Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
4 online now:
Newest Member: popoi
Post Volume: Total: 915,817 Year: 3,074/9,624 Month: 919/1,588 Week: 102/223 Day: 13/17 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   What is an ID proponent's basis of comparison? (edited)
DevilsAdvocate
Member (Idle past 3101 days)
Posts: 1548
Joined: 06-05-2008


Message 91 of 315 (516568)
07-26-2009 8:42 AM
Reply to: Message 90 by Smooth Operator
07-26-2009 8:10 AM


SO writes:
And how is this evidence for a designer?
Because in the first place all genetic material is evidence for a designer.
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.
Percy: How do you know this is evidence that the car is blue?
SO: Because in the first place all cars are blue.
WTF?!?
SO writes:
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.
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.
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.
Smooth Operator writes:
And if they can't mutate, they can't evolve.
Mutation is part of the evolutionary process, yes. It is like saying if someone can't walk they can't run very fast. Duh!
Smooth Operator writes:
If they can't evolve, they can't develop those mechanisms.
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.
And since everything is supposed to be evolved from one-celled organisms, the path to all other living organisms is effectively blocked.
Wrong. Define the mechanisms you are talking about and then we can continue to debate the problems with your argument.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : Correct misspelling and quoting errors

For me, it is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring.
Dr. Carl Sagan

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 93 by Smooth Operator, posted 07-26-2009 9:34 AM DevilsAdvocate has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


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

Smooth Operator
Member (Idle past 5114 days)
Posts: 630
Joined: 07-24-2009


Message 93 of 315 (516578)
07-26-2009 9:34 AM
Reply to: Message 91 by DevilsAdvocate
07-26-2009 8:42 AM


quote:
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.
Because genetic material is information exhibiting CSI. And CSI is evidence of an intelligence.
quote:
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.
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.
I already posted a link showing what the LexA protein can do.
quote:
Mutation is part of the evolutionary process, yes. It is like saying if someone can't walk they can't run very fast. Duh!
So how have bacteria been supposed to evolve the mutation inducing mechanisms without mutations?
quote:
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.
The Lexa proteins without which bacteria can't mutate.
quote:
Wrong. Define the mechanisms you are talking about and then we can continue to debate the problems with your argument.
I already did.

This message is a reply to:
 Message 91 by DevilsAdvocate, posted 07-26-2009 8:42 AM DevilsAdvocate has replied

Replies to this message:
 Message 95 by DevilsAdvocate, posted 07-26-2009 11:39 AM Smooth Operator has replied

Smooth Operator
Member (Idle past 5114 days)
Posts: 630
Joined: 07-24-2009


Message 94 of 315 (516579)
07-26-2009 9:38 AM
Reply to: Message 92 by Percy
07-26-2009 9:23 AM


quote:
Uh, okay. I guess this brings us back to the thread's topic. By what evidence and rationale do you conclude this?
Since only intelligence has been observed to create CSI, and DNA exhibits CSI, we logically infer, that genetic material has been designed.
quote:
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."
They can't? How do you know that?
quote:
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.
No, it specifically says that bacteria can not evolve resistance without the LexA proteins.
quote:
From reading the article it appears that some bacteria can repress and derepress their mutation repair facility in response to external stimuli.
If that is only the case, and the mutations are still happenbing, why can't bacteria evolve resistance?
quote:
How this implies design will have to be explained.
I already explained it.
Edited by Smooth Operator, : No reason given.

This message is a reply to:
 Message 92 by Percy, posted 07-26-2009 9:23 AM Percy has replied

Replies to this message:
 Message 99 by Percy, posted 07-26-2009 2:44 PM Smooth Operator has replied

DevilsAdvocate
Member (Idle past 3101 days)
Posts: 1548
Joined: 06-05-2008


Message 95 of 315 (516606)
07-26-2009 11:39 AM
Reply to: Message 93 by Smooth Operator
07-26-2009 9:34 AM


SO writes:
Myself writes:
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.
Because genetic material is information exhibiting CSI. And CSI is evidence of an intelligence.
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.
SO writes:
Myself writes:
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.
If you are saying transposition 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.
I already posted a link showing what the LexA protein can do.
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.
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).
SO writes:
Myself writes:
Mutation is part of the evolutionary process, yes. It is like saying if someone can't walk they can't run very fast. Duh!
So how have bacteria been supposed to evolve the mutation inducing mechanisms without mutations?
Because these 'mechanisms' aka proteins perform other functions than just enabling or inhibiting genetic mutation (this was the undoing of ID’s irreducible complexity argument) and also these mechanisms do not control all forms of genetic mutations.
SO writes:
Myself writes:
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.
The Lexa proteins without which bacteria can't mutate.
BS, you have poor reading comprehension. They are talking about resistance to specific antibiotics not all types of genetic mutations.
Edited by DevilsAdvocate, : No reason given.
Edited by DevilsAdvocate, : No reason given.

For me, it is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring.
Dr. Carl Sagan

This message is a reply to:
 Message 93 by Smooth Operator, posted 07-26-2009 9:34 AM Smooth Operator has replied

Replies to this message:
 Message 96 by Smooth Operator, posted 07-26-2009 1:13 PM DevilsAdvocate has replied

Smooth Operator
Member (Idle past 5114 days)
Posts: 630
Joined: 07-24-2009


Message 96 of 315 (516617)
07-26-2009 1:13 PM
Reply to: Message 95 by DevilsAdvocate
07-26-2009 11:39 AM


quote:
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.
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 Error
It 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 Error
It 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.
quote:
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.
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).
Well obviously you misread something.
quote:
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.
quote:
If you inhibit this pathway, the bacteria cannot evolve, says Scripps Research Assistant Professor Floyd Romesberg, Ph.D., who led the study.
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.
quote:
Because these 'mechanisms' aka proteins perform other functions than just enabling or inhibiting genetic mutation
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?
quote:
(this was the undoing of ID’s irreducible complexity argument)
This has nothing to do with IC which you misunderstand.
quote:
and also these mechanisms do not control all forms of genetic mutations.
If that is true, why can't bacteria evolve resistance without them?
quote:
BS, you have poor reading comprehension. They are talking about resistance to specific antibiotics not all types of genetic mutations.
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?

This message is a reply to:
 Message 95 by DevilsAdvocate, posted 07-26-2009 11:39 AM DevilsAdvocate has replied

Replies to this message:
 Message 103 by DevilsAdvocate, posted 07-26-2009 4:01 PM Smooth Operator has replied

Stagamancer
Member (Idle past 4916 days)
Posts: 174
From: Oregon
Joined: 12-28-2008


Message 97 of 315 (516627)
07-26-2009 2:15 PM
Reply to: Message 82 by Smooth Operator
07-25-2009 3:29 PM


The facts contradict you. Transposons induce mutations. They are not random.
OK. This is obviously a really difficult concept for you. If you induce mutations, what that means is you increase the chance that a mistake is made in copying the code. However, the kind of mistake that is made is still random. The outcome of this mistake is random. This is still random mutation, there's just a higher probability that it will occur when it is induced. Inducing mutation is just like rolling multiple dice instead of just one (or rolling one die more often). It increases the chances of getting the desired roll, but it does not decrease the randomness of each individual roll. Just because there are mechanisms that allow for this increased mutation rate doesn't mean it's not random.
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.
Ah, they can't get resistance within the scope of the experiments, not no matter how long it takes. A key distinction. Yes, bacteria have ways of increasing the rate of mutation. But, you keep saying it's not random, and yet you also say it's not directed to a specific goal. So which is it? Be consistent. Either bacteria have the ability to direct their mutation to a specific goal, or they have the ability to increase the rate of random mutation at a specific site in order to take a chance that they will develop a beneficial mutation. I'll give you a hint, it's the latter.

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

This message is a reply to:
 Message 82 by Smooth Operator, posted 07-25-2009 3:29 PM Smooth Operator has replied

Replies to this message:
 Message 98 by traderdrew, posted 07-26-2009 2:42 PM Stagamancer has replied
 Message 101 by Smooth Operator, posted 07-26-2009 3:58 PM Stagamancer has replied

traderdrew
Member (Idle past 5154 days)
Posts: 379
From: Palm Beach, Florida
Joined: 04-27-2009


Message 98 of 315 (516630)
07-26-2009 2:42 PM
Reply to: Message 97 by Stagamancer
07-26-2009 2:15 PM


Mutations
However, the kind of mistake that is made is still random. The outcome of this mistake is random. This is still random mutation, there's just a higher probability that it will occur when it is induced. Inducing mutation is just like rolling multiple dice instead of just one (or rolling one die more often). It increases the chances of getting the desired roll, but it does not decrease the randomness of each individual roll. Just because there are mechanisms that allow for this increased mutation rate doesn't mean it's not random.
The above really depends on what any of us lurkers want to believe. I for one have a problem believing that a new function such as digesting nylon could be formed by random mutations simply because of the complexities inside of the cell. How many things can go wrong and look at the error correction mechanisms inside the cell that catches and corrects something like a 99.99999999% of all errors. From a previous link:
Because of the potential harm of mutations, humans and other mammals have evolved to make as few as possible. The machinery inside our cells has the ability to replicate our genomes extremely well, and the polymerase enzymes that replicate our DNA rarely make mistakes. Even when they do, we have multiple, redundant repair and proofreading mechanisms that would make even the most six-sigma-compliant NASA engineer jealous.
The quoted statement from above would be more plausible if one of the first Darwinian predictions (below) was correct.
"The cell is a simple homogenous globule of plasm" - T. H. Huxley - "Darwin's Bull Dog".
Either bacteria have the ability to direct their mutation to a specific goal, or they have the ability to increase the rate of random mutation at a specific site in order to take a chance that they will develop a beneficial mutation. I'll give you a hint, it's the latter.
So what does the bacteria do with all of those mutations that it can't use?
Smooth Operator,
You are doing very well in this debate, much better than I would have done. You seem to be losing some of your patience but I don't blame you. Also, I don't believe the one who wins the debate is the last one who posts. Intelligent design is for those who can discern what is real from what is not.
"Computers are no more able to create information than iPods are capable of creating music." - Dr. Robert Marks - Professor of Electrical and Computer Engineering at Baylor University
Edited by traderdrew, : Just adding more "Complex Specified Information"
Edited by traderdrew, : No reason given.

This message is a reply to:
 Message 97 by Stagamancer, posted 07-26-2009 2:15 PM Stagamancer has replied

Replies to this message:
 Message 115 by Stagamancer, posted 07-27-2009 12:56 AM traderdrew has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


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

traderdrew
Member (Idle past 5154 days)
Posts: 379
From: Palm Beach, Florida
Joined: 04-27-2009


Message 100 of 315 (516633)
07-26-2009 2:59 PM
Reply to: Message 99 by Percy
07-26-2009 2:44 PM


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.
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.

This message is a reply to:
 Message 99 by Percy, posted 07-26-2009 2:44 PM Percy has replied

Replies to this message:
 Message 104 by Percy, posted 07-26-2009 4:06 PM traderdrew has replied

Smooth Operator
Member (Idle past 5114 days)
Posts: 630
Joined: 07-24-2009


Message 101 of 315 (516637)
07-26-2009 3:58 PM
Reply to: Message 97 by Stagamancer
07-26-2009 2:15 PM


quote:
OK. This is obviously a really difficult concept for you. If you induce mutations, what that means is you increase the chance that a mistake is made in copying the code. However, the kind of mistake that is made is still random. The outcome of this mistake is random. This is still random mutation, there's just a higher probability that it will occur when it is induced.
It's not random if it was induced, by definition. Random mutations have no cause.
quote:
Inducing mutation is just like rolling multiple dice instead of just one (or rolling one die more often). It increases the chances of getting the desired roll, but it does not decrease the randomness of each individual roll. Just because there are mechanisms that allow for this increased mutation rate doesn't mean it's not random.
Well no, I never said that the mechanism is mutating for an exact goal. I said it is using mutations to get over time the desired goal. But the point is that mutations are not happening out of thin air.
quote:
Ah, they can't get resistance within the scope of the experiments, not no matter how long it takes. A key distinction.
Obviously long enough to conclude they can't get it.
quote:
Yes, bacteria have ways of increasing the rate of mutation. But, you keep saying it's not random, and yet you also say it's not directed to a specific goal. So which is it? Be consistent. Either bacteria have the ability to direct their mutation to a specific goal, or they have the ability to increase the rate of random mutation at a specific site in order to take a chance that they will develop a beneficial mutation. I'll give you a hint, it's the latter.
I am consistent. I said from the start that they mutate specific regions and wait for the positive outcome. They don't actually know what's going to happen.

This message is a reply to:
 Message 97 by Stagamancer, posted 07-26-2009 2:15 PM Stagamancer has replied

Replies to this message:
 Message 106 by DevilsAdvocate, posted 07-26-2009 4:15 PM Smooth Operator has replied
 Message 116 by Stagamancer, posted 07-27-2009 1:10 AM Smooth Operator has replied

Smooth Operator
Member (Idle past 5114 days)
Posts: 630
Joined: 07-24-2009


Message 102 of 315 (516638)
07-26-2009 3:59 PM


quote:
Smooth Operator,
You are doing very well in this debate, much better than I would have done. You seem to be losing some of your patience but I don't blame you.
Oh, trust me, I'm used to people just not geting it.

DevilsAdvocate
Member (Idle past 3101 days)
Posts: 1548
Joined: 06-05-2008


Message 103 of 315 (516640)
07-26-2009 4:01 PM
Reply to: Message 96 by Smooth Operator
07-26-2009 1:13 PM


SO writes:
Actually it was invented by Leslie Orgel, an evolutionist. Anyways...
Not the way Demski uses it. Orgel never used the entire phrase "complex specified information" and his usage of this concept is completely contradictory to how Demski uses it. This is another case where creationists hijack the academic work of real scientists. Anyways...
SO writes:
CSI is reliable measure of information
Says who?
SO writes:
and it is suitable to detect design
Says who?
SO writes:
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.
I assume you got this second hand from Demski referring to Seth Lloyd's 'Computational capacity of the universe' article in which Llyod is allegorically representing the physical universe as a computation device aka a computer and trying to determine the information capacity & computation power the universe entails. In other words this is a metaphore. He even states this:
Dr. Lloyd writes:
In this metaphor we actually have a picture of the computational universe, a metaphor which I hope to make scientifically precise as part of a research program. We have a picture for how complexity arises, because if the universe is computationally capable, maybe we shouldn't be so surprised that things are so entirely out of control.
SO writes:
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.
How can you determine that the product is not a result of a natural law? This is to assume that something exists outside of natural law (i.e. supernatural); which by definition you cannot determine using empirical evidence which is itself based on natural laws and the scientific method. You are in a catch-22 situation here with your assertion.
SO writes:
When those both conditions are met, we have design.
Or so you thinkanyways
SO writes:
o 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.
What 400 bits in nature? What are you talking about?
SO writes:
It 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 reason we can determine that it was designed by humans is because we as human beings are indoctrinated on what human-made objects look like both by through observation of other objects designed by humans and through our own trial and error. Besides, it is still subject to the same natural laws for its creation as does other phenomena not created/designed by man. There is nothing magical about this. You see design from a supernatural entity because that is what you want to see you.
How about termite mounds are they intelligently designed by termites?
How about stromatolites, are they intelligently designed by cynobacteria?
How about natural phenomena formed through the wind and water erosion and seismic activity that earily look like human-made objects, this is called :
You are conditioned to see what you want to see. It is called apophenia. Look it up.
Myself writes:
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.
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).
SO writes:
Well obviously you misread something.
LOL, is that the best you can come back with? What are you 10 years old?
SO writes:
Well are you not able to extrapolate what that means?
You are no extrapolating you are making shit up out of thin air to back up your preconceived notions.
The point is that to evolve the bacteria needs specific mechanisms.
No, that is not what this article is saying. Now you are deliberately lying. The evolution of this bacteria in this article is only taking into consideration its adaption to resist certain antibiotics not the entire evolutionary history of the bacteria.
SO writes:
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.
It does evolve without LexA. The presence of LeXA just enables mutation in a certain area of the bacterium’s genome which enables it to be resistant to certain types of antibiotics. Stop making shit up.
SO writes:
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.
No, this is not how adaption/evolution works. How are you defining random mutations. All these protein inhibitors are doing is increasing the mutations in one specific area of the genome. This does not mean that mutations are not occurring elsewhere in the genome.
SO writes:
How did the bacteria evolve those mechanisms, if they need the mechanisms in the first place?
Who is saying that these bacterium need these ‘mechanisms’ to evolve overall? These mechanisms are only needed to evolve resistance to certain types of chemical agents. You really need to study some basic biology and molecular biology before you try to attack scientific concepts you are ignorant of.
SO writes:
This has nothing to do with IC which you misunderstand.
How do you know I misunderstand IC when we have not even discussed it. This statement went over your head so nevermind.
SO writes:
If that is true, why can't bacteria evolve resistance without them?
Sweeping generalization and incorrect one at that. Did this article state that all bacteria require this mechanism to be resistant to all chemical agents much less all antibiotics.
SO writes:
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?
We don’t know uncategorically and 100% that they cannot evolve resistance without LexA. It is assumed based on these studies that they can’t at this time. However, given enough time, the bacteria very well may evolve to build resistances without LeXa. If enough mutations occur who knows this may occur, no one knows. Again why would not having this mechanism inhibit the bacterium from evolving in the past since many of these synthetic antibiotics were non-existent until the last half of this century anyways.
Smooth Operator, you are the epitome of someone who has does not have the scientific background necessary to be able to determine true scientific truths from the pseudoscience crap you find on the internet and in creationist/ID propoganda.

For me, it is far better to grasp the Universe as it really is than to persist in delusion, however satisfying and reassuring.
Dr. Carl Sagan

This message is a reply to:
 Message 96 by Smooth Operator, posted 07-26-2009 1:13 PM Smooth Operator has replied

Replies to this message:
 Message 107 by traderdrew, posted 07-26-2009 4:29 PM DevilsAdvocate has replied
 Message 109 by Smooth Operator, posted 07-26-2009 4:36 PM DevilsAdvocate has not replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


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

Smooth Operator
Member (Idle past 5114 days)
Posts: 630
Joined: 07-24-2009


Message 105 of 315 (516644)
07-26-2009 4:07 PM
Reply to: Message 99 by Percy
07-26-2009 2:44 PM


quote:
Oh. Then why do you care about evolution of the nylon-feeding trait if the mere existence of DNA infers design?
Because evolutionists keep claiming you can get information by evolutionary algorithms. Which is false.
quote:
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, 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.
quote:
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.
It's not perfect, but it doesn't have to fail in the way you think it does. If the bacteria can't evolve resistance, than that's what we have.
quote:
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.
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.
Edited by Admin, : Fix quoting.

This message is a reply to:
 Message 99 by Percy, posted 07-26-2009 2:44 PM Percy has replied

Replies to this message:
 Message 114 by Percy, posted 07-26-2009 7:04 PM Smooth Operator has replied

Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024