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Author Topic:   Irreducible Complexity and TalkOrigins
TheWay
Junior Member (Idle past 5874 days)
Posts: 27
From: Oklahoma City, Ok
Joined: 08-21-2007


Message 1 of 128 (434189)
11-14-2007 8:54 PM


I just ordered Behe's book, I haven't read it yet so please no spoilers!
I was reading a review on it and someone posted that IC (irreducible complexity) had been completely refuted on TalkOrigins.org. I simply had to read as much as I could. So here is what I found, and I present these questions to the knowledgeable partakers of the EvC. Thanks and much love.
talkorigins writes:
How might an IC system evolve? One possibility is that in the past, the function may have been done with more parts than are strictly necessary. Then an 'extra' part may be lost, leaving an IC system.
I find this answer fascinating. How did the original IC system evolve? Dr. Spetner suggests that there is a limit to the mutations of an organism based off "how many essential nucleotides it has in its active genome." [spetner 1998 Not by Chance! pg.81] So if this is the case and the variability of a genome of a mammal is roughly 10 to the 24,082,400 power, which is taken on the assumption that the genome only consists of 1% of its dna being "real" information and the rest carrying no information,
How possible is it that the parts will transpose randomly in the genome to result in even one mutation that could result in an IC system?
The odds, according to Dr. Spetner, are very slim to even get a mutation much less one that is advantageous to the organism. Here are some questions Spetner poses to this unlikely event:
What is the chance of getting a mutation?
What fraction of the mutations have a selective advantage?
How many replications are there in each step of the chain of cumulative selection?
How many of those steps do their need to be for a new species to form?
Probably a very small chance of these accumulating especially those that need to result in order to achieve an IC system.
talkorigins writes:
. Or the parts may become co-adapted to perform even better, but become unable to perform the specified function at all without each other.
Sounds like a guess, has anyone ever seen this? Is there any evidence that this has occurred?
talkorigins writes:
This brings up another point: the parts themselves evolve. Behe's parts are usually whole proteins or even larger. A protein is made up of hundreds of smaller parts called amino acids, of which twenty different kinds may be used. Evolution usually changes these one by one
As I understand it, if one amino acid in a chain is altered or mutated we can't really expect the same result in the phenotype as was prior the mutation. Correct me if I am wrong. Please don't bog me down with questions I can't answer, that is what you are for. Unless you can't answer please do not respond or lie. Thanks.
talkorigins writes:
Another important fact is that DNA evolves.
Not following...
talkorigins elaborates and writes:
If you think about it, each protein that your body makes is made at just the right time, in just the right place and in just the right amount. These details are also coded in your DNA (with timing and quantity susceptible to outside influences) and so are subject to mutation and evolution. For our purposes we can refer to this as deployment of parts. When a protein is deployed out of its usual context, it may be co-opted for a different function.
EVOLUTION TO THE RESCUE! Seriously though it sounds interestingly too precise for random chance to produce. When has a protein been "co-opted for a different function?" I thought enzymes played a part somehow?
talkorigins writes:
A fourth noteworthy possibility is that brand new parts are created. This typically comes from gene duplication, which is well known in biology. At first the duplicate genes make the same protein, but these genes may evolve to make slightly different proteins that depend on each other.
Is the author talking about copying errors? Or is something else? He sure says "may" many times when speaking of evolution as a process. (just a quick jab to the ribs )
Alright, this is a section titled "How Might Irreducible Complexity Evolve?" from the article "Irreducible Complexity Demystified" by Pete Dunkelberg. Check it out here: Irreducible Complexity Demystified
And I just realized that it is from the website talkdesign and not talkorigin where I linked from it, I don't feel like correct myself, I pointed that out so I wouldn't be mobbed by the dissecting carnivores of EvC.
I know there is probably more I left out, bring it up as I am strapped for time these days we will eventually get to it. Thanks!

"Sometimes one pays most for the things one gets for nothing." --Albert Einstein

Replies to this message:
 Message 3 by Wounded King, posted 11-15-2007 10:05 AM TheWay has replied
 Message 4 by Rahvin, posted 11-15-2007 11:09 AM TheWay has not replied
 Message 8 by RAZD, posted 11-15-2007 7:55 PM TheWay has not replied

  
TheWay
Junior Member (Idle past 5874 days)
Posts: 27
From: Oklahoma City, Ok
Joined: 08-21-2007


Message 6 of 128 (434330)
11-15-2007 12:33 PM
Reply to: Message 3 by Wounded King
11-15-2007 10:05 AM


A few questions...
Hello Wounded King,
Thanks for taking time to reply to my questions, you have to excuse me as I am studying hard and sometimes lack in comprehensible statements. I am also relatively new to the material.
Enough excuses, I have some questions.
How did the original IC system evolve?
The idea is that the original larger system was not IC, that there were redundancies in the system which meant that the loss of one part did not impair its function. However it could not subsequently sustain the further loss of the complementary component. Or alternatively components which were initially capable of substituting for each other may diverge to such a degree that they lose that ability and the loss of either subsequently compromises the function of the system. There may be other routes to non IC systems becoming IC but those are two that spring to mind.
I will begin with this,
quote:
...there were redundancies in the system which meant that the loss of one part did not impair its function. However it could not subsequently sustain the further loss of the complementary component.
Correct me if I am wrong, the idea is that a more complex system or a system with more ?parts? evolved and then lost ?parts? to reduce into IC? Is this a documented event as a whole or is this a speculation on how it could have happened?
quote:
Or alternatively components which were initially capable of substituting for each other may diverge to such a degree that they lose that ability and the loss of either subsequently compromises the function of the system.
  —Wounded King
So again is the idea that originally an IC system wasn't an IC system and it reduced itself into a situation where it could reduce no further? Many articles, from talkorigins, seem to imply that creationists think that an IC system cannot evolve now. I would use the word adapt but whatever; Has an IC system been shown to add information or adapt new parts?
I think this idea begs the question of how much information must be added to supply a genome to reduce itself before a cell can be functional? As I understand it, information can only be added to the genotype one bit at a time and for every random positive mutation there must be consequentially a bit of information added most of the time. Spetner, as I quoted earlier (if I make a mistake regarding this topic please do not suggest that Spetner is lying, the blame is on me unless I specifically quote him, thanks), suggests that this is the only way a genotype can add information. Whether or not this is theoretical or observable I fail to remember. Is this accurate or are there other ways to add information and please list if they are observed or hypothetical?
I have more questions about information and genetics, I will save them after I have understood more about the above question.
Dr. Spetner suggests that there is a limit to the mutations of an organism based off "how many essential nucleotides it has in its active genome." [spetner 1998 Not by Chance! pg.81] So if this is the case
This is a massive assumption given that there isn't a scrap of evidence to support that contention.
I would like to focus on this a bit. It isn't a main part of the book but it definitely, IMO, would effect some of his calculations if wrong. Really all he says is this:
quote:
Some time ago I looked at how the rate of copying errors affects the rate of evolution [Spetner 1964]. It turns out that the mutation rate is limited by the need to maintain the integrity of the species. If the mutation rate is too high, too many individuals would have one or more of their genes damaged. Because experiments have shown that most mutations are harmful, genes that already built up to be useful would suffer damage.* The mutation rate has to be low, making the rate of evolution slow - once again, too slow for evolution to work the way the NDT says it does.
The * is a reference to the index of the chapter where he gives a hypothetical example.
He suggests that experiments have somewhat verified this postulate. I assume he is referring to his experiments in 1964. Is it possible that you are not aware of any such experiments or is he lying?
How possible is it that the parts will transpose randomly in the genome to result in even one mutation that could result in an IC system?
Unless you are using it in a strange way the word transpose is a strange one to use here. Transposition is only one of many forms of mutation. While there might be one particular mutation which would repredent the last step in a system becoming IC there would be a long history of mutations and evolution in place before in the prior development of the system. This is only a problem if you expect IC systems to spring into being fully formed from no precursors.
I used transpose to mean basically change, I now understand I was potentially writing to geneticists. I apologize. I however, do not understand the use of the word "repredent," I could not find a definition anywhere I can only surmise what it means and I think it is an important adjective to unlocking your point.
Of course, the main ingredient to evolutionary biology is time, I wouldn't refute that. However I hardly accept that any function or system in the genotype would "spring" into being fully formed. I accept that a Highly intelligent being created these systems as one would create a computer program for example. Although, there would be obvious differences in the efficiency and accurateness among other things.
What is the chance of getting a mutation?
There have been lots of studies on mutation rates and indeed there have been a number of threads on the forum dealing both with mutation rates and with theoretical limits to variation. I won't go into it in derail but a look at the scientific literature would produce a considerable body of evidence indicating the chances of a mutation occurring.
I would like your opinion. You are qualified enough to give a reasonable answer correct? Also, I would like to ask what is the chance of getting a positive mutation as opposed to a neutral and detrimental mutation?
What fraction of the mutations have a selective advantage?
This is also something which has been extensively studied and can be found in the literature. It isn't something that can be easily stated however. For a start the fitness, i.e. beneficial or detrimental character, of a mutation is highly dependent on the environmental context in which it arises. What may be beneficial in one context may not be in another. It is however widely accepted that beneficial mutations are less frequent than detrimental mutations.
Are you suggesting that environmental context plays the majority role in natural selection? Does natural selection have any other methods of giving a higher selective value to a mutant organism?
I think this is a good time to bring out the probability of survival in a mutant that has had a positive mutation. Assuming there is such a thing as a positive mutation as described by the Neo-Darwinian Theory. A mutant must have an above average offspring survival rate resulting in a higher selective value. The higher the selective value, the higher the chance that the mutant will survive to take over a population. Am I missing something?
Spetner reduces Ronald Fisher's mathematical archetype of natural selection into a single sentence:
quote:
Fisher has shown that most mutants, even if they have positive SV's, will be wiped out by random effects.
So he suggests that even if the positive mutation creates a positive value for natural selection to occur, it only minutely raises the odds that it will be selected and further take over the population.
There is more, however it seems that odds such as these very slim, and very slim to happen around the 500 times, that G. Ledyard Stebbins Processes of Organic Evolution1966, predicted it would take to gain a new species.
How many replications are there in each step of the chain of cumulative selection?
I'm not sure I understand this question. Does replications mean generations? Does the chain of cumulative selection mean the progress of the various mutations which result in the resulting system?
Spetner doesn't seem to put much stock in any other model of evolution other than copying errors to produce random mutations. He believes the other ways such as transposition fail to conclusively show their true randomness. So he rules out these early on, sticking to evolutions main pony - copying errors. Let's look at all of the ways evolution can produce random mutations in another thread, that I imagine would be an immense topic.
For now though, How many copying errors would it take to produce an active cumulative evolution? Also, how much information would need to be added with each corresponding mutation?
How many of those steps do their need to be for a new species to form?
This seems to be based on the assumption that the differences leading to speciation need to be based on adaptive traits
, which may not be the case. There is no definitive answer for this as there are multiple routes to the genetic establishment of reproductive isolation which are all going to be of varying lengths. There are single mutations which can be shown to be sufficient to produce reproductive isolation, as seen in studies of reproductive isolation in Drosophila (Orr, 2005).
I'm not sure I originally put it into the proper context. As Spetner seems to think that copying errors are the overriding factor in true random mutation. Does mutations such as copying errors result in speciation? Also, Is this the cause of reproductive isolation? I was under the impression that speciation as reproductive isolation was reversable and not subject to complete isolation in the genera or family. What is the stipulations for a complete speciation?
Sounds like a guess, has anyone ever seen this? Is there any evidence that this has occurred?
Well there are lots of examples of genes which have undergone duplication and subsequent divergence. I don't know if any of these are necessarily components of an IC system but they certainly occur and there is considerable evidence that such genes may substitute for each other, either spontaneously in the embryo or if they are geentically engineered to be expressed in place of the related gene.
In this divergence has it been shown to increase the amount of information in the genome? Also, what amount of divergence has been seen in a natural setting without the use of engineering? Also, is the embryo the only known place these can occur outside of physical tampering? How scientific would it be to assume that this process can create the neccessary level of complexity we see in an IC system and even the amount of information prior to its subsequent devolution?
There are situations where the change of a single amino acid, it would not be a mutation as mutations occur in DNA not proteins the mutation in the DNA would produce the change in the protein, could entirely destroy a proteins function but there are also instances where it would have no effect whatsoever.
Are there any documented cases where a change causes a positive effect? Is the smallest change restricted to a single nucleotide? Also, is it that we know a change has no effect or is it believed that it has none?
When has a protein been "co-opted for a different function?"
In many cases in controlled experiments. One such example is the evolution of antibiotic resistance genes from other metabolic enzymes , of multidrug resistance in cancerous cells and of insecticide resistance in numerous species. If you want to look at any of these in greater detail I can provide references.
How probable is this in a natural setting and how likely, by your best estimates, is this to occur in a natural setting? Your examples make me wonder how much "evolution" is to credit and how much adaptation resulting from prior information in the genome is to credit? I would very much like more information on this, I have read about resistences credited to evolution only to wonder how this would eventually effect the phenotype as we see in the phylogeny of our organisms.
There is clear evidence of the processes described but that doesn't stop creationists denying their existence on the grounds that it is merely inferred and we haven't directly observed whole new species arise through genome duplication and divergence.
Are you saying we shouldn't be skeptical of unobserved phenomena that claims itself a scientific fact? Evidences of processes that could have well been established by a designer and interpreted poorly by the design only gives me more of a reason to question what exactly is the evidence.
I hope you will continue in our discussion, I appreciate all the well mannered answers you have given. Thanks for your responses.

"Sometimes one pays most for the things one gets for nothing." --Albert Einstein

This message is a reply to:
 Message 3 by Wounded King, posted 11-15-2007 10:05 AM Wounded King has replied

Replies to this message:
 Message 7 by Wounded King, posted 11-15-2007 2:59 PM TheWay has replied
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TheWay
Junior Member (Idle past 5874 days)
Posts: 27
From: Oklahoma City, Ok
Joined: 08-21-2007


Message 10 of 128 (435914)
11-23-2007 7:15 PM
Reply to: Message 7 by Wounded King
11-15-2007 2:59 PM


Re: A few questions...
Hi Wounded King,
Thanks for the reply, I know it was kind of lengthy.
I haven't been idle on this topic, so a few more questions are in order for you.
First I would very much like to hear what you think about genetic information. What is it? How can it be measured? Can it be measured?
This is what BioPortal has as a definition for genetic information:
Genetic information
Information contained in a nucleotide base sequence in chromosomal DNA or RNA.
I am unsure of why there is a controversy over "information" in the genome. However, I will give it issue and use what is in Spetner's book to try to explain what he thinks it is, and what I think he has related to me.
quote:
The DNA contains the information that tells the cell how to make its protein. It carries a coded list of the string of amino acids making up each protein the cell may have to assemble. The amino acids are encoded in the DNA in the same order in which they appear in the protein. The DNA encodes each amino acid with a string of three bases, and the RNA does the same. A triplet of bases that encodes an amino acid is known as a codon. A codon encodes one amino acid. A molecule of mRNA will encode a complete protein. A typical protein of 300 amino acids is encoded by an mRNA having 300 codons, or 900 nucleotides. This code can be traced back to 900 nucleotides in the DNA.
There are 64 different codons corresponding to the 64 ways of forming a triplet of DNA symbols. These 64 codons encode the 20 amino acids that make up the proteins. Note that there are more codons (64 of them) than there are amino acids (20 of them). More than one codon can therefore encode the same amino acid. For any code, if the same clear text can be encoded in more than one way, the code is called redundant. The genetic code is redundant.
...The bases play the role of the letters of the DNA alphabet, and the genes play the role of the DNA words. In the protein alphabet, the amino acids play the role of the letters, while the proteins themselves play the role of words. Three DNA letters translate into one protein letter, and on DNA word encodes one protein word. The stop codes in the DNA translate into the spaces between the protein words.
This is, from what I can gather, Spetner's best definition of information storage as relating to the genotype.
quote:
A binary digit, or symbol, is one that can take on either of two values, usually denoted by 0 (zero) and 1 (one). The amount of information that can be carried by one binary digit is defined as one bit. The volatile memory of a computer uses 5 volts to represent one, and 0 volts to represent zero. A memory chip that holds eight binary digits, for example, can hold eight bits of information. (In computer jargon, a group of eight bits is called a byte.)
A symbol of a large alphabet can hold more information than can a symbol of a small alphabet. For example, a letter of the English alphabet can hold up to 4.7 bits of information. A symbol of a binary alphabet, on the other hand, can hold up to 1 bit. For a device to store a symbol of a 26-letter alphabet it has to have 26 stable states. To store a symbol of a binary alphabet it needs only two stable states. A DNA nucleotide has four states one for each of its four possible bases. So we could call a DNA symbol a quadrinary digit, and we can encode it with 2 binary digits. (I made up this word to mean that the symbol is from an alphabet of size four. Alternatively we might call it a quadrit, or maybe a quit.) Each DNA symbol can hold up to 2 bits of information.
Edward O. Wilson is quoted as saying,
quote:
Artificial selection has always been a tradeoff between the genetic creation of traits desired by human beings and an unintended but inevitable genetic weakness in the face of natural enemies.
{The Diversity of Life 1992}
Let me set up the context. This is from Spetner's book Not by Chance! btw. If there is any mistakes, they are probably mine as I am summarizing his writing. I'll start with a direct quote from page 138.
quote:
All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not to increase it.
In earlier chapters, I believe he states that there is a switch type mechanism in the genome that activates certain things or deactivates certain things and that this system is what ultimately governs mutations. Is that right? If not I'll go back and read it more carefully.
Anyways he states that "new" information, like what the NDT requires for macroevolution, can only be added by a binary like system. Such as one bit at a time. I could have got that screwy, anyways lets move on to some examples he gives.
Resistance of bacteria to antibiotics and of insects to pesticides. He states, "Some bacteria have built into them at the outset a resistance to some antibiotics." This resistance results from an enzyme that makes the drug inactive and this doesn't build up through mutation. He then cites J. Davies as proposing that the purpose of this particular type of enzyme had a completely unrelated primary function. Basically, a lucky side effect. He also cites a study done on antibiotics and how they are the natural products of "certain fungi and bacteria." Which we should expect to see some natural resistance to. Also non resistant bacteria can become resistant by picking up a resistant virus and the virus may have picked up the gene from a naturally resistant bacteria. Apparently, scientists can genetically modify organisms to become resistant.
quote:
But some bacteria can mutate to become resistant to a drug to which it had been sensitive. In these cases the function is new.
For example, streptomycin and other mycin drugs have caused bacteria to "keep from growing." He then says that the point mutation that made the resistance was the result of losing information.
quote:
Several different mutations in bacteria have indeed been found to result in streptomycin resistance [Gartner & Orias 1966]. We see then that the mutation reduces the specificity of the ribosome protein, and that means losing genetic information. This loss of information leads to a loss of sensitivity to the drug and hence to resistance. Since the information loss is in the gene, the effect is heritable, and a whole strain of resistant bacteria can arise from the mutation.
The more specific the system or code, the more information it would contain. When it a gene's specificity is reduced by a mutation the information is lost to the subsequent generations. So based on this, how can an organism gain complexity yet lose specificity and ultimately information?
Spetner claims, with help from a citation, that a change in an amino acid often affects the way a protein functions. So with resistances, the loss of specificity would result in a degradation of the organism in other ways.
----
Part two; back to your re-post.
Well in the particular context of IC it is hard to say if it has happened since there is no agreement upon exactly what constitutes an IC system or which systems are IC.
What about the bacterium phlagellum? Also, wouldn't it be required to have an abundant amount of information to start with, for any system to even reduce? And doesn't this seem unlikely given that the evidence is tentative for macro-evolution?
The answer was right in front of you on your keyboard the d is right next to the s, unless you use Dvorak, it was simply a typo, my bad! The word should have been 'represent'.
sry about that, should put on the ol' spectacles from time to time...
However I hardly accept that any function or system in the genotype would "spring" into being fully formed. I accept that a Highly intelligent being created these systems as one would create a computer program for example.
What are you? A Raelian?
I know this isn't relevant, but I don't see how a completely organized universe that is very fine tuned came from nothing. God could have spoke a lot?
the chances of getting some positive mutation are higher and the chances of positive mutations persisting tends to be higher than either neutral or detrimental mutations although the degree varies dramatically depending on the specific case.
Isn't this related to the environment such as the bacteria I mentioned above? If there wasn't an introduction of the antibiotics, would the mutation have been neccessary or relevant, or would it have persisted?
I'm not familiar with the basis of Stebbins calculation but I don't think 500 could be taken as anything but a very approximate average even if it was reliable...
Sorry, I originally took that WAY out of context. Thanks for the answer anywho.
Spetner doesn't seem to put much stock in any other model of evolution other than copying errors to produce random mutations.
Well I might agree with this depending on what exactly constitutes a copying error. If it just means point mutations then I would be less likely to agree. If it includes large scale gene duplications I would be happier.
I believe he leans more towards point mutations, although I am unsure of what you mean by "large scale gene duplications." He talks about gene duplications, but it is rather limited. This book was pressed in 1998, if that matters.
You got it back to front, it is the mutations that are one of the things that produce evolution. That might be an interesting thread, I tried to start a similar one before, Mutation and its role in evolution: A beginners guide, but everyone thought it was too technical.
Yep I did, thanks for pointing that out. I would like you to reopen that if you could, I bet I could learn a lot. If we move slow enough.
I don't know that the phrase 'active cumulative evolution' makes any sense. As to how many 'copying errors' might be required I couldn't say offhand, especially since I'm not sure what you mean. I would tend to think it would be however many would have occured in a population in the time until two de novo beneficial mutations, i.e new to the population, were both present in some individual, but it might just be the number until 2 mutations affecting the same trait occurred independently, as no further point mutations would be involved in the mutations being present together in some individual.
I did want to bring this up...It doesn't seem very likely that two de novo beneficial mutations could possibly occur in a population. Wouldn't natural selection have to select both of these and then would at some point these mutations have to "mate."
Or am I completely confused?
Also, could you comment on how things like the sonar-like systems in bats and whales are similar yet aren't related to a common ancestor in the sense that these would have to have developed in both populations randomly? I know there are other examples, I'll have to look those up...
If I sequence the genomes of two identical twins then I should be able to infer that they are twins and therefore that they have the same parent, I don't have to have met the parents. Similarly patterns of similarity between organisms lead us to conclusions about their relatedness which don't rely on us having the genetic information of every preceeding generation inbetween from both lineages.
I think the similarity is good evidence of design, now I know you disagree but without similarity we couldn't assimilate our environment which encourages me to think that that was the plan.
No I'm saying we shouldn't be skeptical of phenomena just because they haven't been directly observed when there is a huge body of directly observed evidence that supports their existence.
Like UFO's? Some could argue using the same reasoning. It's a bit of a stretch, but hey might as well point it out.
I hesitate to say it but the evidence is considerably greater than the evidence for there being any sort of creator. Why couldn't it be the ID camp that is poorly interpreting the design. Perhaps the designer just set up a minimal genome and let it go upon its own merry way through random mutation and natural selection, perhaps he made everyone and everything in a poof exactly as they are 5 minutes ago. Without knowing what sort of designer we are talking about or having any evidence for design its pretty much just empty speculation.
I just don't understand how randomness can create such highly organized complexity. I think simple intuition is the greatest evidence for creation. That's just me.
I know I skipped some stuff, I wanted to focus on the information aspect (not sure I did such a good job). Maybe there are some resources I can pick up on information theory that would broaden my involvement in this topic. Well thanks again, I'll be back some time.

"Sometimes one pays most for the things one gets for nothing." --Albert Einstein

This message is a reply to:
 Message 7 by Wounded King, posted 11-15-2007 2:59 PM Wounded King has replied

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TheWay
Junior Member (Idle past 5874 days)
Posts: 27
From: Oklahoma City, Ok
Joined: 08-21-2007


Message 45 of 128 (437768)
12-01-2007 12:17 PM
Reply to: Message 38 by Dr Adequate
11-25-2007 7:26 PM


Re: Thank you. I'm slow
Hi Everyone, Great discussion.
However you define and quantify information, if some point mutation reduced the information, then the opposite point mutation would of course increase it.
What would constitute an opposite point mutation?
Also, by this logic we could assume that no information would ultimately be removed or added. And that the genome operates under a equilibrium type state? Or is there another type of mutation that can add up information? Also, is adding up information relevant to the ToE?
Spetner's main idea, IMO, is that complexity as we see in various organisms have required information that the idea of the ToE cannot supply through mutations. Complexity requires complex information, which has not yet been shown to have been accumulated through natural processes, as the NDT had imagined.
And however you choose to measure information, if one mutation reduces the information in the genome, the opposite mutation must increase it. Otherwise you could have two identical DNA sequences containing different amounts of information, which would be nonsense.
Could you elaborate? Or supply some material, I can't find anything.

"Sometimes one pays most for the things one gets for nothing." --Albert Einstein

This message is a reply to:
 Message 38 by Dr Adequate, posted 11-25-2007 7:26 PM Dr Adequate has replied

Replies to this message:
 Message 46 by Dr Adequate, posted 12-01-2007 1:31 PM TheWay has replied
 Message 48 by Wounded King, posted 12-01-2007 5:52 PM TheWay has replied

  
TheWay
Junior Member (Idle past 5874 days)
Posts: 27
From: Oklahoma City, Ok
Joined: 08-21-2007


Message 49 of 128 (438089)
12-02-2007 6:25 PM
Reply to: Message 46 by Dr Adequate
12-01-2007 1:31 PM


Re: Mutations and information, part 2
Thanks for the reply, it is starting to make more sense.
In that case, though, in particular a deletion mutation would not remove information. In which case any series of deletion mutations would not remove information. In which case, there is no information in any genome. In which case it is not an objection to evolution to say that mutations can't create information, since there isn't any information.
Are you not re-defining information from the abstract? If I laid out a 1 1 1 1 (four ones) sequence we could say that it is information because we can add these up to get something new like the number four. So abstractly a sequence can manifest a certain idea. Also, we can attach meaning to each (1) number and have it be represented accordingly. Furthermore, without a standard, we could no more say that it isn't information as it is information.
As far as I know, the phenotype reflects the genotype and is an expression thereof. So, in the abstract, I do not understand how you can say that there is no information other than redefining information to fit the evolutionary model.
I looked at the article you provided at: NCBI
and was mentally confounded.
That was a tough paper to read. A few questions from it:
They created a self replicating RNA structure from what? They purified the replicase of 95% nucleic acids, I take it that this replicase is now a deadened version of the bacteria? They added the oligonucleotide to the template free RNA and it induced production of different RNA species, so is this like reconstructing RNA from scratch? Or is there another point to this experiment? After they added the bromide and acridine orange some species couldn't reproduce without it, is this evidence of speciation due to environment? Or am I missing the point of the article?
It also sounds as if they are unsure of why this phenomena is occuring. The information could be in the protein as they suggested or influenced by the oligonucleotides. It is rather strange though.

"Sometimes one pays most for the things one gets for nothing." --Albert Einstein

This message is a reply to:
 Message 46 by Dr Adequate, posted 12-01-2007 1:31 PM Dr Adequate has replied

Replies to this message:
 Message 51 by Dr Adequate, posted 12-02-2007 8:47 PM TheWay has not replied
 Message 53 by Percy, posted 12-03-2007 8:02 AM TheWay has not replied

  
TheWay
Junior Member (Idle past 5874 days)
Posts: 27
From: Oklahoma City, Ok
Joined: 08-21-2007


Message 50 of 128 (438093)
12-02-2007 6:31 PM
Reply to: Message 48 by Wounded King
12-01-2007 5:52 PM


Re: Thank you. I'm slow
Complexity requires complex information
Well that is something of an assumption. There are a number of obvious mathematical formulae showing complexity from very simple initial information, for instance many of Wolfram's cellular automata programs are very simple but they produce very complex patterns.
I believe I over simplified it. Specificity would be an example of small "information" resulting in complexity. I guess I tried to push the idea that the complexity is overwhelming and that subsequently information would be the main factor regardless of the amount.
How can we show it to you unless we agree what it would look like? Without a usable definition for this 'complex information' the IDists can just shift the goalposts any time a counterexample is given.
Do you think Spetner knows how to measure it? Does he give any examples?
I doubt that Spetner knows if no one here knows. As for me, I haven't the slightest clue. So I'll stick around this thread and try to learn more as well as looking for more details externally. Although, abstractly, information would be synonymous with knowledge as one would expect from a design. From a layman's perspective it seems that genetics would fill this requirement. Just tossing that out there.

"Sometimes one pays most for the things one gets for nothing." --Albert Einstein

This message is a reply to:
 Message 48 by Wounded King, posted 12-01-2007 5:52 PM Wounded King has not replied

Replies to this message:
 Message 52 by Dr Adequate, posted 12-02-2007 9:19 PM TheWay has not replied

  
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