Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
5 online now:
Newest Member: popoi
Post Volume: Total: 915,808 Year: 3,065/9,624 Month: 910/1,588 Week: 93/223 Day: 4/17 Hour: 1/1


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   What is an ID proponent's basis of comparison? (edited)
Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 71 of 315 (516424)
07-24-2009 9:22 PM
Reply to: Message 68 by Smooth Operator
07-24-2009 8:41 PM


Smooth Operator writes:
Not only that but this can be achived in 9 days in the lab. It doesn't take lots of time you see. You just place the bacteria in the presence of nylon, and they will get the ability to digest nylon every time. That's because of the mechanisms they have. Not because of chance.
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?
--Percy
Edited by Percy, : Minor clarification.

This message is a reply to:
 Message 68 by Smooth Operator, posted 07-24-2009 8:41 PM Smooth Operator has replied

Replies to this message:
 Message 72 by Smooth Operator, posted 07-24-2009 11:50 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 74 of 315 (516450)
07-25-2009 6:19 AM
Reply to: Message 72 by Smooth Operator
07-24-2009 11:50 PM


Hi Smooth!
The Yomo paper can be found here:
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.
Still, this is the kind of thing you should be looking for as evidence for ID. You believe that nylon-eating behavior is not an example of the evolution of new traits, but that such traits were programmed in from the beginning by the designer. Therefore it was the designer who put in place the mechanism that prevents these long nonstop frames from picking up stop codon mutations. So the next step is to discover and understand this mechanism.
Yomo's paper was written in 1992, seventeen years ago, so it is possible that we've learned a great deal about this mechanism since then. You might want to look into the subsequent research.
By the way, transposons are only one of many mutational mechanisms.
--Percy

This message is a reply to:
 Message 72 by Smooth Operator, posted 07-24-2009 11:50 PM Smooth Operator has replied

Replies to this message:
 Message 76 by Smooth Operator, posted 07-25-2009 11:10 AM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 77 of 315 (516481)
07-25-2009 12:24 PM
Reply to: Message 76 by Smooth Operator
07-25-2009 11:10 AM


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

This message is a reply to:
 Message 76 by Smooth Operator, posted 07-25-2009 11:10 AM Smooth Operator has replied

Replies to this message:
 Message 79 by Smooth Operator, posted 07-25-2009 2:52 PM Percy has seen this message but not replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 78 of 315 (516482)
07-25-2009 12:40 PM
Reply to: Message 75 by Smooth Operator
07-25-2009 11:08 AM


Smooth Operator writes:
Bacteria are a bit more complicated than dice, don't you agree?
The argument wasn't that bacteria are like dice. Dice were used to illustrate the relevant principle of probability.
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.
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:
quote:
After 9 days of incubation at 30oC, hypergrowing colonies were obtained at a frequency of 10-3.
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

This message is a reply to:
 Message 75 by Smooth Operator, posted 07-25-2009 11:08 AM Smooth Operator has replied

Replies to this message:
 Message 80 by Smooth Operator, posted 07-25-2009 3:01 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 83 of 315 (516500)
07-25-2009 3:47 PM
Reply to: Message 80 by Smooth Operator
07-25-2009 3:01 PM


Smooth Operator writes:
This shows that they need a certain chemical to be present to get the 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

This message is a reply to:
 Message 80 by Smooth Operator, posted 07-25-2009 3:01 PM Smooth Operator has replied

Replies to this message:
 Message 84 by Smooth Operator, posted 07-25-2009 3:55 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 86 of 315 (516514)
07-25-2009 5:58 PM
Reply to: Message 84 by Smooth Operator
07-25-2009 3:55 PM


Smooth Operator writes:
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.
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

This message is a reply to:
 Message 84 by Smooth Operator, posted 07-25-2009 3:55 PM Smooth Operator has replied

Replies to this message:
 Message 88 by Smooth Operator, posted 07-25-2009 10:46 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 89 of 315 (516555)
07-26-2009 5:24 AM
Reply to: Message 88 by Smooth Operator
07-25-2009 10:46 PM


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

This message is a reply to:
 Message 88 by Smooth Operator, posted 07-25-2009 10:46 PM Smooth Operator has replied

Replies to this message:
 Message 90 by Smooth Operator, posted 07-26-2009 8:10 AM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 92 of 315 (516576)
07-26-2009 9:23 AM
Reply to: Message 90 by Smooth Operator
07-26-2009 8:10 AM


Smooth Operator writes:
Because in the first place all genetic material is evidence for a designer.
Uh, okay. I guess this brings us back to the thread's topic. By what evidence and rationale do you conclude this?
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.
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." 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.
The paper itself can be found here: oi/10.1371/journal.pbio.0030176]-->Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance (there's a link on the page to download the PDF). What it says is a bit more measured and much less spectacular. For example, on page 1031 there's this:
...the model described above suggests that bacteria play an active role in the mutation of their own genomes by inducing the production of proteins that facilitate mutation...
From reading the article it appears that some bacteria can repress and derepress their mutation repair facility in response to external stimuli. How this implies design will have to be explained.
--Percy

This message is a reply to:
 Message 90 by Smooth Operator, posted 07-26-2009 8:10 AM Smooth Operator has replied

Replies to this message:
 Message 94 by Smooth Operator, posted 07-26-2009 9:38 AM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 99 of 315 (516631)
07-26-2009 2:44 PM
Reply to: Message 94 by Smooth Operator
07-26-2009 9:38 AM


Smooth Operator writes:
Since only intelligence has been observed to create CSI, and DNA exhibits CSI, we logically infer, that genetic material has been designed.
Oh. Then why do you care about evolution of the nylon-feeding trait if the mere existence of DNA infers design?
About preventing mutations, ask yourself how you would prevent copying errors? Reproduction is very complex chemistry, and while highly reliable, it isn't perfect. All known cells have non-zero mutation rates. Even when the DNA repair mechanism is active, it, too, is just chemical reactions and imperfect. When it is active the mutation rate is smaller, but it never reaches zero.
The average mutation rate for normal bacteria (meaning their mutation repair mechanism is active) is 10-8 per base pair per generation. When the bacteria disables the repair mechanism in response to the presence of an antibiotic (disabling this response is what that research paper is about, oi/10.1371/journal.pbio.0030176]-->Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance), the mutation rate goes up. The mutation rate was never zero. Evolution is never "halted in its tracks." That could only happen if you prevented all mutations, and since the copying of millions of nucleotides is only rarely perfect, almost all reproductive events are accompanied by mutations.
No, it specifically says that bacteria can not evolve resistance without the LexA proteins.
Yes, you're right, they do say that. For some reason they're overstating the case. Please understand that they don't really mean that for the reasons explained before. There's no way to make reproduction perfect.
In some ways it's a little like typing a message here. If you type your message and then immediately click "Submit Reply," there will be a number of typos (more for some than others). Those that proof read their messages before posting appear to have far fewer typos, and this is analogous to the mutation correction mechanisms in cells. This doesn't mean he never has typos, he just has far fewer typos. Prevent him from proof reading, analogous to the bacteria disabling the mutation correction mechanism, and the number of typos per message will suddenly jump.
I already explained it.
Oh, I must have missed it.
--Percy

This message is a reply to:
 Message 94 by Smooth Operator, posted 07-26-2009 9:38 AM Smooth Operator has replied

Replies to this message:
 Message 100 by traderdrew, posted 07-26-2009 2:59 PM Percy has replied
 Message 105 by Smooth Operator, posted 07-26-2009 4:07 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 104 of 315 (516643)
07-26-2009 4:06 PM
Reply to: Message 100 by traderdrew
07-26-2009 2:59 PM


traderdrew writes:
This point was made to me in a previous debate. However, superficially it doesn't explain the complexities it would have to overcome such as the right mutations at the right places with the right expressions. I am thinking about the wrong places where random mutations could occur.
The reason favorable mutations pop up in bacteria so frequently and in such short time periods is because of sheer numbers. The number of base pairs in your average bacteria is around 5 million (5x106). The mutation rate in your average bacteria is 10-8 per base pair per generation. Multiplying these two numbers together gives you the likely number of mutations each time an average bacteria divides, which is .01 mutations/generation. Another way to express this number is to say that every 100 or so cell divisions you get a bacterium with a mutation.
So you place a single bacterium in a petri dish with a growth medium that divides every 20 minutes. At the end of a single day you would have 5 thousand billion billion bacteria (5x1021), and about the same number of cell divisions, so this means there have been 50 billion billion mutations (5x1019). What do you think the odds are of at least one mutation occurring both where it's needed and to the precise base pair that is needed? Well in a genome of approximately 5 million base pairs, the odds are pretty close to one. In fact, it would be very unusual if the necessary mutation didn't occur many, many times.
This is why students in biology lab have no problem obtaining the desired bacterial mutation. When such large numbers are involved the unlikely becomes a certainty.
--Percy

This message is a reply to:
 Message 100 by traderdrew, posted 07-26-2009 2:59 PM traderdrew has replied

Replies to this message:
 Message 121 by traderdrew, posted 07-27-2009 9:25 AM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 114 of 315 (516675)
07-26-2009 7:04 PM
Reply to: Message 105 by Smooth Operator
07-26-2009 4:07 PM


Smooth Operator writes:
Because evolutionists keep claiming you can get information by evolutionary algorithms. Which is false.
Except it's true. If it were false then models of the evolutionary algorithm couldn't produce new information. If it were false then you would be able to identify the location in the cell of the information for where to place the mutation and which base pairs to substitute.
I understand that you believe it is false. But believing and proving are two different things.
No, when the mechanism was disabled, than there was no ability to evolve, not when it was active. You are confusing mutation inducing, and mutation repair mechanisms.
The evidence we have says that the mutation rate goes up when the mutation repair mechanism is disabled. If you think a mutation inducing mechanism exists then you have to provide evidence of one.
This could be true in higher organism. Or yes, maybe even in bacteria. But it could be that all other mutations in bacteria are also induced. And the only reason why we called mutations mistakes, was because of ignorance.
Interesting idea that all mutations are deterministically induced, but there's no evidence for it.
--Percy

This message is a reply to:
 Message 105 by Smooth Operator, posted 07-26-2009 4:07 PM Smooth Operator has replied

Replies to this message:
 Message 129 by Smooth Operator, posted 07-27-2009 2:25 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 117 of 315 (516727)
07-27-2009 7:04 AM
Reply to: Message 115 by Stagamancer
07-27-2009 12:56 AM


Re: Mutations
Stagamancer writes:
And yet we have observable, calculable mutation rates. Bacterial mutation rates are far higher than human mutation rates and your 99.99999999% correction rate is not based on any real information.
This might be misinterpreted by Smooth Operator, so for him let me add that the mutation rates of human and bacterial cells are fairly close in value, but bacteria can produce tens of generations a day, and consequently bacterial populations produce many more mutations per day even with their generally smaller genomes. Humans produce only about .0006 generations per day, and our numbers are not only dwarfed by bacteria, but even by total weight they exceed us.
AbE: The link provided by TraderDrew in Message 120 provides a wealth of useful information, including his 99.99999999% correction rate figure, but also that E. coli replicates its DNA at the rate of 4000 base pairs per second. Who knew!
I think the important point for TraderDrew to understand is that the bacterial mutation rate of 10-8 per base pair per generation includes the corrections.
But I'd challenge that 99.99999999% figure, because if it is accurate then the error rate without correction is 1. In other words, not a single base pair is copied without error. That just makes no sense, so that figure cannot be correct, not even close.
--Percy
Edited by Percy, : Add additional information after TraderDrew posted his Message 121.
Edited by Percy, : Correctly refer to Message 120 from TraderDrew.

This message is a reply to:
 Message 115 by Stagamancer, posted 07-27-2009 12:56 AM Stagamancer has seen this message but not replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 122 of 315 (516748)
07-27-2009 9:50 AM
Reply to: Message 121 by traderdrew
07-27-2009 9:25 AM


traderdrew writes:
But when there are multiple coherent mutations that are required to produce new structures or to take large steps, I remain unconvinced.
As evolutionary mechanisms are currently understood, new structures or large steps in a single generation would be very unlikely.
Evolution produces only minute change in each generation, selecting traits from the pool of individuals who survived to reproduce. The procedure of selection and reproduction is repeated from scratch in each generation, each generation producing minute change. Over thousands of years the changes gradually accumulate.
What I do know is that just after the first time I left this forum, I became a better debater. As my jiu-jitsu teacher taught me, "You will learn more when you risk exposing yourself than when you don't."
This tells me two things. One, your Jiu-Jitsu teacher was very wise. Two, keep disagreements with you on a verbal level.
--Percy

This message is a reply to:
 Message 121 by traderdrew, posted 07-27-2009 9:25 AM traderdrew has replied

Replies to this message:
 Message 124 by traderdrew, posted 07-27-2009 11:55 AM Percy has seen this message but not replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 132 of 315 (516808)
07-27-2009 3:00 PM
Reply to: Message 129 by Smooth Operator
07-27-2009 2:25 PM


Smooth Operator writes:
No, I already explained why it's false. And I gave links that describe the NFL theorem that explains why algorithms do no produce new information. Why didn't you read them?
Here at EvC Forum you're expected to produce arguments in your words and use links only as supporting references. This is from the Forum Guidelines:
  1. Bare links with no supporting discussion should be avoided. Make the argument in your own words and use links as supporting references.
So what you need to do is explain how NFL theorems disallow the possibility of genetic algorithms producing new information.
But I can save you some time. Genetic algorithms that model evolutionary behavior are already in use today producing novel designs. They're a practical reality. There really isn't much point to arguing that something that works before our very eyes doesn't really happen. And then how do you explain the design innovations produced by the algorithm since they're not figments.
But we don't want to turn this thread into a discussion of GA's. The more relevant point is that new information is being created all the time throughout the universe, including through the process of mutation. If you think that the information identifying where mutations should occur and which base pairs should be involved is already part of the cell, then you have only to find the source of this information, and you have to find it for all possible mutations. Since mutations are known to occur anywhere throughout a genome, and since bacterial genomes range from around 500,000 base pairs up to 10 million base pairs, you need information somewhere in the bacterial cell for the production of each and every possible mutation, as well as the molecular triggers for each one.
I did, few posts ago. It's caleld LexA. When it is turned off no evolution is possible on the specific part of the genome.
It has already been explained that this isn't true. What LexA does is control whether the genetic repair mechanism is enabled or not. When it is enabled then there are still mutations, just fewer of them. The average bacterial mutation rate of 10-8 is when the repair mechanism is enabled. Note that it isn't 0.
--Percy

This message is a reply to:
 Message 129 by Smooth Operator, posted 07-27-2009 2:25 PM Smooth Operator has replied

Replies to this message:
 Message 133 by Smooth Operator, posted 07-27-2009 3:23 PM Percy has replied
 Message 149 by Wounded King, posted 07-27-2009 6:10 PM Percy has replied

Percy
Member
Posts: 22389
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 150 of 315 (516876)
07-27-2009 8:42 PM
Reply to: Message 149 by Wounded King
07-27-2009 6:10 PM


Wounded King writes:
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.
Whoa! That seemed a little weird, so I've read up on this a bit more, and I think I can make sense out of it if more details are added. Tell me if I've got this straight.
Uncleaved LexA represses the SOS response, the name given to a DNA repair system that operates after replication begins. Because uncleaved LexA is present in normal bacteria, the SOS repair response is repressed under most circumstances. It doesn't matter that this repair system is repressed when the bacteria isn't replicating, since there's nothing to repair.
Normal bacteria also possess the RecA protein, but it only plays a significant role during replication when (among other things) it cleaves the LexA repressor, thus enabling the SOS repair response, just when it is needed.
Some antibiotics work by inducing DNA damage in bacteria. Cause enough damage and the bacteria dies. But antibiotics can also somehow stimulate the RecA protein to cleave the LexA repressor, even though the bacteria is not replicating. The SOS repair response is no longer repressed, and it goes to work repairing the DNA damage caused by the antibiotic. This process of simultaneous destruction and repair produces many mutations. The possibility of all mutations become more likely, including those with resistance-conferring ability.
But no matter how close I've come to grasping the details, I don't think it changes the argument I was directing at Smooth Operator, which is what I think you were saying next. I wasn't trying to get to this level of detail because Smooth Operator's argument fails for much more basic reasons. Resistance-conferring mutations are selected from out of the random mutations that occur while under stress from antibiotics and are not specifically induced.
--Percy
Edited by Percy, : Add minor clarification.

This message is a reply to:
 Message 149 by Wounded King, posted 07-27-2009 6:10 PM Wounded King has replied

Replies to this message:
 Message 178 by Wounded King, posted 07-29-2009 11:12 AM Percy has seen this message but not replied

Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024