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

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No, not always.

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Yes always. Can a calculator give you a number that hasn't been programmed into it?

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The generation of random numbers is programmed into an algorithm, but the output of the algorithm is a genuine set of (very nearly) random numbers.

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The ones that have been programmed into it.

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Random number generators often 'measure' things to generate the seeds for random number generation, eg the system time, or mouse movements on a PC. So the behaviour of a machine can be genuinely random.

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But it's not random. It's programmed. Whatever the time is, and whatever the number the generator get, the result is always the same. It's much more complex than without the random number generator, but it's still the same. Just because it's heavier to visualise it, and it seem like the robot is acting randomly, it doesn't mean it is. Because we know that it is beaing led by it's programming.

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Then the selection / mutation / reproduction algorithms are applied, so that the most effective random movements are kept,combined and varied.

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Yes, and all of these actions are already programmed in advance.

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In this way the random start point rapidly coverges on effective movement for the robot.

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And for any given start point, the robot will do exactly as it was programmed to do.

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except that we don't!

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Well you can't always ask for everything!

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good, hopefully I'm laying some evidence out for you post by post.

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So far so good...

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The Japanese researchers you mentioned believe that the genetic change responsible for nylon-eating behavior was caused by random mutation, but you seem to believe that it's something else, that there's some mechanism already inherent in this bacterium that produces the necessary genetic changes when in the presence of nylon. That's an interesting idea. Is there any evidence for this mechanism?

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No, they do not. Read carefully.

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Some statements by Yomo et al., express their consternation:

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‘These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes.

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‘The presence of a long NSF (non-stop frame) in the antisense strand seems to be a rare case, but it may be due to the unusual characteristics of the genes or plasmids for nylon oligomer degradation.

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‘Accordingly, the actual existence of these NSFs leads us to speculate that some special mechanism exists in the regions of these genes.’

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The adaptation of bacteria to feeding on nylon waste - creation.comAnd yes, the mechanisms that produce mutations are called transposons.Transposable element - Wikipedia

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Just because something happens predictably, doesn't mean it's not by chance. If I roll a 6 sided die, I will come up with a 2 at least once within an hour. EACH TIME! Holy moley! there must be something else besides chance happening here! Or, maybe it's that the probability of developing the mutation is such that within 9 days, and in the presence of nylon, the bacterium will develop the mutation that allows it to digest nylon.

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Bacteria are a bit more complicated than dice, don't you agree? If it was that easy to evolve nylon degradation ability by chance, than they would have done it before. Yet they didn't, they only do it in the lab, and in only 9 days.

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Yes, some bacteria have an adaptation that causes them to increase mutation rates when they are under stress. Sometimes they increase the overall mutation rate of the whole genome, sometimes they increase the mutation rate at a specific place. However, that does not mean that there is any particular mutation they are going for. Nylon is not a naturally occurring polymer. There's no possible way the bacterium could "know" what kind of mutation it could need. Instead, it increases it's mutation rate when under stress which gives it a better chance of creating a beneficial mutation. There is no predetermination. There is no guarantee that the right mutation will occur.

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I never said that there is a particular mutations that bacteria want that it happens. Nor are they directing to a specific mutation. Sometimes this can happen with other mechanisms but not with transposons. But the point is that when in the presence of nylon, transposons will start to mutate a specific region of the genome untill bactria can degrade it. That's why they can't do it instantly, but have to wait for about 9 days. Yet the point is that this happens not by random undirected mutations. This happens by an already existing mechanism. Without it, they would not be able to do it.

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But, lucky for the bacteria, there are billions upon billions of them, and even if the right mutation only has a 1 in 10000000000 chance of happening, chances are, in 9 days, through hundreds of generations, it will. It's still a novel mutation that confers a new function, not a physiological response

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A mechanism that is already existing can not give you any new information. This is not a new function but a fine-tuning of an existing one. The initial function was digestion, the new one is also digestion with a wider posibility of materials to digest. No new structures were built. As I said earlier, you need at least 400 informational bits to have new CSI.

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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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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.

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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.

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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.

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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?

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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.

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Um, this begs the question how do you know all genetic material demands a designer. You have done nothing to answer Percy's question but provide a baseless assertion as your first point. This is called circular reasoning i.e.

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Because genetic material is information exhibiting CSI. And CSI is evidence of an intelligence.

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I assume by the term 'mechanism' you are referring to the transposons you mentioned earlier, correct? Or are you referring to other genetic 'mechanisms' as well for inducing genetic mutation? If so what.

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If you are saying ransposition is the only method for causing genetic changes you are wrong. I trust this is not what you are saying so if you could elaborate I would appreciate it.

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I already posted a link showing what the LexA protein can do.

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Mutation is part of the evolutionary process, yes. It is like saying if someone can't walk they can't run very fast. Duh!

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So how have bacteria been supposed to evolve the mutation inducing mechanisms without mutations?

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Um, you lost me. Which mechanisms? You ever heard of genetic frameshifting, single base mutations, insertions, deletions, etc which are not always caused by transposition.

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The Lexa proteins without which bacteria can't mutate.

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Wrong. Define the mechanisms you are talking about and then we can continue to debate the problems with your argument.

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I already did.

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Uh, okay. I guess this brings us back to the thread's topic. By what evidence and rationale do you conclude this?

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Since only intelligence has been observed to create CSI, and DNA exhibits CSI, we logically infer, that genetic material has been designed.

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Oh, okay, I see now why you've concluded this. If you read the entire article (To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists) you'll see that the second paragraph you quoted is bit overstated. Evolution (and the mutations behind it) cannot be "halted in its tracks."

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They can't? How do you know that?

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Later the article correctly describes how mutations always occur, it's just that they seem to occur faster in certain bacteria under certain environmental pressures.

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No, it specifically says that bacteria can not evolve resistance without the LexA proteins.

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From reading the article it appears that some bacteria can repress and derepress their mutation repair facility in response to external stimuli.

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If that is only the case, and the mutations are still happenbing, why can't bacteria evolve resistance?

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How this implies design will have to be explained.

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I already explained it.Edited by Smooth Operator, : No reason given.

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I assume you are using Dembski’s term he conjured up out of thin air. Repeating over and over that CSI is evidence for intelligence does not make it so. You must provide evidence.

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Actually it was invented by Leslie Orgel, an evolutionist. Anyways...CSI is reliable measure of information and it is suitable to detect design. By complexity I mean a pattern that has a low probability of occurence. The probability should be lower than 1:10^120. Becasue that is the number of bit operations that the observable universe could have performed from it's origin. And there are 10^120 states in about 400 bits.Next we have to have a specification. That is a patern that the object we are investigating exhibits. But it can't be just any pattern, it has got to be an independently given pattern. Meaning, that the object you are examining should should represent a patternt that already exist and is not producet due to a natural law.When those both conditions are met, we have design. So when we find 400 bits in nature we are right to infer that they are a product of intelligence, since intelligence is known to produce much higher amounts of information. Chance is not.For an example look at this mountain.
Wikimedia ErrorIt is complex right? But it doesn't represent anything. Therefore it lacks a specification. Therefore we do not infer design for that mountain.But now look at this mountain.
Wikimedia ErrorIt is clear to anyone that this mountain is also complex and specified. It has an independently given pattern. It represents 4 US presidents. So we can without a doubt say that this mountain was designed, without us actually seeing the design in process, or knowing who designed it.The same thing applies to DNA. It is a carrier of information. It has 3 billion base pairs. Which is actually 6 billion bits. Which is far larger than chance could have ever produced. So by this method we infer that the genome itslef was designed.

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This article is talking about the LexA protein controlling the capability of the bacterium to evolve a resistance to the antibiotics ciprofloxacin and rifampic. It is not stating that the bacterium is not able to evolve at all as a result of inhibiting this protein? You are misinterpreting what this article is stating.

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Again there are many different varieties of genetic mutations that can occur. This protein is just enables or inhibits the mutation of certain areas of the genome resulting in resistance to certain chemical agents (in this case specific antibiotics).

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Well obviously you misread something.

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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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If you inhibit this pathway, the bacteria cannot evolve, says Scripps Research Assistant Professor Floyd Romesberg, Ph.D., who led the study.

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Well are you not able to extrapolate what that means? The point is that to evolve the bacteria needs specific mechanisms. If it was only up to random mutations, than there would be no reason why bacteria couldn't evolve witout LexA. If by definition mutations were random and couldn't be stopped. This just means that they found specific mechanism for specific region of the genome. It is obvious that this is how the whole of adaptation works. And not by purely random mutations.

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Because these 'mechanisms' aka proteins perform other functions than just enabling or inhibiting genetic mutation

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Even if they did, that still doesn't answer my question. How did the bacteria evolve those mechanisms, if they need the mechanisms in the first place?

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(this was the undoing of ID’s irreducible complexity argument)

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This has nothing to do with IC which you misunderstand.

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and also these mechanisms do not control all forms of genetic mutations.

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If that is true, why can't bacteria evolve resistance without them?

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BS, you have poor reading comprehension. They are talking about resistance to specific antibiotics not all types of genetic mutations.

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I am talking about the specific region of the genome maintained by LexA. The protein can induce all kinds of mutations it want's on that specific region. If there were still random mutations on that specific region without LexA, why can't bacteria evolve resistance without LexA?