Rilke's Granddaughter
Posts: 311
Joined: Jan. 2005
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| Quote (afdave @ May 24 2006,05:43) | OK. I said I was going to let this thread die, but I got to thinking that I really don't want to clutter up my "God Hypothesis" thread with Anti-Evolution arguments. And I learned something new this morning which dispels a persistent myth that I have heard. It's amazing how many good scientists are jumping the Darwinist ship and writing good new articles which support Creationist Theory.
RESISTANT BACTERIA: NO PROOF OF EVOLUTION
I have always thought that most mutations are harmful, but that there are a few that are beneficial. Bacterial mutations which confer resistance to anti-biotics have been cited most often to me as an example of beneficial mutations.
So, I thought I would investigate. Here's a recent article which appears to dismantle the idea of resistant bacteria supporting the ToE. What do you think?
| Quote |
Is Bacterial Resistance
to Antibiotics an Appropriate Example of Evolutionary Change?
Kevin Anderson, Ph.D.
© 2005 by Creation Research Society. All rights reserved. Used by permission.
This article first appeared in Vol. 41, No. 4 of the Creation Research Society Quarterly, a peer-reviewed journal published by the Creation Research Society.
Abstract
Evolutionists frequently point to the development of antibiotic resistance by bacteria as a demonstration of evolutionary change. However, molecular analysis of the genetic events that lead to antibiotic resistance do not support this common assumption. Many bacteria become resistant by acquiring genes from plasmids or transposons via horizontal gene transfer. Horizontal transfer, though, does not account for the origin of resistance genes, only their spread among bacteria. Mutations, on the other hand, can potentially account for the origin of antibiotic resistance within the bacterial world, but involve mutational processes that are contrary to the predictions of evolution. Instead, such mutations consistently reduce or eliminate the function of transport proteins or porins, protein binding affinities, enzyme activities, the proton motive force, or regulatory control systems. While such mutations can be regarded as “beneficial,” in that they increase the survival rate of bacteria in the presence of the antibiotic, they involve mutational processes that do not provide a genetic mechanism for common “descent with modification.” Also, some “relative fitness” cost is often associated with such mutations, although reversion mutations may eventually recover most, if not all, of this cost for some bacteria. A true biological cost does occur, however, in the loss of pre-existing cellular systems or functions. Such loss of cellular activity cannot legitimately be offered as a genetic means of demonstrating evolution. |
Now here is an excerpt from the discussion of what is required to support the idea of Common Descent With Modification ... | Quote | Thus, common “descent with modification” provides a more appropriate and functional definition of the theory of evolution, and this article will refer to evolution in this context. This definition also entails several “predictions” regarding the types of genetic change necessary for common evolutionary descent (predictions that are in sharp contrast to the “predictions” of a creation model). Such changes must provide more than mere changes in phenotype; they must provide a genetic mechanism that accounts for the origin of cellular functions and activities (i.e., regulatory systems, transport systems, enzyme specificity, protein binding affinity, etc.).
Genetic changes that reduce or eliminate any of these cellular systems provide no genetic mechanism for common “descent with modification.” Rather, such changes are actually the antithesis of this descent, reducing or eliminating a pre-existing system of biological complexity (a reversal of “descent with modification”). Therefore, these genetic changes offer no example of a genetic mechanism for the “evolutionary” acquisition of flight by non-flying organisms, cognition by non-cognitive organisms, photosynthesis by non-photosynthesizing organisms, etc. Yet the theory of evolution requires such events to have occurred, and requires mutations capable of such genetic changes. Hence, the predictions of evolution require specific types of changes, not just so-called “beneficial” mutations. Therefore, despite the great claims that have been made, it is imperative to question whether acquisition of antibiotic resistance is a valid example of evolutionary change that supports the predictions of the evolutionary theory (i.e., the theory of common “descent with modification”). |
Here is a particularly telling table showing LOSS of function, not gain.
| Quote |
In the presence of a particular antibiotic (or other antimicrobial), any mutation that protects the bacterium from the lethality of that compound clearly has a “beneficial” phenotype. Natural selection will strongly and somewhat precisely select for those resistant mutants, which fits within the framework of an adaptive response. But, molecular analysis of such mutations reveals a large inconsistency between the true nature of the mutation and the requirements for the theory of evolution (Table I).
Table I. Mutation Phenotypes Leading to Resistances of Specific Antibiotics. Antibiotic Phenotype Providing Resistance
Actinonin Loss of enzyme activity
Ampicillin SOS response halting cell division
Azithromycin Loss of a regulatory protein
Chloramphenicol Reduced formation of a porin or a regulatory protein
Ciprofloxacin Loss of a porin or loss of a regulatory protein
Erythromycin Reduced affinity to 23S rRNA or loss of a regulatory protein
Fluoroquinolones Loss of affinity to gyrase
Imioenem Reduced formation of a porin
Kanamycin Reduced formation of a transport protein
Nalidixic Acid Loss or inactivation of a regulatory protein
Rifampin Loss of affinity to RNA polymerase
Streptomycin Reduced affinity to 16S rRNA or reduction of transport activity
Tetracycline Reduced formation of a porin or a regulatory protein
Zittermicin A Loss of proton motive force
Bacterial resistance to the antibiotic, rifampin, can result from a commonly occurring spontaneous mutation. Rifampin inhibits bacterial transcription by interfering with normal RNA polymerase activity (Gale et al., 1981; Levin and Hatfull, 1993). Bacteria can acquire resistance by a point mutation of the ß-subunit of RNA polymerase, which is encoded by the rpoB gene (Enright et al., 1998; Taniguchi et al., 1996; Wang et al., 2001; Williams et al., 1998). This mutation sufficiently alters the structure of the ß-subunit so that it loses specificity for the rifampin molecule. As a result, the RNA polymerase no longer has an affinity for rifampin, and is no longer affected by the inhibitory effect of the antibiotic.
In fact, the level of rifampin resistance that a bacterium can spontaneously acquire can be extremely high. In my laboratory, we routinely obtain mutant strains with a resistance level that is orders of magnitude greater than that of the wild-type strain. When rifampin is present, this mutation provides a decided advantage for survival compared with those cells lacking these specific mutations. But, each of these mutations eliminates binding affinity of RNA polymerase for the rifampin. As such, these mutations do not provide a mechanism accounting for the origin of that binding affinity, only its loss. |
Dr. Anderson summarizes thusly ...
| Quote | Summary
Resistance to antibiotics and other antimicrobials is often claimed to be a clear demonstration of “evolution in a Petri dish.” However, analysis of the genetic events causing this resistance reveals that they are not consistent with the genetic events necessary for evolution (defined as common “descent with modification”). Rather, resistance resulting from horizontal gene transfer merely provides a mechanism for transferring pre-existing resistance genes. Horizontal transfer does not provide a mechanism for the origin of those genes. Spontaneous mutation does provide a potential genetic mechanism for the origin of these genes, but such an origin has never been demonstrated. Instead, all known examples of antibiotic resistance via mutation are inconsistent with the genetic requirements of evolution. These mutations result in the loss of pre-existing cellular systems/activities, such as porins and other transport systems, regulatory systems, enzyme activity, and protein binding. Antibiotic resistance may also impart some decrease of “relative fitness” (severe in a few cases), although for many mutants this is compensated by reversion. The real biological cost, though, is loss of pre-existing systems and activities. Such losses are never compensated, unless resistance is lost, and cannot validly be offered as examples of true evolutionary change. |
Now you can read the rest of the article if you like HERE.
OK. Shoot me down if you can!
AFD |
For 2nd Lt. Dave
Young Dave is uncommonly dense,
For he thinks that his 'theory' makes sense.
But for it be
A theory, you see,
He has to show real evidence!
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look up
So I think the became more homogeneous after that.
