Fri Aug 17, 2012 3:46 pm
Resistance to tetracycline may be mediated by one of three different mechanism:
(I) an energy-dependant efflux of tetracyclines carried out by by transmembrane spanning proteins which results in reduction of the concentration of tetracycline in the cytosol:
(II) ribosomal protection, whereby tetracyclines no longer bind productively to the bacterial ribosome; or
(III) chemical modification requiring oxygen and NADPH and catalysis by enzymes.
Efflux and ribosomal protection, mediated by plasmid or chromosomal determinants, are the two major mechanism of bacterial resistance of clinical significance......
Levy and co workers discovered that efflux is a major mechanism of tetracycline resistance in bacteria. They demonstrated that tetracycline-resistant cells lose accumulated drug faster than susceptible cells do and that tetracycline enters the bacterial cell by an energy-dependant process. The determinants which confer resistance by removing tetracycline from the cytosol encode transporter proteins located in the cytoplasmic membrane. These proteins mediate energy-dependant efflux of the tetracycline.
The ribosomal protection proteins are all polypeptides …. These proteins interact with the ribosome, making it insensitive to tetracycline inhibition. |The exact mode of interaction of these proteins with the ribosomes is not well understood.
Tetracycline resistance is often due to the acquisition of new genes, which code for energy-dependent efflux of tetracyclines or for a protein that protects bacterial ribosomes from the action of tetracyclines.
We have shown that the tet genes are found in the producing Streptomyces spp. and the otr genes are found in the nonproducing Mycobacterium spp. (Table (Table5).5). Eighteen of the tet genes and one of the otr genes code for efflux pumps, and seven of the tet genes and one of the otr genes otr(A) code for ribosomal protection proteins (Table (Table3).3). The presence of both tet and otr genes with similar efflux or ribosomal protection mechanisms of resistance is consistent with the hypothesis of lateral gene transfer from the tetracycline-producing streptomycetes to other bacteria (16)
Both efflux and ribosomal protection proteins are found in antibiotic-producing streptomycetes …...
Thus, bacteria exposed to antibiotics in the environment or in animals can ultimately influence antibiotic resistance in bacteria of human origin
The low level of occurrence of tetracycline resistance among isolates from wild animals is presumably due to their low exposure to these antibiotics. Most of these isolates either had a high level of resistance or none at all, suggesting that the acquisition of a mobile genetic element accounts for resistance.
[/quote]“Thus, a gene for antibiotic resistance that evolves via natural selection may be shared.”
Thu Sep 13, 2012 11:43 am
A modern working definition of a gene is "a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions, and or other functional sequence regions ".
Natural selection is the gradual, non-random process by which biological traits become either more or less common in a population as a function of differential reproduction of their bearers.
It is a key mechanism of evolution
Amino acids serve as the building blocks of proteins, which are linear chains of amino acids. Amino acids can be linked together in varying sequences to form a vast variety of proteins. Twenty amino acids are naturally incorporated into polypeptides and are called proteinogenic or standard amino acids. These 20 are encoded by the universal genetic code. Nine standard amino acids are called "essential" for humans because they cannot be created from other compounds by the human body, and so must be taken in as food. (Again although not strictly correct we get the picture)
Wed Sep 19, 2012 2:55 am
Wed Sep 19, 2012 3:23 am
scottie wrote:This is not exactly correct and at least 5 years out of date, but let's stick with it for the moment.
scottie wrote:Wouldn't it be nice to see some real science showing how Natural Selection produces a gene.
Thu Sep 20, 2012 4:13 pm
There are random mutations that rearrange the DNA of the cell. These mutations are invariably the result of copying errors, breakdown in regulating functions like error correction, and DNA damage from environment like from chemical or UV radiation sources.
There are also more mutations in DNA, by orders of magnitude, as a result of regulated cell processes, than those that are random in nature.
The random mutations that do occur are invariably deleterious to the organism and are quite naturally the subject of intense study to solve or prevent health problems like cancers.
The point I make is this.
The reality is that most genetic changes occur as a result of cellular processes in response to stress, damage and copying errors and are rectified in various ways, (I have not taken account of the developmental changes that occur) while most other mutations which for some reason not corrected, are deleterious to the organism.
I haven't even begun to talk about transposons and their part in genome restructuring. All these processes are under the control and regulation of the cell as it responds to stress and the maintaining of it's own equilibrium.
In the light of all this actual evidence (and with respect, not logic that you appear to rely upon) what does Natural Selection actually have to do?
Where are the functional phenotypes that random mutation is supposed to have produced in order for NS to select from?
It is no wonder that Darwin himself acknowledged he could recount no evidence for species change by NS.
The reality is that NS has very eloquently described how species may survive but has nothing to say about how they arrived.
Let me see if I've got this straight. Someone says to you, "beneficial mutations exist. Example: antibiotic resistance." And your response is, "this bacterium got antibiotic resistance from lateral gene transfer, therefore beneficial mutations do not exist."
What the empirical evidence shows is that, it is the direct clinical intervention that induces the acquisition of these natural occurring mobile genetic elements in tetracyclines that produces the resistance.
I also went on to state
Even if a mutation occurs in the ribosome that may provide an advantage to the bacterium, it would come at a cost. Ribosomal mutations, while providing antibiotic resistance for the organism, slow the process of protein synthesis, slow growth rates, and reduce the ability of the affected bacterium to compete in an environment that is devoid of a specific antibiotic.
Furthermore, a mutation that confers resistance to one antibiotic may make the bacterium more susceptible to other antibiotics.
These are deleterious effects and are completely inconsistent with the evolutionary model of natural selection acting on random mutations.
Antibiotics are among the most valuable compounds used for fighting human diseases. Unfortunately, pathogenic bacteria have evolved towards resistance. One important and frequently forgotten aspect of antibiotics and their resistance genes is that they evolved in non-clinical (natural) environments before the use of antibiotics by humans.
Sun Sep 23, 2012 6:57 am
scottie wrote:My position is not that random mutations do not happen. They do. Does NS act upon random mutations. Yes I believe that may also happen. In other words, does evolution (change over time) happen. Yes.
scottie wrote:All I have argued is that this resistance is already there in nature. The question is not how did the resistance in humans come about. We know that, well sort of! The question is how did these genes come about in the first place.
scottie wrote:Ok so you are not interested in discussing the origin of genes with me but you do know the simple answer. Genes are legos made of legos. My my, however did I miss that one. Errr yep I've got it. I have been accused of lacking imagination, that's what it must be. Got to keep working at it.!!
Wed Sep 26, 2012 7:56 pm
But if we can agree that a random mutation might confer a benefit for the mutated organism, then we can agree that the variation on which natural selection acts is, at least in part, the result of random mutation.
“Yes I believe that may also happen.”
First, the bacteria evolves a gene that confers resistance to some dangerous substance. This substance is "natural" in the sense that it is not man-made (not an artificial antibiotic).
Thu Sep 27, 2012 10:01 am
Thu Oct 04, 2012 5:09 pm
scottie wrote:Please don't take my statement any further than what I have said.
scottie wrote:How does one distinguish between what is a random and what is a prescribed cellular response to outside pressure.
scottie wrote: I am not aware of any biologist that disagrees that most random mutations are deleterious.
scottie wrote:Could you explain please; How does the bacteria “evolve” a gene?
Sat Jul 13, 2013 1:44 am
Luxorien wrote:scottie wrote:Please don't take my statement any further than what I have said.
What pressure is a colony of bacteria being subjected to when you keep them in their optimal environment? How do you account for steady rates of mutation in populations of organisms kept under controlled laboratory conditions?
Luxorien wrote:scottie wrote: I am not aware of any biologist that disagrees that most random mutations are deleterious.
Sat Aug 10, 2013 7:47 am
Fri Sep 27, 2013 12:22 pm