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

Hi Percy,I have to go with Smooth Operator on this one. In its uncleaved form LexA does repress the activity of certain DNA repair mechanisms. When it is cleaved these mechanisms become activated. However, along with DNA repair elements the cleavage also allows the expression/activation of a set of polymerases which are highly error prone, which is probably why Smooth Operator focuses on LexA cleavage as a mutation inducing mechanism instead.You and Devil's advocate are right about the rates of mutation in the LexA mutant and therefore presumably in the presence of a LexA cleavage blocking drug, the authors (Cirz et al., 2005) state that ... So 104 fold less frequently is pretty substantial and certainly sufficient for the authors to state ... Of course in the long term evolution can afford to be inefficient but perhaps not in the face of a sudden environmental challenge such as the introduction of antibiotics.TTFN,WK

It isn't the replication of the bacteria necessarily that is the important issue but of the DNA. The way fluoroquinolones work is to block the action of a set of enzymes which allow changes to the coiling of the circular DNA found in bacteria (these enzymes are called gyrases as they cut the DNA and allow it to gyrate).The SOS response is not specific to replication but is started by the binding of the RecA protein to single stranded DNA, which catalyses LexA auto-cleavage. Single stranded DNA normally only occurs either during replication, usually when something is blocking the normal progress of replication, or when the DNA is significantly damaged. One of the effects the cleavage of LexA has is that the increased levels of the error prone polymerases allows them to act on undamaged DNA which does not happen during the normal course of things. This isn't necessarily the case, there may be structural elements either sequence or higher level in certain regions of DNA that make mutations more or less probable or the frequency of different types of mutation may change. So the higher induced mutation rate need not be simply an increased level of the mutation rate seen in the absence of the SOS response, it may be qualitatively different as well.In terms of LexA and E. coli I don't know that there is any evidence for this. RecA recruits error prone polymerases to sites where single stranded DNA is available, but I don't see that this would favour specific mutations in genes allowing the evolution of resistance, unless they were more susceptible to damage than other regions. One interesting possibility is that since higher levels of transcriptional activation are associated with higher levels of mutation if gyrase encoding genes were induced downstream of the SOS response we would have a mechanism which would preferentially target a subset of genes including the gyrases.Sadly, looking at literature on the targets upregulated when LexA is cleaved I see no sign of the gyrases (Khanin et al., 2006). Intriguingly however the transcription of gyrases is upregulated when gyrase activity is blocked (Menzel and Gellert, 1983; Franco and Drlica, 1989).It is also interesting to note that the different subunits A and B of the gyrase enzyme have different transcriptional responses to change in supercoiling with A being strongly upregulted and B having no noticeable response (Neumann and Quiones, 1997). This could be significant given that the largest proportion of resistant mutants that have been isolated for Ciprofloxacin have been in the gene coding for the GyrA subunit(Morgan-Linnel et al., 2008).TTFN,WK

Wikipedia has an extensive page covering the Dover case. This includes the judges final decision and transcripts of the majority of the proceedings.There is quite a lot of Behe testimony, I think the part that is being focused on is during the afternoon of day 12.TTFN,WKEdited by Wounded King, : No reason given.

OK, that whole article is ridiculous but that table simply doesn't support your claim.In what way is a mutation which changes gyrase in such a way as to reduce its affinity to Fluoroquinolones a loss of information for the gyrase?The author is simply demented. He wants us to think that Gyrase has evolved to bind Fluoroquinolones? Does he even understand what these antibiotics are? These are synthetic chemicals which have been developed specifically to inhibit bacterial growth or kill bacteria. It is like thinking that my car has a cigar lighter plug point because it was designed so I could plug my iPod car charger into it. He is getting cause and effect mixed up. So since gyrases clearly didn't evolve to function as Fluoroquinolone binding molecules how on Earth can it be considered a loss of function when their affinity is reduced?There are numerous valid cases where resistance is the result of a genuine information loss such as null mutations removing an entire gene. But the whole argument is undermined by this idiotic attempt to describe every form of resistance as a loss of information/function when you are defining function as being 'binds to antibiotic'.I think this is all bound up with the approach that whatever the starting state was of an organism, protein or gene sequence when it was first studied is somehow enshrined for IDist/creationists as being the ideal state so any change from that state must necessitate a loss of function/information.Will you at least concede that to consider binding affinity for an antibiotic to be an evolved function of the bacteria is nonsensical?TTFN,WKEdited by Wounded King, : No reason given.

This seems a rather strange example. Does you test not show intelligence if the rat becomes so exhausted that it dies? You realise that a random walk through the maze will tend to eventually lead to the rat escaping without any intelligence required at all? How can the rat intelligently choose the right turns? Did you show it a map beforehand? What you are really showing is that rats have enough memory not to go back down a dead end.This seems about as objective as most 'explanatory filter' approaches, you set an arbitrary complexity of maze and an arbitrary time frame for completion and simply declare it to be an objective test because you can make some sort of measurement.TTFN,WK

Um, that was rather my point. The antibiotics are designed to bind to gyrase. Are you claiming that after the antibiotics were designed the information content of gyrase just magically went up without any change in its genetic sequence because it suddenly had a high affinity binding molecule created for it?If you are talking about a loss of specificity in the gyrase are you claiming that the binding affinity is a result of complex specified information in the gyrase? If so then how are you not claiming that the gyrase had evolved or been designed to bind the antibiotic, rather than the other way round. And unless this is the case how can it possibly be a loss of information for the gyrase when it mutates in such a way as to lose this affinity? Then how can it be considered a loss of information for the gyrase? The only 'functional' element lost to the gyrase is that of binding a molecule which makes it damaging or possibly lethal to the organism, and that was a function that didn't exist until the antibiotic was developed.Are you saying that gyrase was intelligently designed to be susceptible to the antibiotics in the future? That seems a lot of effort for the intelligent designer to go to for only a few decades of antibiotic protection.Simply saying 'it's a loss of specificity' is not a sufficient answer. How is this substantially different? Are you saying 'this is the range of informational variation we know about, anything beyond this is a loss of information'? If not how can we measure this existing range? This can hardly be anything other than pure speculation since we don't know what all the existing genetic variations have been for a whole species ever. So how can you possibly know what the existing 'informational range' is for anything? Than why haven't bacteria simply vanished over the billions of generations of their existence?TTFN,WK

It wasn't a jury trial. I shouldn't imagine judges are so easily swayed by cheap courtroom theatrics, although I'm sure it looked good for the press and other interested parties.TTFN,WK

That was subsequently according to you, when the gyrase lost binding affinity. What I'm asking is did the gyrase have complex specified information in the pre-mutated sequence even though it had no binding partner to have an affinity for prior to the development of the antibiotic? No problem, but the gyrase's job isn't to bind an antibiotic that would impair its function. If you are claiming the mutation had an effect other than to change the affinity of gyrase and the antibiotic then that would be a good thing to provide evidence for. All the paper you directed me to does is claim that the loss of affinity between the gyrase and the antibiotic represents a loss of information for the gyrase.So tell me what job the gyrase no longer performs as well? So it functioned to bind and antibiotic for millenia before that antibiotic was developed? In what way does that fulfil the concept of function? Please state this explicitly, you are saying the designer designed gyrase to have a specific genetic sequence which it maintained for thousands of years simply so humans could develop an antibiotic that would be effective for a few decades before the gyrase mutated and made the antibiotic ineffective?Is that what you are saying? Well we don't know that, you may claim that but it is a quite different thing. So bacteria have a generation time of 1 or so years do they? I'm glad you have helped us gauge your knowledge of biology so succinctly.Your argument seems to do nothing except make a nonsense of the concept of function as useful in terms of information.TTFN,WK

I know this is open to interpretation but wasn't it rather that the creationists went straight to the schools, through the school board, and that the actual case was bought by a parent unhappy with the teaching of ID?I'm sure one could see the instatement of ID into school curricula as an open invitation to sue but is this the same as ID deciding to go the way of the courts?Indeed they seem to much prefer holding their own faux court cases like the one in Kansas organised by the state board of education. Unfortunately as long as people keep voting religious fundamentalists onto boards of education this problem is unlikely to go away, but is likely to waste thousands or indeed millions of dollars of tax payers money that is supposed to be paying for education.TTFN,WK

Its also worth remembering that simple gene duplications certainly can produce selectable phenotypes whether or not they constitute an 'increase in information'.It seems to me that as these discussions progress IDist notions of information and function get more and more divorced from the actual biological functionality that is the substrate for natural selection.TTFN,WK

I magically answered your question before you asked it, see above at Message 235.TTFN,WK

I was trying to leave Rrhain some wiggle room since he was saying it was creationist taking things to the courts.TTFN,WK

The point about the moving of goalposts is that it is bad form for the team whose goal it is to move it just before the ball goes between the posts. Or if you prefer to be the kicker, it would be unfair surely to adjust your opponents goal posts to be twice as wide apart as your own?TTFN,WK

Apparently not since you don't seem to be making any sense. I talk about billions of generations of bacteria and you convert that into billions of years. How else are we to understand this unless you think bacteria have generation times close to a year, as opposed to the 20 minutes something like E.coli actually has. Did it? the amino acid changed, how do you know that this lead to a loss of information since there is no change in function to tie it to? Aren't you the one propounding Abel and Trevors idea of 'functional information'? If this mutation doesn't change the gyrase's function why should it be a loss of information? You are making a nonsense of the whole CSI argument. There is no deterioration of its structure, you can show absolutely no change in the functionality of the gyrase. It makes no sense to say,'yes but if I change all of the amino acids the protein will cease to function' as that says nothing to what this particular amino acid change does. How is the structure damaged? Change need not equal damage, either at the nucleotide or amino acid level. Then what function do you think this amino acid was specified for? You presumably mean CSI here or 'functional information' since information streams into us from the universe all the time from a countless number of material entities.TTFN,WK

Then I suggest reading peoples posts twice perhaps to make sure you are actually understanding what is written. I usually re-read any post I am replying to, its easy to miss things. It hasn't lost its strucuture. Its structure has change in a way that has no effect on its biological function but makes it less susceptible to antibiotics. It could have as many structural changes as it could stand that wouldn't effect its function and unless you have a wholly unique understanding of ID, as I'm beginning to think you do, surely you would have to accept that such changes don't represent a loss of information, since they don't affect function. To argue that since changing all the amino acids would render the protein non-functional that therefore any mutation must make the protein less functional is clearly wrong, it isn't even logical. But you haven't lost it in this case, it has simply changed. So you have had a change in information. Which given that the original information is probably still extant in the population leads us straight to Percy's examples of how allelic variants can represent informational change. And its replacement is an equally effective part of Gyrase's structure. Now you are just talking nonsense. In what way is a mutation that does nothing but benefit the protein by giving it resistance to an antibiotic comparable to sickle cell, other than that they are both mutations. As an aside aren't fine tunings supposed to be improvements albeit small ones? If not then what is the point of fine tuning?You now seem to be actually arguing that information is independent of biological function since you don't seem to care if the mutation affects it or not.Wouldn't it just be more sensible to agree that the source you quoted was overstating the case? I'm not asking you to accept increases in information even, simply that not all beneficial mutations need to be through a loss of information.TTFN,WK