The darwinists evolutionary scams reminds me of old men--little boys having an orgy over imaginary inter specie sex-- for fame--fortune--glory--dynasties too!
44 posted on 09/29/2001 12:20:02 AM PDT by f.Christian
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To: John Locke
Once you understand how random mutation interacts with non-random selection, most of the puzzle goes away. Except that it presupposes objective observers.
45 posted on 09/29/2001 12:29:11 AM PDT by RobbyS
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To: ecoli
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.

Shhhhhhh!!!!!

46 posted on 09/29/2001 5:42:30 PM PDT by jennyp
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To: netman
You're spamming.
47 posted on 09/29/2001 5:49:13 PM PDT by dbbeebs
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To: f.Christian
Boom going... BUST!!

"Blank Out!

48 posted on 09/29/2001 5:50:22 PM PDT by dbbeebs
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To: dbbeebs
bttt
49 posted on 09/29/2001 5:53:00 PM PDT by f.Christian
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To: Charlotte Pearce
Ken Ham is an utter and complete fraud, if there is one thing creationists excel in, it is keeping con-artists in the money,

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,

50 posted on 09/29/2001 6:06:54 PM PDT by ContentiousObjector
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To: ContentiousObjector
Did God create evolution...or did evolution(govt-hoax-science) decreate God?

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??

51 posted on 09/30/2001 2:03:39 AM PDT by f.Christian
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