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Author Topic:   Evolving New Information
NosyNed
Member
Posts: 8996
From: Canada
Joined: 04-04-2003


Message 361 of 458 (524747)
09-18-2009 11:08 AM
Reply to: Message 359 by Hyroglyphx
09-18-2009 10:46 AM


Benefits vs Problems
Sickle Cell Anemia is a recessive trait that tends to have more problems than benefits.
Define "more" please. How do you measure it?
If it had more problems than benefits it would be selected out of the population would it not? If a person has only 1 copy of the gene it is beneficial in a malarial area. Two copies are a net detriment.
In fact, it has a net benefit to a population in the right circumstances. This is enough to bring the single copy up to about 1/3 of a population. Higher than this and there are too many two copy individuals born.
It isn't so easy to be absolute about what is beneficial and what isn't. One example that appears to be easy is the mutation in a strain of Italians that appears to make them immune to cardiovascular disease (this arose some centuries ago in one individual). Another example that is a bit less clear is the boy who has super muscular development. Being very strong should be beneficial should it not? However, in an environment that has limited food availability it may not be. This selective pressure can reduce the average size of populations under some circumstance (foor shortages) but under other circumstances push a population to larger sizes (cold weather).

This message is a reply to:
 Message 359 by Hyroglyphx, posted 09-18-2009 10:46 AM Hyroglyphx has replied

Replies to this message:
 Message 362 by RAZD, posted 09-18-2009 12:20 PM NosyNed has not replied
 Message 363 by Hyroglyphx, posted 09-18-2009 12:26 PM NosyNed has replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 362 of 458 (524755)
09-18-2009 12:20 PM
Reply to: Message 361 by NosyNed
09-18-2009 11:08 AM


Re: Benefits vs Problems
Hi Nosyned,
In fact, it has a net benefit to a population in the right circumstances. This is enough to bring the single copy up to about 1/3 of a population. Higher than this and there are too many two copy individuals born.
Doesn't the proportion in the population depends on the incidence of malaria in the environment of the individuals?
Mating people with 1 copy (SN) to people with no copy (NN) we get:
      S   |   N   
N NS | NN
N NS | NN
So ~half would be new carriers, and ~half would be no carriers. With no malaria in the environment all would survive, with endemic malaria infecting the whole population nearly all the no carriers would die leaving mostly new carriers.
Mating people with 1 copy (SN) to people with other with 1 copy (SN) we get:
      S   |   N   
S SS | SN
N NS | NN
So again ~1/2 would be new carriers, ~1/4 would be no carriers and ~1/4 would be double carriers. Double carriers normally die before reaching reproductive age, so in areas with no malaria in the environment the no carriers and single carriers would survive, with single carriers making up ~2/3's of the population, while with endemic malaria infecting the whole population nearly all the no carriers would die in addition to all the double carriers, leaving mostly new carriers.
Thus where malaria is endemic the population would quickly shift to mostly single carriers, while in areas with no malaria the proportion would be gradually reduced by the survival of the no carriers.
This would be similar to the peppered moths with a change in the environment affecting the distribution and frequency of the existing mutations with the population.
Enjoy.
Edited by RAZD, : corrected table, clarity

we are limited in our ability to understand
by our ability to understand
Rebel American Zen Deist
... to learn ... to think ... to live ... to laugh ...
to share.


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This message is a reply to:
 Message 361 by NosyNed, posted 09-18-2009 11:08 AM NosyNed has not replied

  
Hyroglyphx
Inactive Member


Message 363 of 458 (524756)
09-18-2009 12:26 PM
Reply to: Message 361 by NosyNed
09-18-2009 11:08 AM


Re: Benefits vs Problems
Define "more" please. How do you measure it?
How I rationalize it is that all human beings, regardless of where they live, need oxygenated blood cells, even those who live in an malaria-stricken area.
If it had more problems than benefits it would be selected out of the population would it not?
That all depends on how long sickle-cell anemia has been around. If we can definitively conclude that it has been around for centuries upon centuries then, yes, what you say is true. But if this is a relatively new mutation, then we wouldn't expect it to be selected out or in just yet.
In fact, it has a net benefit to a population in the right circumstances. This is enough to bring the single copy up to about 1/3 of a population. Higher than this and there are too many two copy individuals born.
How would this be the case? Wouldn't it be the opposite? If Africans tend to procreate with other Africans, then the more people who have the hetereozygous trait run a greater risk of procreating with someone with the same condition, so that their children might be the homozygous carrier. Would not that homozygous trait increase as population increases?
It isn't so easy to be absolute about what is beneficial and what isn't. One example that appears to be easy is the mutation in a strain of Italians that appears to make them immune to cardiovascular disease (this arose some centuries ago in one individual). Another example that is a bit less clear is the boy who has super muscular development. Being very strong should be beneficial should it not? However, in an environment that has limited food availability it may not be. This selective pressure can reduce the average size of populations under some circumstance (foor shortages) but under other circumstances push a population to larger sizes (cold weather).
Very true. Even the greatest benficial mutation may have some unforseen drawback. That could be said of all traits I suppose.
Edited by Hyroglyphx, : fixed html

"Three passions, simple but overwhelmingly strong, have governed my life: the longing for love, the search for knowledge and unbearable pity for the suffering of mankind." -- Bertrand Russell

This message is a reply to:
 Message 361 by NosyNed, posted 09-18-2009 11:08 AM NosyNed has replied

Replies to this message:
 Message 364 by NosyNed, posted 09-18-2009 2:26 PM Hyroglyphx has not replied

  
NosyNed
Member
Posts: 8996
From: Canada
Joined: 04-04-2003


Message 364 of 458 (524774)
09-18-2009 2:26 PM
Reply to: Message 363 by Hyroglyphx
09-18-2009 12:26 PM


Re: Benefits vs Problems
How I rationalize it is that all human beings, regardless of where they live, need oxygenated blood cells, even those who live in an malaria-stricken area
I read that those with only one copy of the allele are asymptomatic as far as anemia is concerned but much more (or completely?) resistant to malaria.
That all depends on how long sickle-cell anemia has been around. If we can definitively conclude that it has been around for centuries upon centuries then, yes, what you say is true. But if this is a relatively new mutation, then we wouldn't expect it to be selected out or in just yet.
Genetics suggests it has been around for 60 to 150 thousand years.
How would this be the case? Wouldn't it be the opposite? If Africans tend to procreate with other Africans, then the more people who have the heterozygous trait run a greater risk of procreating with someone with the same condition, so that their children might be the homozygous carrier. Would not that homozygous trait increase as population increases?
That is why with the balance of the selective pressure of malaria (very high) and the selective pressure of those who are homozygotic (even higher) the percent of carriers levels out at about 1/3. It is not dependent on population size at all.

This message is a reply to:
 Message 363 by Hyroglyphx, posted 09-18-2009 12:26 PM Hyroglyphx has not replied

  
LucyTheApe
Inactive Member


Message 365 of 458 (524801)
09-18-2009 9:30 PM
Reply to: Message 340 by Percy
09-11-2009 10:30 AM


Re: What is information?
Percy writes:
In everyday usage information can mean representations of facts or thoughts or ideas. When used in this way information is understood to have meaning. But Shannon information theory provides a very specific mathematical definition of information that excludes meaning. People can associate meaning with information, but information itself is independent of meaning.
All of Shannons experiments were the result of a deliberate, intelligent message. Otherwise he couldn't do his maths.
Yes he dealt with the efficiency of the transfer of information without considering the meaning and of course he realised that it requires the positive intelligent use of energy to ensure that the transmission was recieved as expected.
One very simple example of this is the famous message of Paul Revere's ride, "One if by land, two if by sea." The meaning of "land" is not inherent in one lantern, nor is the meaning of "sea" inherent in two lanterns. The code could have been, "One if by sea, two if by land," and it would have worked just as well. In information theory, meaning and information are two different things, and meaning is not part of information theory. Specifically, thoughts and ideas are not included in information theory.
A predefined binary information system. Take the meaning away and its just flashing lights.
You never mentioned a "shell" before, so I don't know what you're referring to, and I can't figure out how you calculated the number of bits of information. Could you describe this for me?
Just like a function doesn't make any sense outside its program, an eye colour machine makes no sense outside a cell. The shell is simply the encapsulation program, in this case a java executable.
public class Swap {

    public static void main(String args) {

    }

}
If you want to know how I calculated the information content then just complile the following files:
public class Swap {
    public static void main(String args) {
	Object a = new Object();
	Object b= new Object();
	swap(a,b);
    }
private static void swap(Object a, Object b) {
  Object temp = new Object();
  temp = b;
  b=a;
  a=temp;
}
}
and;
public class Swap1 {
    public static void main(String args) {
	Object a = new Object();
	Object b= new Object();
	Object c= new Object();
	swap(a,b,c);
    }
private static void swap(Object a, Object b, Object c) {
  Object temp = new Object();
  temp = c;
  c=b;
  b=a;
  a=temp;
}
}
I'm using the definition of redundancy from information theory. This is the first sentence from the Wikipedia article on "Redundancy (information theory)":
your reference should actually read;
quote:
Redundancy in information theory is the number of bits used to transmit a message minus the number of bits of actual information in the message. Informally, it is the amount of wasted "space" used to transmit certain data. Data compression is a way to reduce or eliminate unwanted redundancy, while checksums are a way of adding desired redundancy for purposes of error detection when communicating over a noisy channel of limited capacity.
which is exactly my interpretation. When we are talking about a cell that has to pass on its information into a different time, it has no memory, the term redundancy changes is normal meaning.
Since a message from a message set of size 3 can be represented in 1.585 bits, and since the DNA representation actually uses 12 bits, the extra 10.415 bits are redundant.
I disagree, the 12 choices are determined by the environment or "situation" the cell finds itself. It's not redundancy but rather the inbuilt ability to adapt.
The example I provided is a simplified model of what we observe happening in nature. My simple gene of 3 alleles experienced a single point mutation, something that is observed to happen all the time. This single point mutation caused the number of alleles of this gene to grow from 3 to 4 in our population. This represents a change in information from 1.585 bits to 2 bits, an increase of .415 bits.
Again I disagree. You are talking about expression. You're calling expression new information; its not. You claim on one hand that certain possible outcomes are redundant but then you use one and claim its new information. Now you need to use my model just as I have asked greyseal to do. Smash it to produce new information. If you are successful then I will reconsider my poisition.

There no doubt exist natural laws, but once this fine reason of ours was corrupted, it corrupted everything.
blz paskal

This message is a reply to:
 Message 340 by Percy, posted 09-11-2009 10:30 AM Percy has replied

Replies to this message:
 Message 366 by PaulK, posted 09-19-2009 2:53 AM LucyTheApe has not replied
 Message 367 by Percy, posted 09-19-2009 8:42 AM LucyTheApe has replied
 Message 370 by greyseal, posted 09-22-2009 6:48 AM LucyTheApe has not replied

  
PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


Message 366 of 458 (524811)
09-19-2009 2:53 AM
Reply to: Message 365 by LucyTheApe
09-18-2009 9:30 PM


Lucy's thinking
You stated that Percy's definition of "redundancy" was obviously different from yours.
You then stated that Percy should have quoted additional sentences which do not add to the definition and that your meaning was "exactly" your interpretation.
Obviously your claim to come from another universe must be true, since in ours "obviously different" does not mean "exactly the same".

This message is a reply to:
 Message 365 by LucyTheApe, posted 09-18-2009 9:30 PM LucyTheApe has not replied

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


Message 367 of 458 (524822)
09-19-2009 8:42 AM
Reply to: Message 365 by LucyTheApe
09-18-2009 9:30 PM


Re: What is information?
LucyTheApe writes:
All of Shannons experiments were the result of a deliberate, intelligent message. Otherwise he couldn't do his maths.
Shannon's experiments? Shannon was a mathematician and did not conduct experiments to develop information theory. Obviously Shannon used his intelligence to do his work, we all do.
Yes he dealt with the efficiency of the transfer of information without considering the meaning and of course he realised that it requires the positive intelligent use of energy to ensure that the transmission was recieved as expected.
This erroneous conceptual picture you have is at the core of your misunderstanding of information theory. In everyday terms information includes meaning, but information theory is a very specialized way of thinking about information. Information theory is concerned solely with the problem of transmitting sequences of bits from one point to another. In information theory those bits have no meaning. Measures of information are based upon bits, and there's no meaning.
All transmissions of electromagnetic radiation are in effect just streams of bits, whether they come from the sun or from the local TV station. Humans attach meanings to those bits after they arrive, but the bits themselves have no inherent meaning.
If you want to know how I calculated the information content then just complile the following files...
You think the amount of information in a program is equal to the number of bits output by its compiler? So when the new, more efficient version of the compiler is released and produces a more compact compiled file, your program now contains less information, even though you made no changes? Or you move the compiled file from a Unix to a Dos system and suddenly the file size is different and now your program has a different amount of information, even though you didn't change your program? Or you run the compiled file through gzip to reduce its size, and now the program has less information? In fact, gzip can only reduce file size when redundancy is present. Care to rethink how you should measure the amount of information in your program?
As both Cavediver and I suspected, you have no idea how to calculate how much information is in your program, and not even a clue of how complicated a task you have set yourself.
Any workable example must be simple to enough that we can accurately quantify how much information is involved. To do this you need to know the size of your message set. My simple genome example illustrated how a message set of size 3 (1.585 bits of information) can grow to a message set of size 4 (2 bits of information) through a simple point mutation. I think you should focus on this simple example. Here's the message set with just three alleles before the mutation:
  • GGAAGC (green eyes)
  • GGAAGA (blue eyes)
  • GGCACG (yellow eyes)
And here's the message set with four alleles after the mutation produces a new allele:
  • GGAAGC (green eyes)
  • GGAAGA (blue eyes)
  • GGCACG (yellow eyes)
  • GGCAAG (brown eyes)
I'm using the definition of redundancy from information theory. This is the first sentence from the Wikipedia article on "Redundancy (information theory)":
your reference should actually read;
quote:
Redundancy in information theory is the number of bits used to transmit a message minus the number of bits of actual information in the message. Informally, it is the amount of wasted "space" used to transmit certain data. Data compression is a way to reduce or eliminate unwanted redundancy, while checksums are a way of adding desired redundancy for purposes of error detection when communicating over a noisy channel of limited capacity.
which is exactly my interpretation. When we are talking about a cell that has to pass on its information into a different time, it has no memory, the term redundancy changes is normal meaning.
As PaulK has already noted, you've misinterpreted what Wikipedia is saying. The more complete excerpt does not change the meaning at all, it just repeats the definition in the first sentence in different terms, and it provides the example of checksums. Redundancy is the unnecessary bits used to transmit or store information. You said in Message 339, "It depends how we define redundancy. I obviously have a different interpretation than you do." But if you agree with the Wikipedia article then we have the identical interpretation. Since you apparently still disagree with me, it's more likely that you misinterpreted Wikipedia.
Since a message from a message set of size 3 can be represented in 1.585 bits, and since the DNA representation actually uses 12 bits, the extra 10.415 bits are redundant.
I disagree, the 12 choices are determined by the environment or "situation" the cell finds itself. It's not redundancy but rather the inbuilt ability to adapt.
You still have no idea what redundancy is. As the Wikipedia article states, redundancy is the number of bits used to transmit information above the actual number of bits in the message. Therefore a message from a message set of size 3 can be represented in 1.585 bits, and since the DNA representation actually uses 12 bits, the extra 10.415 bits are redundant. You can't argue with this, it's just a mathematical fact.
Now you need to use my model just as I have asked greyseal to do. Smash it to produce new information. If you are successful then I will reconsider my poisition.
If by "my model" you're referring to your Java code examples, since you are unable to quantify the amount of information in them, I think it's time for you begin addressing the simple example I provided, or to provide one of your own where the amount of information can be quantified.
--Percy
Edited by Percy, : Minor clarification.

This message is a reply to:
 Message 365 by LucyTheApe, posted 09-18-2009 9:30 PM LucyTheApe has replied

Replies to this message:
 Message 398 by LucyTheApe, posted 10-03-2009 12:01 PM Percy has replied

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


Message 368 of 458 (525105)
09-21-2009 4:34 PM
Reply to: Message 347 by Wounded King
09-11-2009 1:31 PM


Re: Persistent twittery
I have been busy lately on a totally different project so I haven't had the time to respond. I don't mean to sound sarcastic, once again I haven't found any good evidence to disprove ID except maybe common descent. I have mined various quotes around here and I have found answers to them. I thought of an answer to it that the intelligent designer isn't concerned with linear time the way we are concerned with it. Also, there might be some good reasons for an old Earth such as petroleum production. And also, my hypothesis of Assemblism which basically says biological life forms have been built and evolved (evolved through intelligent engineering) through natural laws with a precision that we are probably currently incapable of.
An example of another brief counterpoint from mining quotes from this thread is: Saying that the physics of the universe somehow fits together through some sort of random dumb luck and it just happens to support life as we know it isn't a scientific explanation. At best, there is evidence for natural processes but in my opinion design wins as the better explanation.
Do you agree that there is in fact also evidence to substantiate the claim?
No, I have not found evidence to support that quote in message 9 in the Meyer thread. I have found evidence that contradicted it. I also found quotes saying that what determines the 3D structure of proteins in controversial in itself. But what would determine the folding structures if it wasn't precise information. I also recall reading that proteins can fold and form in other ways the ways they are supposed to but that has lead to malfunctions and diseases.
Are you claiming that the MotA from one of those bacteria is in fact the product of convergent evolution from an entirely unrelated gene rather than simply a member of the same lineage with a high proportion of sequence divergence?
I am not claiming this. I guess you can make a case for convergent evolution. I will refesh your memory quoting from Sean Carroll. The most stunning discovery of Evo Devo [that similar genes shapes dissimilar animals]... was entirely unanticipated.
For example certain control proteins found in wings are also found in crustacean gills. As pointed out by Behe in "The Edge of Evolution", this says absolutely nothing about how gills could be converted to wings by a Darwinian process. So convergent evolution would be or remain a possible pathway for exploration.
I don't quite know what the point of this paragraph is
I was referring to the 3D stuctures of proteins.
It is quite possible for similar but not identical amino acid substituttions to allow similar conformations, so there is no reason why a non-identical 2ary structure can't give rise to a similar functional fold.
I have to agree. This is most likely a truth.
No it isn't, it is exactly the subject Shapiro's work addresses and the answer is that much of the engineering comes from transposable elements in the DNA and mechanisms which promote genetic re-arrangement as a response to certain environmental cues or in specific cell lineages, i.e. the immune system in mammals.
The thinking behind this is based on what Behe and Meyer have stated. In a conference at the Heritage Foundation Stephen Meyer briefly spoke about Shapiro and he told us Shapiro rarely thinks about where the engineering came from. Also, Behe states the more complex the biochemical machinery is the more hurdles there is for Darwinism and the more we discover how complex all of it is the more design becomes apparent.
Edited by traderdrew, : No reason given.
Edited by traderdrew, : No reason given.

This message is a reply to:
 Message 347 by Wounded King, posted 09-11-2009 1:31 PM Wounded King has replied

Replies to this message:
 Message 369 by Wounded King, posted 09-21-2009 5:51 PM traderdrew has replied

  
Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 369 of 458 (525113)
09-21-2009 5:51 PM
Reply to: Message 368 by traderdrew
09-21-2009 4:34 PM


Follow the actual evidence
Drew, all you are doing is regurgitating the claims of the ID crowd, claims which you simply seem to accept at face value.
No, I have not found evidence to support that quote in message 9 in the Meyer thread.
Then the reason can only be because you haven't looked. I directed you to specific proteins sequences and the tools you could use to analyse them yourself to determine the degree of conservation. Did you do it? If so did you get a different result to me?
If you want to make a case that the different MotA proteins are functionally distinct then make the argument. Just saying over and over again taht there is no evidence is the purest bull when I have given you the best evidence you can have short of us getting together in a lab and sequencing the genes ourselves.
But what would determine the folding structures if it wasn't precise information.
Environmental factors such as the pH it was working in, the presence of other proteins, the phosphorylation state of certain resides and a number of other physicochemical factors. But all of these things being equal we would still expect the same sequence to produce the same folds.
This is irrelevant though since you concede that other sequences can produce functionally similar, if not the same, folds.
In a conference at the Heritage Foundation Stephen Meyer briefly spoke about Shapiro and he told us Shapiro rarely thinks about where the engineering came from.
And Meyers attribution is enough for you? Do you see why we get the impression you are doing nothing more than cutting and pasting points from ID sites? You don't seem to want to do any research into these topics that doesn't consist of looking up the recieved ID wisdom on them.
Take the MotA claim as an example, just give lookign at the actual evidence a shot. Nick Matzke says that the MotA sequences from two species have a conserved function despite having an amino acid sequence identity of only ~80%. If we look at the sequences for the MOTA protein in Treponema pallidum and Agrobacterium tumefaciens then we do indeed find that they differ by around 80%. If you don't trust the links I gave you in Message 335 then go to the ENTREZ site and find the sequences for yourself.
If you don't disagree about the percentage then you must be disagreeing about the function, so what evidence are you using to conclude that the MOTA protein does not fulfill a similar function in both bacteria? Do you have specific evidence contradicting the quote or just vague ID platitudes about how unlikely it all is and what delicate fragile unique special flowers every protein is?
You could show us a dozen proteins which absolutely require 100% conservation at the amino acid level to function at all and none of them would be evidence contradicatory to Nick Matzke's claim, because none of them would be the MotA proteins he is discussing.
Do you think he is talking about different proteins or that I just picked a random protein which has homologues with 80% sequence divergence and claimed that was what he was talking about? I can show you the trail I followed to identify which proteins he meant if you like.
Why not look at the actual evidence for once rather than a potted digest handed down from the ID movement?
I'm also not sure what you think convergent evolution is, none of the things you talk about are convergent evolution in the sense it is generally understood in biology. Are you saying that homologous genes in the developing wing and the gills are the result of convergent evolution at the molecular level? That the same molecular strutures evolved (or were created/intelligently designed if you will) seperately twice for 2 different functions?
As usual of course Behe is talking nonsense. The fact that we find teh same genes in the same sort of regulatory pathways in multiple organisms and multiple organs says masses as to how they have evolved, and the differences in the molecular constitution of those genes and their regulation and the relationship between these and the differences in the actual structures produced is the entire basis of Evo-Devo. And Sean Carroll is right, it was very unexpected. People expected to see much greater divergence and diversity at the genetic level and the existence of such fundamental similar genetic building blocks as the HOX genes and numerous signalling pathways was a radical discovery. But the similarity of these pathways, and indeed the patterns of their diversity, are a strong argument for a natural history of life on Earth based on common descent with modification from common ancestral populations. And the nature of that diversity is consistent with mutational mechanisms with which we are already familiar at levels stretching from the single nucleotide to entire genomes.
TTFN,
WK

This message is a reply to:
 Message 368 by traderdrew, posted 09-21-2009 4:34 PM traderdrew has replied

Replies to this message:
 Message 371 by traderdrew, posted 09-22-2009 5:10 PM Wounded King has replied

  
greyseal
Member (Idle past 3862 days)
Posts: 464
Joined: 08-11-2009


Message 370 of 458 (525180)
09-22-2009 6:48 AM
Reply to: Message 365 by LucyTheApe
09-18-2009 9:30 PM


Re: What is information?
Now you need to use my model just as I have asked greyseal to do.
Hey, woah, now unless real organisms run java code, your model is just a model.
I have given you an example of an analogous real-world occurence to your model.
You have ignored it.
An increase in 3 alleles to 4 is an INCREASE.
A increase in the amount of genetic code in an INCREASE.
I and others have repeatedly shown you this occuring in nature as well as in logical models.
Retract your argument or address the examples.
I notice you've taken a very small step forwards...by doing exactly what I predicted and proclaiming that an increase in the number of alleles isn't an increase "in information" which you have still not defined very well, because everybody else thinks they've met your criteria. I think you're wrong. Percy thinks that's wrong. WK thinks that's wrong.
You've failed to explain why you're right - after all, an increase in the number of alleles IS an increase, and until you can successfully define "information" everybody is of the opinion that it fulfills your requirements (such as they are).
And you've still not even glanced at the syndrome - it replicates your java script example almost perfectly. The syndrome increases the amount of genetic information drastically, and the result doesn't really do what was intended, but then neither does your javascript code.

This message is a reply to:
 Message 365 by LucyTheApe, posted 09-18-2009 9:30 PM LucyTheApe has not replied

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


Message 371 of 458 (525241)
09-22-2009 5:10 PM
Reply to: Message 369 by Wounded King
09-21-2009 5:51 PM


Re: Follow the actual evidence
If you want to make a case that the different MotA proteins are functionally distinct then make the argument. Just saying over and over again taht there is no evidence is the purest bull when I have given you the best evidence you can have short of us getting together in a lab and sequencing the genes ourselves.
I lost my train of thought. I just read your message 335 and i'm sure you are correct, however I still remain unconvinced that Darwinism is the only explanation. Obviously there is a great deal of variation in three dimensional protein structures. And I have stated before there are different enzymes that can perform the same function.
Drew, all you are doing is regurgitating the claims of the ID crowd, claims which you simply seem to accept at face value.
Yes, I am pretty much reverberating what the ID crowd says. I am not a scientist and they know more than me. I do have a few original ideas such as Assemblism. I don't see what is wrong with repeating them to see how people react to it.
But all of these things being equal we would still expect the same sequence to produce the same folds.
This is irrelevant though since you concede that other sequences can produce functionally similar, if not the same, folds.
Well apparently they can but I wouldn't expect this to happen between different sets of sequences most of the time. I would think there should be a great amount of variation among specific protein shapes.
And Meyers attribution is enough for you? Do you see why we get the impression you are doing nothing more than cutting and pasting points from ID sites? You don't seem to want to do any research into these topics that doesn't consist of looking up the recieved ID wisdom on them.
Well that is why I have been here. I want to hear more counterpoints.
Why not look at the actual evidence for once rather than a potted digest handed down from the ID movement?
I like Meyer and Behe and I agree most of the time with the few IDists who post on this website. I thought of challenging them but they seem to have their hands full with you guys. Very few times I have totally disagreed with their content but most of the time they could have done a better job in persuading me in favor of their views.
Are you saying that homologous genes in the developing wing and the gills are the result of convergent evolution at the molecular level?
That thought did occur to me.
That the same molecular strutures evolved (or were created/intelligently designed if you will) seperately twice for 2 different functions?
It would serve as a casual explanation.
As usual of course Behe is talking nonsense.
Then where is the crustacean gill to wings theoretical pathway?
And Sean Carroll is right, it was very unexpected. People expected to see much greater divergence and diversity at the genetic level and the existence of such fundamental similar genetic building blocks as the HOX genes and numerous signalling pathways was a radical discovery.
Well then, I would think these similar genetic building blocks should give you clues as to specific Darwinian pathways various ancient organisms took. Where are the gills to wings pathways? I would think the thinking and conjecture says, "The genes were dominant at one point in crustaceans but then became hidden within junk DNA and then expressed themselves again when it was time for wings to evolve." I still can think you all are saying, "It was a surprise but it still can be explained with Darwinian conjecture." Darwinian conjecture is beginning to sound 'amorphous' just as Paul K described ID. And the amorphous description doesn't persuade me the other way a tiny bit because a designer can do what a designer wants.
But the similarity of these pathways, and indeed the patterns of their diversity, are a strong argument for a natural history of life on Earth based on common descent with modification from common ancestral populations.
That is a strong statement and if you can point me to a place that can elaborate on that then I 'might' be persuaded even though I might honestly be afraid to read it.
Edited by traderdrew, : No reason given.

This message is a reply to:
 Message 369 by Wounded King, posted 09-21-2009 5:51 PM Wounded King has replied

Replies to this message:
 Message 372 by Wounded King, posted 09-22-2009 7:43 PM traderdrew has replied

  
Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 372 of 458 (525275)
09-22-2009 7:43 PM
Reply to: Message 371 by traderdrew
09-22-2009 5:10 PM


Re: Follow the actual evidence
I am not a scientist and they know more than me.
But for some reason actual evolutionary biologists know less about evolution than you do? Indeed you are prepared to believe Stephen Meyer, a historian and philosopher of science on the details rather than people doing actual primary research?
Very few times I have totally disagreed with their content but most of the time they could have done a better job in persuading me in favor of their views.
Well sure, you already agree with them and apparently you think the word of an ID proponent is always better than that of someone arguing for evolution.
It would serve as a casual explanation.
It certainly is casual. These sort of ad hoc explanations have no value, like many of the speculative strong adaptationist 'just so' stories that plague evolutionary biology.
Then where is the crustacean gill to wings theoretical pathway?
You haven't really given me much to go on here. Are we talking insect wings? Bird wings? I'm going to assume you mean insect wings, although I wouldn't be at all surprised to find homologous genes in bird wings as well. Indeed I just found one on google in about 10 seconds.
I suspect that a number of these genes we are discussing are in fact common also to the crustacean and insect leg. The genes engrailed and Distal-less are expressed in both the developing wings and legs of insects and in the compound arthropod leg which includes the 'leggy' bit, the endopod, and the 'gilly' bit, the epipod. Both of these genes also have homologues involved in the patterning of vertebrate limbs, including birds wings. The engrailed homologues are called Engrailed-like 1 and 2 and the principal Distal-less homologues are called Dlx genes which stands for 'distal-less homeobox' genes.
The more wing/gill specific genes discussed by Averof and Cohen (1997) which I think you were refering to are called apterous and nubbin or pdm, Interestingly while these genes are, with the exception of a small region in the leg for apterous, not expressed in the leg they do have homologues in vertebrate limb development. The homologues of apterous are called Lmx-1 and Lhx2 while nubbin has a homologue called Pou2F1.
I would think the thinking and conjecture says, "The genes were dominant at one point in crustaceans but then became hidden within junk DNA and then expressed themselves again when it was time for wings to evolve."
This isn't how darwinian theory would explain it. Evolutionary biologists would look at the fossil and currently extant species of insects and crustacea and realise that in fact you don't need to lose your gills and regain them as wings. You just hang on to your gills and over many many generations they become modified and allow for a new function to be acquired such as modifying descent (pun unintentional) and eventually allowing powered flight. I admit that the last elements are true conjecture and just the sort of 'just so story' I was complaining about myself, but it hardly seems unreasonable. The larval mayfly has gills highly remiscent of the crustacean gill and also structurally similar to the insect wing.
That is a strong statement and if you can point me to a place that can elaborate on that then I 'might' be persuaded even though I might honestly be afraid to read it.
It isn't in one place, it is throughout the whole of developmental biology. Your own gill/wing example is just one where we see a pattern of one or 2 genes in what are considered more 'primitive' organisms, i.e. the invertebrates, which in the vertebrates have diversified snd giving rise to homologous gene families which have both retained and modified the function of the ancestral proteins from which both they and their invertebrate homlogues derive.
Virtually any developmental pathway tells the same story. I'd be happy to discuss some of them with you since developmental biology is both my job and my passion.
As I say, I don't really know what a good place to start is for a novice. Apart from some SJ Gould articles I hadn't really encountered development until I got to university. There are plenty of evo-devo blogs out there, including the infamous Pharyngula. Maybe Sean Carroll's book would be good, but I haven't read it myself.
So I can't point you to a place which will tie this all together with a bow, science doesn't usually work like that, but I can certainly elaborate on evo-devo if you like, and direct you to the primary literature which discusses these things.
TTFN,
WK

This message is a reply to:
 Message 371 by traderdrew, posted 09-22-2009 5:10 PM traderdrew has replied

Replies to this message:
 Message 373 by NosyNed, posted 09-22-2009 8:30 PM Wounded King has replied
 Message 375 by traderdrew, posted 09-25-2009 1:09 PM Wounded King has replied

  
NosyNed
Member
Posts: 8996
From: Canada
Joined: 04-04-2003


Message 373 of 458 (525293)
09-22-2009 8:30 PM
Reply to: Message 372 by Wounded King
09-22-2009 7:43 PM


references
So I can't point you to a place which will tie this all together with a bow, science doesn't usually work like that, but I can certainly elaborate on evo-devo if you like, and direct you to the primary literature which discusses these things.
I would stick my neck out and say that the primary literature is never the right place to direct someone unless they are a professional (or RAZD).
That is a bit strong since I can get a fair amount out of it myself but only part of the time and only with some difficulties. But I am pretty well read in a number of areas.
For example your post presumes too much understanding of what terms like "homologue" etc are. I think you have to spell it out a bit more.

This message is a reply to:
 Message 372 by Wounded King, posted 09-22-2009 7:43 PM Wounded King has replied

Replies to this message:
 Message 374 by Wounded King, posted 09-23-2009 6:00 AM NosyNed has not replied

  
Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 374 of 458 (525361)
09-23-2009 6:00 AM
Reply to: Message 373 by NosyNed
09-22-2009 8:30 PM


Re: references
I would stick my neck out and say that the primary literature is never the right place to direct someone unless they are a professional (or RAZD).
Meh, this is developmental biology, not rocket science. It isn't like reading a maths heavy physics paper or an abstruse information theory argument. There are pretty pictures and once you understand really only a few key techniques, in fact you might get by with just understanding what an in-situ hybridisation was for the majority of papers, the only tricky things to interpret are some of the comparative anatomies.
Anyway I prefer to explain things in my own words and use the primary literature simply as a reference as your title suggests.
I may not have a very objective view on this I realise. One commentary on the wing/gill relationship was on the old Pharyngula site here.
The only real problem I see with references to the primary literature is that so much of it is still not open access.
As to homologues, Drew seemed to have understood the way I have been using the term previously in the thread and my reply was specifically directed to him, but I agree that for some lay lurker it might be quite unclear and it would be good to make posts as accessible to all as possible.
TTFN,
WK

This message is a reply to:
 Message 373 by NosyNed, posted 09-22-2009 8:30 PM NosyNed has not replied

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


Message 375 of 458 (526006)
09-25-2009 1:09 PM
Reply to: Message 372 by Wounded King
09-22-2009 7:43 PM


Re: Follow the actual evidence
But for some reason actual evolutionary biologists know less about evolution than you do? Indeed you are prepared to believe Stephen Meyer, a historian and philosopher of science on the details rather than people doing actual primary research?
I'm sure Meyer is smart enough to understand the research. Not that I can argue with you on that point.
Well sure, you already agree with them and apparently you think the word of an ID proponent is always better than that of someone arguing for evolution.
No I don't always agree with them. I have a brain. I know that I don't have deep understanding of the subject matter on a lilliputian level. (I was just reading your link to NosyNed.) I am not a creationist and neither is Mike Behe. Here is something from one of your latest posts that I have been thinking about:
Environmental factors such as the pH it was working in, the presence of other proteins, the phosphorylation state of certain resides and a number of other physicochemical factors. But all of these things being equal we would still expect the same sequence to produce the same folds.
Using my brain I can see protein folding is more complex than I thought it was. Phosphorylation (I had never heard of it) is apparently part of a system called the phosphotransferase system. What regulates the pH and how do these systems work together??? Seems like more irreducible complexity to me.
Looking at your links I can say at least you are providing some detail and not making blank statements. Just to clear up what some of you might be thinking about me, I am not against your research Wounded King. I wish you well.

This message is a reply to:
 Message 372 by Wounded King, posted 09-22-2009 7:43 PM Wounded King has replied

Replies to this message:
 Message 376 by Wounded King, posted 09-25-2009 4:58 PM traderdrew has replied

  
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