What is an ID proponent's basis of comparison? (edited)

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If you read the paper you'll find that it isn't about mechanisms that might produce the mutations causing nylon-eating capability. It's about the prior evolution of the relevant genes. Apparently these genes have long nonstop frames (lengthy DNA sequences with no stop codons), and the length is unlikely because random mutations should have inserted stop codons and broken them up into much shorter frames. Their speculation about "some special mechanism" concerns what might prevent these mutations.

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This has already been addressed.The adaptation of bacteria to feeding on nylon waste - creation.com

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The antisense DNA strand of the four nylon genes investigated in Flavobacterium and Pseudomonas lacks any stop codons.8 This is most remarkable in a total of 1,535 bases. The probability of this happening by chance in all four antisense sequences is about 1 in 1012. Furthermore, the EIII gene in Pseudomonas is clearly not phylogenetically related to the EII genes of Flavobacterium, so the lack of stop codons in the antisense strands of all genes cannot be due to any commonality in the genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid is not necessary for the normal growth of Flavobacterium, so functionality in the wild-type parent DNA sequences would appear not to be a factor in keeping the reading frames open in the genes themselves, let alone the antisense strands.

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Hi Smooth!Your excerpt focused on something else, the unlikelikhood of mutations failing to insert stop codons in long nonstop frames. I was responding to your claim of "some special mechanism" that prevents such mutations from occurring.Again, evidence of such mechanisms is the kind of data IDists should be seeking. You might want to check the technical literature on the subject since 1992 when Yomo published his paper, since there may have been progress in identifying such a mechanism since then.--Percy

The argument wasn't that bacteria are like dice. Dice were used to illustrate the relevant principle of probability. Pseudomonas aeruginosa only do it in the lab. Flavobacterium, the first bacteria to evolve nylon-eating ability, evolved this capability in the wild. See Nylon-eating bacteria: Discovery.The "9 days" claim you've mentioned several times comes from the paper Emergence of Nylon Oligomer Degradation Enzymes in Pseudomonas aeruginosa PAO through Experimental Evolution:

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After 9 days of incubation at 30^oC, hypergrowing colonies were obtained at a frequency of 10^-3.

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In other words, they'd get nylon-eating behavior after 9 days one out of a thousand times, so the probability issue is even more a factor than you originally led us to believe.--Percy

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Your excerpt focused on something else, the unlikelikhood of mutations failing to insert stop codons in long nonstop frames. I was responding to your claim of "some special mechanism" that prevents such mutations from occurring.

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Again, evidence of such mechanisms is the kind of data IDists should be seeking. You might want to check the technical literature on the subject since 1992 when Yomo published his paper, since there may have been progress in identifying such a mechanism since then.

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That would be a mutation repair mechanism. It's inside every cell...

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Pseudomonas aeruginosa only do it in the lab. Flavobacterium, the first bacteria to evolve nylon-eating ability, evolved this capability in the wild.

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Yes they can also do it in the wild if they get exposed to nylon. It's not the lab that's the difference, it's the presence of nylon. I said they can only do it in the lab, because there is always nylon present there. If by chance they get to some nylon in nature, they will also get the ability to digest it.

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In other words, they'd get nylon-eating behavior after 9 days one out of a thousand times, so the probability issue is even more a factor than you originally led us to believe.

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No, it's not the issue. It's obvious they didn't all get it at day 9. It means one out of 1000 them got it and either spread it around with LGT, or it just replicated itself. The point remains that they do it while there is nylon that is present, and they don't do it by chance alone.Just look at the next statement in the text:

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As a control experiment, the same culture broth was spread on an M9 plate containing no carbon source. However, no colonies were observed even after 9 days of incubation.

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This shows that they need a certain chemicl to be present to get the ability to digest nylon.

No kidding. But the same principle still applies. Just because it's by chance does not mean it's not predictable. There are a lot of things bacteria do only in the lab, and many things they do in predictable amounts of time. But it's always random mutation. No, they wouldn't have done it before, because nylon is not a naturally occurring polymer. You obviously did not understand what I said. Just because transposons start mutating a specific region, does not mean that they're specifically directing it to mutate to digest nylon. When stressed by a lack of their usual food source, the bacteria increase their mutation rate a specific site in the genome (one that has to do with digestive enzymes), just in case a beneficial mutation pops up. It just so happens, that a single frameshift mutation is all that is required for the bacteria to digest nylon. Another novel food source may require multiple mutations and may take longer to adapt to, if they can at all.

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

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No kidding. But the same principle still applies. Just because it's by chance does not mean it's not predictable.

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Yeah, but in this case it's not by chance. A dice has no mechanisms, a bacteria does.

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There are a lot of things bacteria do only in the lab, and many things they do in predictable amounts of time. But it's always random mutation.

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The facts contradict you. Transposons induce mutations. They are not random.

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In the June issue of the open-access journal PloS Biology, the team describes how a protein called LexA in the bacterium Escherichia coli promotes mutations and helps the pathogen evolve resistance to antibiotics. The scientists also show that E. coli evolution could be halted in its tracks by subjecting the bacteria to compounds that block LexA. Interfering with this protein renders the bacteria unable to evolve resistance to the common antibiotics ciprofloxacin and rifampicin.

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There are alos cases of mechanisms which induce mutations, and if they are blocked, a bacteria can't get resistance, no matter how long it takes.To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists – Uncommon Descent

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No, they wouldn't have done it before, because nylon is not a naturally occurring polymer.

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But if it's compounds like carbon, are found near bacteria, and they have no other source of food, they wil get the ability to digest it.

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You obviously did not understand what I said. Just because transposons start mutating a specific region, does not mean that they're specifically directing it to mutate to digest nylon.

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And I never said they did!

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When stressed by a lack of their usual food source, the bacteria increase their mutation rate a specific site in the genome (one that has to do with digestive enzymes), just in case a beneficial mutation pops up. It just so happens, that a single frameshift mutation is all that is required for the bacteria to digest nylon. Another novel food source may require multiple mutations and may take longer to adapt to, if they can at all.

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First of all we don't know how much mutations are needed. Teh secon obvious point you mised is that mutations were by definition NOT random. They were induced. Without the mechanism for inducing mutations there would be no ability to digest nylon.

While some chemicals in the environment *can* cause mutations, nylon isn't thought to be one of them. Nylon-eating ability in bacteria comes about through random mutation. The mutations for nylon-eating ability happen whether or not nylon is present in the environment. When nylon is present then these mutations are advantageous and are selected for.--Percy

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While some chemicals in the environment *can* cause mutations, nylon isn't thought to be one of them.

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Neither did I say that it is. I said that in the presence of nylon (or it's compound carbon), and in absence of other food source, the bacteria will self-induce the mechanism to produce mutations. This process will continue untill it can feed on nylon.

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Nylon-eating ability in bacteria comes about through random mutation.

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It comes about by induced mutations.

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The mutations for nylon-eating ability happen whether or not nylon is present in the environment.

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That is becasue some other compound could be present, besides oxygen and standard food source for the bacteria could be absent.

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When nylon is present then these mutations are advantageous and are selected for.

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Maybe, a big maybe. Not always are benefitial mutations selected for.

How can I learn to self-induce an ability to eat oak leaves? If I could eat oak leaves I won't have to carry so much food with me when I go camping.

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Ridicule is the only weapon which can be used against unintelligible propositions. Ideas must be distinct before reason can act upon them.

If nylon is required before the necessary mutations occur, then the mutations are not self-induced but are caused in some way by the presence of nylon.But that's not the way nylon-eating behavior is thought to come about. You say "in absence of other food source," so maybe you're thinking of the tendency of organisms under stress to experience more mutations.So what is the mechanism you think is evidence for a designer?--Percy

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How can I learn to self-induce an ability to eat oak leaves? If I could eat oak leaves I won't have to carry so much food with me when I go camping.

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You can't unless you have the mechanism for it, like the bacteria do.

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If nylon is required before the necessary mutations occur, then the mutations are not self-induced but are caused in some way by the presence of nylon.

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Exactly, they are caused by the mechanism which is trying to get the bacteria a new source of food. The mechanism doesn't know what food the bacteria actually needs, so it mutates the specific region of the genome untill the bacteria can digest the new substance.

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But that's not the way nylon-eating behavior is thought to come about. You say "in absence of other food source," so maybe you're thinking of the tendency of organisms under stress to experience more mutations.

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Yes, and that's how it goes. But the random mutations have no reason to thave their rate of occurance increased simply because the bacteria is under stress. There is a mechanism which induces the mutations when the bacteria is under stress.

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So what is the mechanism you think is evidence for a designer?

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The one that let's bacteria acquire resistance when it is activated. But when it is deactivated, the bacteria can't mutate and cant acquire resistance.To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists – Uncommon Descent

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In the June issue of the open-access journal PloS Biology, the team describes how a protein called LexA in the bacterium Escherichia coli promotes mutations and helps the pathogen evolve resistance to antibiotics. The scientists also show that E. coli evolution could be halted in its tracks by subjecting the bacteria to compounds that block LexA. Interfering with this protein renders the bacteria unable to evolve resistance to the common antibiotics ciprofloxacin and rifampicin.

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And how is this evidence for a designer?--Percy

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And how is this evidence for a designer?

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Because in the first place all genetic material is evidence for a designer.Second, this is especially evidence, since it shows that living organisms, at least bacteria could not have evolved without those mechanisms, because they can't mutate without them. And if they can't mutate, they can't evolve. If they can't evolve, they can't develop those mechanisms. And since everything is supposed to be evolved from one-celled organisms, the path to all other living organisms is effectively blocked.