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Antibiotic resistance through nitric oxide-producing enzymes

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So how did these nitric oxide-producing enzymes arise? By Darwinian processes?

…Nudler’s team found that many antibiotics kill bacteria through the production of harmful charged particles known as reactive oxygen species, otherwise called oxidative stress.

“Antibiotics cause bacteria to produce a lot of reactive oxygen species. Those damage DNA, and bacteria cannot survive. They eventually die,” Nudler said in a telephone interview.

“We found nitric oxide can protect bacteria against oxidative stress.”

He said bacteria produce nitric oxide to resist antibiotics. The defense mechanism appears to apply broadly to many different types of antibiotics, he said.

Nudler said many companies are testing various nitric oxide-lowering compounds called nitric oxide synthase inhibitors for use as anti-inflammatory drugs.

He thinks a compound in this class could be made to reduce the amount of nitric oxide bacteria can produce, reducing their ability to resist antibiotics. That would mean researchers would not need to discover new antibiotics.

SOURCE

Comments
Course if the down regulation is broken via mutation, this wouldn't work. In fact it would be pretty easy to mutate so that it did break. An ID solution would be to find something that attacks a critical function that the bacteria can't break and remain viable.tragic mishap
September 29, 2009
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Just a thought on the original topic. Somebody should do a study on the effect of using nitric oxide with antibiotics versus straight anti-biotics. If nitric oxide synthase is down regulated by higher conentrations of its product, nitric oxide, then higher levels of nitric oxide would reduce expression of nitric oxide synthase. If this study is correct then that would give a big assist to the antibiotics. You could do this in the lab fairly easily, but even a human clinical trial should not be that hard. We already have an FDA approved drug that delivers a healthy dose of nitric oxide - Viagra.tragic mishap
September 29, 2009
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The fact remains that this is not natural selection. The fact remains that even if no fungal toxin were present, T-urf13 provides no positively selectable trait and would likely not persist, low density of the toxin notwithstanding.
??? The fungal toxin isn't really relevant, except for refuting a later statement of tragic mishap's. The primary trait associated with T-URF13 is cms, a characteristic that is not uncommon in nature, and a trait whose general origins (not just in maize, but in plants in general) is often traceable to the occurrence, via natural and random mechanisms analogous to those that gave rise to T-URF13, of novel proteins that have no "parents". Basically, these are numerous cases of multifunctional proteins, each of which likely has many more "CCC's" than Behe could ever stomach, evolving via natural and random mechanisms in circumstances that Behe predicts absolutely preclude such events.
In fact, I’d be willing to bet the binding to the fungal toxin is non-specific to the toxin. In other words I bet there’s other chemicals that could open the channel.
The binding of toxin to protein is rather specific. But that of course does not preclude the existence of chemical mimics. That would not be very surprising.
This should be qualified to mean that no more than one or two mutations can be traversed without each one being visible in some way to natural selection. Behe’s hypothesis is about how far you can go before you get a selectable trait, not how far you can go period.
This makes no sense to me. I think you are just putting words in Behe's mouth, to try and rescue from the fatal insult that is the example we are discussing. Regardless, the "CCC" represented by the toxin-binding site almost certainly involves many more than two amino acids, and it evolved without any selection at all.Arthur Hunt
September 17, 2009
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Okay. So it's believable that CMS would not only persist but perhaps be maintained at a ratio higher than 50/50 to non-CMS. The fact remains that this is not natural selection. The fact remains that even if no fungal toxin were present, T-urf13 provides no positively selectable trait and would likely not persist, low density of the toxin notwithstanding. In fact, I'd be willing to bet the binding to the fungal toxin is non-specific to the toxin. In other words I bet there's other chemicals that could open the channel. Also, my earlier hypothesis:
My hypothesis would be that since this enzyme was not designed, the change from the wild type must be the result of one or at most two mutations, going off Behe’s arguments in Edge of Evolution.
This should be qualified to mean that no more than one or two mutations can be traversed without each one being visible in some way to natural selection. Behe's hypothesis is about how far you can go before you get a selectable trait, not how far you can go period.tragic mishap
September 17, 2009
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Tragic, Hmm. So you eliminate plants with the Turf-13 gene from your experiment, and instead look at another CMS genotype. If the CMS plants rise in frequency vs the hermaphroditic plants in your field over time, how would you know the results weren't just due to chance?Dave Wisker
September 17, 2009
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So apparently you don't seem to care if the results might be affected by your experimental methodology rather than reflect what you are actually trying to examine. Good luck on that grant then.Dave Wisker
September 16, 2009
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tragic mishap, is your expectation that the CMS plants would not persist in the mixed population you describe?Arthur Hunt
September 16, 2009
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The test is not for fungus, it's to see if CMS would be positively selected for by nature. The plants would be exactly the same except one would be CMS and the other not. There would be no need to include a gene for the Turf-13 protein. Anyway, let me know about that grant, and in twenty years after I have tenure I'll see if it's worth my time. Wouldn't want to expose my real beliefs to the thought police before I'm safely home.tragic mishap
September 16, 2009
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tragic, Do you have a grant in mind? Not particularly, but then I don't work with plants or agriculture. Art Hunt might know of some for which you could apply. I'd work a bit more on your experimental design first, however. Just one example of the top of my head: how would you set up your controls for density effects when assessing fungus resistance?Dave Wisker
September 16, 2009
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Dave,
Until our ID friends consider and explore these known selective advantages for CMS, and then compare them to the one selective disadvantage in a natural setting, their objections really don’t hold much water.
Do you have a grant in mind? One in which I could be explicit about the purpose of the experiment? Because I have a perfect test in mind. 1. Take a CMS and non-CMS batch of seeds mixed 50/50, and plant them randomly in a field. 2. Leave them be for several seasons, taking samples of every generation. The plants would be allowed to breed naturally. 3. See which version wins out.tragic mishap
September 16, 2009
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The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize. Art:
And the evidence for this is …. ?
It's pretty simple actually- no maize no maize protein URF 13-T.
And how is this statement not a flat-out assertion that “artificial selection” was in fact an explicit designing, from the ground up, of the protein?
You should explain how it is such an assertion. I know I never thought nor implied such a thing. But anyway you also said:
The maize mitochondrial genome was shuffled without any specific protein-coding purpose, and a protein that far exceeds the limits Behe has placed on random processes was the product.
That is not Dr Behe's argument. When the protein in question "evolves" an new binding site- that is other than the binding sites it had from the beginning, then you will have something.Joseph
September 16, 2009
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I make a point: The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize. Instead of actually addressing that point what do our evolutionist guests do? Ignore it and prattle on about more irrelevancies. All this to hide the fact that Art is wrong because new binding sites did not evolve. The protein in question came with all the binding sites Art sez refutes Behe. Except that Art doesn't know what he is talking about because new binding sites didn't evolve on this protein. What it has it came with.Joseph
September 16, 2009
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Dave Wisker:
1. Turf-13 arose naturally in maize.
Maize arose artificially. The protein in question wouldn't have arisen if we didn't artificially screw around with the plant. As far as anyone knows it arose as a direct consequence of our meddling.
3. Joseph writes “Except that outcrossing isn’t possible if all males are sterile."
That is a true statement. You do understand biology, don't you?
Perusal of literature on the evolutionary dynamics of CMS in the wild
We aren't talking about things in the wild. Why do you keep changing the topic?Joseph
September 16, 2009
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1. Turf-13 arose naturally in maize. That is, it was neither engineered nor planned by humans. 2. That CMS maize plants weren't used in agricultrural settings settings says absolutely nothing abouit how CMS plants fare in the wild. 3. Joseph writes "Except that outcrossing isn’t possible if all males are sterile." This is about as empty a statement as one can get. Perusal of literature on the evolutionary dynamics of CMS in the wild shows that CMS is maintained polymorphically-- females with selective advanatge rise in frequency until they reach an equilibrium with hermaproditic plants (there are no 'male' plants in these situations. This equilibrium is reached via standard population genetic processes.Dave Wisker
September 16, 2009
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BillB:
Joseph, Can maize, or the maize genome, tell the difference between differential reproduction rates caused by human activity and rates caused by a change in climate?
Do you have a point? Neither maize, nor the maize genome, would exist without artificial selection. No corn, no corn-dogs. No popcorn. No children of the corn...Joseph
September 16, 2009
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Joseph, Can maize, or the maize genome, tell the difference between differential reproduction rates caused by human activity and rates caused by a change in climate?BillB
September 16, 2009
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The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.Joseph
September 16, 2009
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Dave Wisker:
1. CMS maize may be susceptible to fungus, but as to whether its ‘devastating’ to fitness, as our ID friends maintain, one has to wonder if the susceptibility is density-dependent.
"Devastating to fitness"? Also if one reads the papers on this one finds out that they STOPPED using the seeds because of the susceptability to fungal toxins. T-URF 13 protein, second sentence.
3. CMS also offers the known selective advantage of outcrossing.
Except that outcrossing isn't possible if all males are sterile. Until the evolutionists can demonstrate that maize can arise without agency involvement, that the protein in question would also arise in that scenario, they don't have a case. Also until the demonstrate the binding sites/ properties in question "evolved", as opposed to being present from the origin of the protein, they don't have anything. Art sez:
Um, Behe’s entire argument was built around the evolutionary response of a parasite that has been exposed to a selective agent of decidedly human origin.
It's called an "arms race".
In this regard, there is no difference between the origins of chloroquine resistance in Plasmodium and the origins of T-URF13.
Just because you can say it doesn't make it so. Again Art uses "debate by declaration" and "debate via straman". And he talks about credibility.Joseph
September 16, 2009
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Art writes:
Um, Behe’s entire argument was built around the evolutionary response of a parasite that has been exposed to a selective agent of decidedly human origin. In this regard, there is no difference between the origins of chloroquine resistance in Plasmodium and the origins of T-URF13.
It seems our ID friends want to have it both ways.Dave Wisker
September 16, 2009
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A couple of things re: Cytoplasmic male sterility. 1. CMS maize may be susceptible to fungus, but as to whether its 'devastating' to fitness, as our ID friends maintain, one has to wonder if the susceptibility is density-dependent. Under densely-packed agricultural conditions, the disdvanatge may be high, but not as much of a problem in the wild. 2.Does the susceptibility of CMS maize to fungus outweigh the known selective advantage of higher yield? It has long been known that CMS plants often have higher yields than their hermaphroditic counterparts. 3. CMS also offers the known selective advantage of outcrossing. Does this outweigh the susceptibility to fungus? Until our ID friends consider and explore these known selective advantages for CMS, and then compare them to the one selective disadvantage in a natural setting, their objections really don't hold much water.Dave Wisker
September 16, 2009
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Also, Mr. Hunt, just because cytoplasmic male sterility exists in the wild doesn't mean that natural selection favored it in any way or that it was formed by Darwinian processes. You are assuming what you are trying to prove.tragic mishap
September 16, 2009
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Mr. Hunt, It's definitely an interesting case. I was fascinated by it. Never did I suggest that scientists designed the protein. All I said was that intelligence was involved in making it, and there is no evidence that anything like this could have been done without intelligence. All this example proves is that intelligent design is more powerful than RM + NS when it's not even trying. It's really a very interesting, fringe case that validates ID predictions about intelligence being necessary for this kind of structure. Just because some of these mutations piggy-backed intelligently selected mutations does not make it random. You could convince me that this was a fully random process by answering the following question: How did all the intermediate steps spread throughout the population leading to subsequent fortuitous mutations? Presumably the mutations occurred originally in a single individual plant. That would have to be the case if they were truly random. The next step would be spreading throughout the population even though they do not confer an advantage visible to natural selection. So how did those mutations spread? I'm talking specifically now about the mutations leading to the Turf-13 protein.tragic mishap
September 16, 2009
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The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize.
And the evidence for this is .... ? And how is this statement not a flat-out assertion that "artificial selection" was in fact an explicit designing, from the ground up, of the protein?Arthur Hunt
September 16, 2009
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Arthur Hunt:
I read this comment and think that tragic mishap and joseph are clsiming that plant breeders in the 50’s and 60’s deliberately and painstakingly designed T-URF13
That thought never crossed my mind. IOW Art has erected yet another strawman. The point is, and I have made it clear before, that without artificial selection this protein would not have arisen in maize. IOW because of artificial selection this type of thing had the opportunity. Without AS thgere wouldn't have been that opportunity. Dr Behe's entire argument is against blind watchmaker type processes. Had maize arisen solely via those types of processes you would have a point. Also it appears that URF13-T came with the ability to form a pore in the membrane. IOW URF13-T didn't form and then evolve those binding sites. That proves Arthur is wrong and has misrepresented Dr Behe's arguments once again.
That’s why cytoplasmic male sterility is a trait that is seen in the wild.
We aren't talking about mere CMS. We are talking about this one particular protein. Try to stay focused.Joseph
September 16, 2009
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the intelligently designed goal of the project was to create a plant that was male sterile, hardly something natural selection would select for. In fact, natural selection would select against both these mutations.
That's why cytoplasmic male sterility is a trait that is seen in the wild. Fact is, plant breeders weren't intelligently designing anything; they were just looking for things that natural mechanisms provide through normal genetic processes.
Also, as Joseph says, these plants were artificially selected for by human beings with a purpose in mind. So we know that it wasn’t natural selection because humans did the selecting. The influence of intelligence cannot be denied here, as intelligence preserved and preferentially propogated all the intermediate steps whereas natural selection would never have done so.
I read this comment and think that tragic mishap and joseph are clsiming that plant breeders in the 50's and 60's deliberately and painstakingly designed T-URF13. Our two IDists here are insisting that scientists in that era: 1. knew that a protein like T-URF13 could incite male sterility; 2. knew exactly how to design, from scratch, this protein; 3. knew how to assemble a gene encoding the protein; and 4. knew how to introduce the gene into the maize mitochondrial genome to yield exactly what is seen in the cmsT mitochondria. Frankly, tragic mishap and joseph have wandered way past the line of respectable credibility in their suggestion. They should read Meyer's latest book so that they can get an inkling of the history of molecular biology and understand how preposterous their claims are. The fact is, T-URF13 arose strictly via random and natural (NOT intelligent) processes. The maize mitochondrial genome was shuffled without any specific protein-coding purpose, and a protein that far exceeds the limits Behe has placed on random processes was the product.
You continue to post about T-urf13 even though it has been pointed out to you that it is a result of artificial selection and therefor does not go against Behe who only argues against NATURAL selection.
Um, Behe's entire argument was built around the evolutionary response of a parasite that has been exposed to a selective agent of decidedly human origin. In this regard, there is no difference between the origins of chloroquine resistance in Plasmodium and the origins of T-URF13.Arthur Hunt
September 15, 2009
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Another thing to consider pertaining to T-URF 13 and Behe's "Edge of evolution": Dr Behe was talking about new bunding sites evolving. Did the T-URF 13 binding sites evolve or were they always present?Joseph
September 15, 2009
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I read both your articles on TREE a long time ago Mr. Hunt. Joseph is correct. The T-urf13 protein resulted in a devastating loss of fitness for the plant by causing it to be vulnerable to a toxin from a certain fungus. Also, the intelligently designed goal of the project was to create a plant that was male sterile, hardly something natural selection would select for. In fact, natural selection would select against both these mutations. Also, as Joseph says, these plants were artificially selected for by human beings with a purpose in mind. So we know that it wasn't natural selection because humans did the selecting. The influence of intelligence cannot be denied here, as intelligence preserved and preferentially propogated all the intermediate steps whereas natural selection would never have done so.tragic mishap
September 15, 2009
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Arthur Hunt, You continue to post about T-urf13 even though it has been pointed out to you that it is a result of artificial selection and therefor does not go against Behe who only argues against NATURAL selection. IOW Hunt is being dishonest and he thinks his dishonesty is meaningful discourse. Thank you for continuing to prove that your only methodology for debate is lying and deception.Joseph
September 15, 2009
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"My hypothesis would be that since this enzyme was not designed, the change from the wild type must be the result of one or at most two mutations, going off Behe’s arguments in Edge of Evolution." The problem with this hypothesis (nicely stated though it is) is that Behe is wrong.Arthur Hunt
September 14, 2009
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ellazimm, First of all, I did not infer design there, but that doesn't mean design didn't happen. It could be a case of a false negative, which as explained by Dembski is unavoidable in the design inference. A real problem would be a false positive. Secondly, this was more a parable than a real analysis. My hypothesis would be that since this enzyme was not designed, the change from the wild type must be the result of one or at most two mutations, going off Behe's arguments in Edge of Evolution. That's a testable prediction. If that prediction was wrong, then according to my test this enzyme was designed. That would be a clear case of a false positive, invalidating my test. So in answer to your question, poor functionality is a result of random mutations from the intended design. Darwinists argue that poor functionality, anywhere they see it, is evidence against design. What we are actually saying is that the original design must not have been poorly functional, but rather exquisitely functional. Therefore a design theorist would hypothesize that any poor function in nature is the result either of mutations away from the original design or there is something we don't yet know about the system that is causing us to erroneously assume poor functionality. This too is a testable prediction and could generate a large amount of fruitful research in every case where Darwinists shrilly claim poor function, like the panda's thumb. NOTE: Causing information loss (destroying a function) is easy and much more than one or two mutations could be evident. Very generally, the one or two mutations limit is for new functions caused by a change in protein structure. Behe goes a bit further and puts a limit of six mutations as the high threshold for new protein-protein binding sites.tragic mishap
September 14, 2009
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