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Author Topic:   AIG has an article up on the nylon-digesting bacteria
Biophysicist
Inactive Member


Message 1 of 27 (98515)
04-07-2004 6:38 PM


As usual, it looks like their arithmetic is correct, given the assumptions they've made, about the open reading frame being very long for this new gene.

However, I believe that both the original plasmid and the result of the mutation have been sequenced, and the nylon-digesting gene has indeed been found to be the result of a frame-shift mutation from a previously useful gene. I think the way the article keeps trying to deny that a frame-shift mutation could have done this is then dishonest. The best argument they make in that line is that there seems to be an extra mechanism to encourage mutations in that region of the plasmid, which is fairly interesting in its own right.

Also, I don't appreciate their argument that this cannot be considered a "gene duplication --> new gene" event. There can be more than one copy of the plasmid in the cell, so you could easily maintain a mixture of the two probabilistically.

Of course, the real problem with the article is the way it keeps referring to evolution as a process simply based on randomness.

Here's a question: do existing genes have a lower probability of having a frame shift mutation generate a stop codon than would be expected given a random sequence of nucleotides with nominal proportions of A, C, T, and G bases? That's one thing I'd like to know before going any further on the subject of AIG's arithmetic. The otehr thing I'll note is that even a chance on the order of 1 in a trillion is not vanishingly small for a population of many billions of bacteria each with multiple copies of the plasmid.


Replies to this message:
 Message 2 by Brad McFall, posted 04-07-2004 6:54 PM Biophysicist has responded
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Brad McFall
Member (Idle past 3205 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 2 of 27 (98519)
04-07-2004 6:54 PM
Reply to: Message 1 by Biophysicist
04-07-2004 6:38 PM


new hope helps
Do you think it "dishonest" that no biophysicst or biophysical geneticist has tried to ordinate sequence data using sets of harmonic conjugates (Non-Euclidean Geometry by HSM OXTER, FRS UofTORONTO press1942...1968p28...)"A large part of our investigation (eg Chapter v) will be concerned with the geometry of poits on a single line, where there is no scope for incidences. This deficiency is compensated by the possibility of defining ths HARMONIC CONJUGATE of a given point with respect to two given points. (We think of this as a one-dimensional concept, even thouh it requires incidences in two dimensions for its construction and in three dimensions for the proof of its uniqueness.) We shall use the abbreviation H(AB,CD) for the statement that D is the har...")??????????????????????????
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Loudmouth
Inactive Member


Message 3 of 27 (98526)
04-07-2004 7:10 PM
Reply to: Message 1 by Biophysicist
04-07-2004 6:38 PM


quote:
Of course, the real problem with the article is the way it keeps referring to evolution as a process simply based on randomness.

Indeed. Do they think that it is random that this species of flavobacterium is able to outcompete its competition when the primary source of energy is nylon derivatives? AiG always manages to skip right over the natural selection part of evolution and instead focus on the randomness of random mutations. They want to focus on the random chipping of stone and not how the sieve sorts them by size. One is random, granted, but the whole process is not.


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Biophysicist
Inactive Member


Message 4 of 27 (98547)
04-07-2004 8:29 PM
Reply to: Message 2 by Brad McFall
04-07-2004 6:54 PM


Re: new hope helps
I'm sorry, but I really don't understand what you're talking about here. Perhaps if you parse your sentences, let me know what the quote is in reference to, and first present the basic point of your argument (hopefully within the scope of the discussion I gave at the start of the thread), I might be able to reply.
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Brad McFall
Member (Idle past 3205 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 5 of 27 (98767)
04-08-2004 7:05 PM
Reply to: Message 4 by Biophysicist
04-07-2004 8:29 PM


Sure, this is part of my "homework" on Quarternions and I havent quite finished it yet, nor brought the source with me today, but I'll key you up to my memory on it and try to apply it more directly to your post next time. All quotes can be found as done by posters in this thread.
quote:

As usual, it looks like their arithmetic is correct, given the assumptions they've made, about the open reading frame being very long for this new gene.
However, I believe that both the original plasmid and the result of the mutation have been sequenced, and the nylon-digesting gene has indeed been found to be the result of a frame-shift mutation from a previously useful gene.



quote:

I think the way the article keeps trying to deny that a frame-shift mutation could have done this is then dishonest. The best argument they make in that line is that there seems to be an extra mechanism to encourage mutations in that region of the plasmid, which is fairly interesting in its own right.

Also, I don't appreciate their argument that this cannot be considered a "gene duplication --> new gene" event. There can be more than one copy of the plasmid in the cell, so you could easily maintain a mixture of the two probabilistically.

Of course, the real problem with the article is the way it keeps referring to evolution as a process simply based on randomness.



quote:

...)"A large part of our investigation (eg Chapter v) will be concerned with the geometry of poits on a single line, where there is no scope for incidences. This deficiency is compensated by the possibility of defining ths HARMONIC CONJUGATE of a given point with respect to two given points. (We think of this as a one-dimensional concept, even thouh it requires incidences in two dimensions for its construction and in three dimensions for the proof of its uniqueness.)

I noticed that this defintion MIGHT? be useful in detailing frameshift mutations"" without reference to chance prima facie.
quote:

Here's a question: do existing genes have a lower probability of having a frame shift mutation generate a stop codon than would be expected given a random sequence of nucleotides with nominal proportions of A, C, T, and G bases?

As I have contined to do this "homework", I have noticed that your "probabiliy" while possibly "framed" by the 2-D nature of harmonic conjugate would not beenough if bioinformatics could actually be bent to a means of Noneuldeian geometry on the whole rather than just as a formal logic in the debate. This is much more complicated than I had first responded in to your post but it might even be easier to approve of as it use plane duplicity rather than chemical chirality in its proof. Meanwhile the reason I started this work was to address something with AbbyLeever where I assert rotations which need not be limited to a "side" which this would remand as to the acutal seqence location of any old stop codon.

quote:

Of course, the real problem with the article is the way it keeps referring to evolution as a process simply based on randomness.


quote:
AiG always manages to skip right over the natural selection part of evolution and instead focus on the randomness of random mutations. They want to focus on the random chipping of stone and not how the sieve sorts them by size. One is random, granted, but the whole process is not.

A corrollary or theorm in this homed work finds that natural selection might not be understood as to the 3-D proof (more than one cell etc)as disruptive selection could possible be critical here but then remands I had gotton back to AL satifactoruily which I do not gain say at this point even if I personally might so express.


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Black
Member (Idle past 3356 days)
Posts: 77
Joined: 11-28-2008


Message 6 of 27 (98784)
04-08-2004 8:41 PM


The only other creationist I know of who has talked about the nylon bug would be Lee Spetner. You can see his comments here:

http://members.tripod.com/aslodge/id89.htm

I emailed him about this. Here is a copy of the revelent portion of my email:


[...]
Your calculations show that it would be near impossible for this new protein to have arisen randomly. I disagree with your conclusion. Let me explain. Please let me know if you think I am wrong.

There are many ways to calculate things. I will use an analogy: take a standard, six-sided dice. What is the chance that you roll a 6 on your first roll? You have one chance in six, of course. However, what is the chance that the dice lands at, let's say, angle X and then comes to rest at 6? Considering that there are many different angles at which the dice could land before coming to rest at 6, the probability of it landing exactly at angle X is quite small. In fact, depending on how precise angle X is, it may appear quite impossible for the dice to land exactly at that angle. However, just because it seems quite impossible to get a 6 by having the dice land at precisely angle X, does not mean it is impossible to get a 6.

Thus, I believe in coming to your conclusion you have made an assumption. Your assumption was that the only way to 'digest' this nylon waste is with this exact protein. I do not believe there is any reason for making such an assumption. Indeed there are reasons not to make it.

It seems to be that there are many different ways proteins can be formed. The evolution of the nylon bug, even if it had not taken this direct route could have probably reached a similar destination simply because there are so many different possible proteins.

One example: researchers created 6 trillion new proteins that can do the same job (bind with APT). Functional proteins were selected by enriching for those that bind to ATP. The paper on this appeared in Nature 401 in 2001. The title of the paper is "Functional proteins from a random-sequence library." It was done by Anthony Keefe and Jack Szostack.

Another example is the cytochrome c protein. Although this protein does the same function every time, it is different in almost every animal.

This shows that the assumption you made is incorrect. There are many potential paths that can be taken in creating proteins.
[...]

I emailed him this several weeks ago and have yet to receive a responce, although I know his email is active because he was responding to other emails! Oh well....


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Brad McFall
Member (Idle past 3205 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 7 of 27 (98911)
04-09-2004 12:37 PM
Reply to: Message 6 by Black
04-08-2004 8:41 PM


This is a systemic'" problem with the central dogma and cross national styles of information flow patterns. If it be admitted that more than one protein can do the fermentation then generally one could reason that more than one cell can ORIENT the protein that does the digestion and if one KNEW that the taxonomy economically was defective (personal oberservation) then one could ARGUE the other way around as well. This of course leads to debate and not rebate. Some day we may know more. I dont today.
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Loudmouth
Inactive Member


Message 8 of 27 (98914)
04-09-2004 12:58 PM
Reply to: Message 7 by Brad McFall
04-09-2004 12:37 PM


Random Mutation
Brad,

The way I see it, the chances of the mutation that lead to the nylonase enzyme is no different than any other mutation in the genome of the flavobacterium. If Spetner were honest, he would show how every divergence in DNA sequence within the flavobacterium genus/species is equally unlikely. Spetner, in no way, shows how the mutation leading to the nylonase gene is any more improbable than a mutation in a non-coding/neutral region. The Hardy-Weinberg Boys sniff a rat on this one.


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Replies to this message:
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Trixie
Member (Idle past 1878 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 9 of 27 (98976)
04-09-2004 7:26 PM
Reply to: Message 8 by Loudmouth
04-09-2004 12:58 PM


Re: Random Mutation
I can't believe that I've spent a Friday evening (Good Friday at that) doing literature searches and Entrez and Blast searches on this blasted bug!!! Also on Pseudomonas. Ho hum, what fun!!! Anyway, first thing to say is that some of the information in the AIG article and some of the interpretations don't make a lot of sense. I had intended to disect it, but my DNA analysis software has led me a merry dance on the sequence alignments and translations in all three reading frames and I don't have time tonight. Hopefully I'll get back to it tomorrow (toddler and his disease permitting).

One thing I will say with regards to the genes in question residing on plasmids and not the Chromosome is that the effects of selection pressure on plasmids in bugs are so much more readily seen. Carrying a plasmid is a bioburden on a bug - it has to use valuable resources copying the pasmid as well as the chromosome when it divides. In an environment devoid of nylon, those bugswhich have the nylon digesting enzyme gene on a plasmid are at a distinct reproductive disadvantage and so become less numerous in the population. However, possession of the pasmid in these conditions is not lethal and so the odd one or two will still carry copies. If all other carbon and nitrogen sources run out and only nylon remains, these very few are now at a distinct advantage, even with their bioburden and so they become more numerous. Under these conditions the non-possession of the plasmid IS lethal because the bugs will starve. Eventually, the entire population in the given environment will contain the plasmid. So, although the bug doesn't change into another species or become extinct, evolution can be seen in the behaviour of the plasmid withn the bugs, even although the plasmid doesn't change its DNA sequence. There is no mutation involved, as no offspring will contain information that the parent didn't, since the parent MUST have the plasmid for the offspring to have it (I believe this plasmid is non-conjugative). The whole thing is population dynamics.

To complicate matters, the presence of a number of transposons on the plasmid CAN cause DNA rearrangements. These jumping genes can jump to new locations in the plasmid, possibly inactivating genes that they jump into and leaving a copy of themselves in the original position. They can also jump into the chromosome under certain circumstances.

The bottom line is that I'm going to have to do a lot more reading before I can explain this in a less garbled manner, but my opinion is that the behaviour of this plasmid and its nylon-digesting gene is a wonderful example of selection pressures acting on a population and demonstrates perfectly the mechanisms behind the ToE.


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Taqless
Member (Idle past 4086 days)
Posts: 285
From: AZ
Joined: 12-18-2003


Message 10 of 27 (98982)
04-09-2004 8:46 PM
Reply to: Message 1 by Biophysicist
04-07-2004 6:38 PM


Hey Biophysicist,
Here's a question: do existing genes have a lower probability of having a frame shift mutation generate a stop codon than would be expected given a random sequence of nucleotides with nominal proportions of A, C, T, and G bases?

Here's my 2 cent answer
1) Technically coding regions are a random conglomeration of A,C,T, and oh Gs that we happen to care about.
2) I think, and therefore I can be wrong, that random mutations occur equally within coding and non-coding regions, HOWEVER the tolerance for mutations (whether or not they result in a frameshift) is higher and can accumulate in non-coding regions of the DNA.
3) Having said the above it would be difficult for me to prove it since many of these mutations in the coding region would result in spontaneous abortions or actually giving birth to a dead baby (in the animal kingdom).


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Brad McFall
Member (Idle past 3205 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 11 of 27 (99485)
04-12-2004 6:08 PM
Reply to: Message 9 by Trixie
04-09-2004 7:26 PM


Re: Random Mutation
T,
I was headed to the issue of behaviorial neophenogenesis which creationism remands be solved in some way that DID not seperate descent and mechanisms but I have not tried to do the same reasoning on this "bug" level. In terms of research I am in the same state I was when Mammuthus and I were discussing strong vs weak PE. There is a tendency to assume that one FIRST addresses the mutation before one shows how some adaptibility IS an adaptation and this rather than the effects of chance are my better guess at what's going on even in GOuld's reading of the "synthesis" but I really dont know. I do know it does not need to be first or foremost. It must be addressed at the end at least. The possiblity of applying "design" at the bug level is much easier as many people have indeed spent many more hours thinknig of cats, cows and hippos for instance given any bird. There was a claim prior (to Provine-Johsonson debate)(to say nothing of my own educated "protestations") that the Baldwin effect, Stablizing Selection and genetic assimilation step or stem from the same cause. The kinematics may be seperable while the mechanics are not. I am in possesion of a physical means to manipulate this trio conceptually and given time I will explain the analysis again. I have already discussed ALL of the relevant individual issues in various threads here (there may have been a few things I said on other web sites that had not been repeated here but I doubt it as to evolutionary interest).
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Wounded King
Member (Idle past 2267 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 12 of 27 (100229)
04-15-2004 12:59 PM
Reply to: Message 6 by Black
04-08-2004 8:41 PM


Dear Black,

What is your point with regards to cytochrome C? That it has evolved independently several times from the same ancestral protein? Isn't it more likely that the diversity of Cytochrome-Cs is due to only certain features being required to be conserved to retain its basic function and the deep evolutionary time for which this particular gene/ protein has been around?

TTFN,

WK


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wj
Inactive Member


Message 13 of 27 (100288)
04-15-2004 8:20 PM
Reply to: Message 12 by Wounded King
04-15-2004 12:59 PM


I think that Black's point of the cytochrome C case was that there are multiple variations of the protein which are completely functional. Therefore trying to perform probability calculations on the formation of a specific version of cytochrome C is pointless. It ignores the fact that a large number of possible outcomes will give a functional protein. Therefore the probability is not say 1 in 10 million but 500,000 in 10 million. Spetner apparently ignores this point because it defuses his argument.

As you rightly point out, the variation found in cytochrome C throughout living organisms is consistent with the theory of evolution: a primative protein which has only a small, critical functional zone and where mutation can occur outside the functional zone without being selected against.

Makes on wonder why Spetner's intelligent designer couldn't stick to a single "intelligent design" for the protein.


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Sylas
Member (Idle past 3432 days)
Posts: 766
From: Newcastle, Australia
Joined: 11-17-2002


Message 14 of 27 (100293)
04-15-2004 9:43 PM
Reply to: Message 9 by Trixie
04-09-2004 7:26 PM


Re: Random Mutation
Trixie writes:

The bottom line is that I'm going to have to do a lot more reading before I can explain this in a less garbled manner, but my opinion is that the behaviour of this plasmid and its nylon-digesting gene is a wonderful example of selection pressures acting on a population and demonstrates perfectly the mechanisms behind the ToE.

I am awaiting with breathless anticipation for a thoroughly informed and referenced careful consideration of the matter from someone who has a some good background knowledge in the matter and has chased up the relevant literature.

Take the time you need; but do take the time! Thanks. This is, by the way, a case where a good post is something that could be made into something for the talkorigins archive. Best wishes to the toddler; I'll be appropriately patient.

Cheers -- Sylas


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Wounded King
Member (Idle past 2267 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 15 of 27 (100350)
04-16-2004 5:36 AM
Reply to: Message 13 by wj
04-15-2004 8:20 PM


I think that if that was the point Black was trying to make he didn't make it very clearly. I think that it is more important than ever to be clear and correct in our thinking if we are engaging in a dialogue with creationists or ID proponents. Black's e-mail, or at least the excerpt he gave us, did not show that sort of clarity.

Black writes:

One example: researchers created 6 trillion new proteins that can do the same job (bind with APT). Functional proteins were selected by enriching for those that bind to ATP. The paper on this appeared in Nature 401 in 2001. The title of the paper is "Functional proteins from a random-sequence library." It was done by Anthony Keefe and Jack Szostack.

Another example is the cytochrome c protein. Although this protein does the same function every time, it is different in almost every animal.

This shows that the assumption you made is incorrect. There are many potential paths that can be taken in creating proteins.

There are a couple of problems with this section. Firstly the cited papers research only produced 4 proteins, from the original pool, which gave rise to protein families with members with physiologically equivalent ATP binding, not 6 trillion which can 'do the same job'. 6x10^12 was the number of random proteins initially screened. What Black writes is easily open to the misinterpretation that 6 trillion proteins was the number pulled out and not the number screened.

The point that a protein does not have to have one specific unique amino acid sequence to fulfil a particular function is an important one but I don't think that Black has presented that point very clearly. The Cytochrome-C example does not show that there are several different paths to create a protein with a specific function, although there are, simply that proteins with amino acid/ structural differences can perform the same function. His first example does illustrate his point but he represents the research in the paper in a very confusing way.


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