Irreducible Complexity and TalkOrigins

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. 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. Sounds like a guess, has anyone ever seen this? Is there any evidence that this has occurred? 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. Not following... 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? 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 DemystifiedAnd 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!

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

Thread moved here from the Proposed New Topics forum.

It turns out that the butler did it. 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. This is a massive assumption given that there isn't a scrap of evidence to support that contention. 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. 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. 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. 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? 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). 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. You are wrong. This is also highly context dependent. 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. 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. Enzymes are proteins. They are a particular class of proteins which act to speed up chemical reactions. It's not a jab to the ribs at all, it is simply that science is tentative and considered and the evidence is primarily inferred from genetic data. 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.TTFN,WKEdited by Wounded King, : No reason given.

You're starting with a false premise - that irreducibly complex structures exist, at all.Short answer: they don't.Medium answer: every single feature of every organism that currently exists or that we have ever examined from fossil evidence is a slightly modified version of the same feature on another organism.Longer answer: Take the eye as an example. IC proponents tend to point out that, if you remove the lens, or cornea, or any other part of the eye, it ceases to be a useful structure. It therefor must be irreducibly complex, and could not have evolved. But this does not match up with the evidence. The eye, as a general structure, has evolved in several completely different, completely separated trees (all of the steps of eye evolution are just that useful). The first step is simply a photoreactive cell - something that can tell light from dark. This is useful - sunlight is a source of energy, so it's useful for an organism to be able to tell when it is sitting in sunlight. There are many examples of these - various bacteria, for example, and plants. The next step towards an eye would be having only a small cluster of photoreactive cells in a recessed portion of the organism's body. It doesn't have to be recessed much to make the simple light/dark detecting cells now able to sense the direction of the light as well as its presence - obviously more useful.Check out the Wiki article - rather than me typing the whole chain out, they have a decent description, along with a few examples of specific organisms with eye-precursors. 100%. Mutation happens literally all the time. You, in fact, have as few as 50 and as many as several hundred mutations in your very own genetic code. The imperfect replication process makes mutation an inevitability. Compared to the sum total of all mutations? Slim. Most mutations confer no selective advantage or disadvantage whatsoever. That's why evolution is only directly observable over multiple generations (not so easy with humans, but easy to observe in bacteria, for example, and some organisms mutate at an incredibly rapid rate, like the HIV virus). You mean how many replications are necessary to fully evolve a given feature? False dilemma - each of the precursors to the feature you're targeting is, in itself, a fully evolved feature conferring a selective advantage. Otherwise, the final feature would not evolve. Evolution is not goal-oriented. If a beneficial mutation pops up, it will survive better than the organisms without the mutation. That's it. The "chain," as we're calling it, is a human construct to help us see all of the steps to evolving a given feature, but the implication that all useful structures require multiple steps of replication and mutation to evolve is not reflected by either reality or the theory of evolution. Many. You really can't get more precise than that, unfortunately - speciation is most commonly defined as when a descendant population is no longer able to reproduce with its ancestor population, creating two reproductively seperated populations. We have observed this in relatively few generations, but it's dependant on far too many variables to give a more precise answer. See, again, the Wiki article.Quite to the contrary - beneficial mutations are forced to accumulate. The better-adapted organisms are the only ones that survive selective pressure, and are thus the ones that continue to reproduce and mutate. If you have an antibiotic-resistant bacteria, and apply antibiotics to an area, the resistant population will be all that survives. This means the next beneficial mutation, whenever it happens, will HAVE to happen in addition to the resistance mutation, since that population is the only one still living.And again - there ARE no irreducibly complex systems.

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Or the parts may become co-adapted to perform even better, but become unable to perform the specified function at all without each other.

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Sure. The human eye again, for example. It's an evolved structure, as shown previously, but if you take one in its current form and, say, remove the retina, the eye no longer functions at all.Irreducible complexity relies on the false premise that evolved features spring in to being fully formed through mutation - ie, a heart's valves must suddenly appear, alone, before the heart can finish evolving. This isn't the way it works at all. Each individual mutation builds on a long history of previous mutations, each of which were beneficial to the organism. When you're taking baby steps, you'll eventually walk from New York to San Francisco, but none of the individual steps look all that different from the ones immediately before and after the current one.

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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

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Wow. Let's try to be polite, shall we?Changing an amino acid changes the protein, which can make significant changes...sometimes. Sometimes, it doesn't do much, or anything. It depends on the gene, and the features the gene controls. Many features are controlled by multiple genes simultaneously, so a change in one will not necessarily cause a change in expression. Others are controlled by a single gene, and altering a single protein will have an effect.

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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.

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It's simple chemistry, TheWay - it's not random at all. Chemical reactions happen in certain, prescribed ways because of the physical properties of the chemicals themselves. While mutation is random, it's random within the set of possible chemical reactions, making it less akin to the moronic "tornado assembling an airplane" metaphor Creationists are fond of, and more like "I have a bunch of different shaped pegs and holes, and some of the pegs are made of gold - by trying the pegs and holes randomly, I'll eventually get some gold pegs on the other side."As for co-opting for a different purpose: much like the "holes and pegs" metaphor, a protein can have more than one chemical reaction possible (like a small enough peg can fit through a hole of a different shape). A protein produced naturally in an organism for one function can be used by a mutation for another, entirely different purpose. Take a look at the evolution of the Bombardier Beetle over at Talkorigins (another wonderfully debunked example of supposed "irreducible complexity"). Each of the chemicals and enzymes used by the beetle for it's trademark explosion are used for different purposes elsewhere in the organism, and had completely different uses in its ancestors. As an example, one of the chemicals used in the explosive reaction is used in other insects as a defense mechanism because it tastes bad to predators - the bad-tasting chemical was used for a completely different purpose in the beetle.

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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.

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I believe he's referring to a case where a gene is transcribed multiple times in a single copy. So, in the sequence "ABC," the gene "A" is replicated an extra time and the sequence becomes "AABC."We use "may" when talking about evolutionary processes because there are so many possibilities. Selective pressure, mutation, everything in evolution takes many, many forms. Sexual selection and genetic drift cause changes in allele frequency over time, just as the more direct "kill a big portion of the population and the strongest will survive" does, for example.Irreducible Complexity is a dead idea. It's been debunked so many times that only the gullible or the uninformed still ascribe to it. Behe keeps writing books because there are still a lot of people who don't understand what evolution really is, and have a preset religious motivation to believe in a designer. Note that Behe never, ever addresses the actual scientific community. He never publishes any papers in scientific journals - all he ever does is try to convince the general public, who know absolutely nothing about the topic and can be fooled so easily as to be embarrassing to the rest of us. What Behe and others like him say is self consistent, so it "makes sense" to the uneducated. It's unfortunately not consistent with reality, and that unfortunately takes more education than the average person receives on the subject to understand.

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Every time a fundy breaks the laws of thermodynamics, Schroedinger probably kills his cat.

I'm not sure what you are talking about here in terms of transcription. Gene duplication is the result of a copying error either at the level of individual genes, chromosomes or entire genomes, so it either occurs during DNA synthesis during S phase or when the cell is dividing if the genetic mterial is not divided equally between the daughter cells. The first case seems to be what you are describing and is what would be thought to have produced genetic features such as the initial clusters of Hox genes for example, these clusters have subsequently been duplicated by whole genome duplication leading to dozens of different forms of Hox genes.TTFN,WK

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. I will begin with this,

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...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.

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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?

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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

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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. 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:

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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.

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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? 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. 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? 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:

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Fisher has shown that most mutants, even if they have positive SV's, will be wiped out by random effects.

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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. 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? 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? 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? 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? 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. 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.

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

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. If the question is if more complex systems can reduce then they certainly can, a prime example would be the numerous instances where independent parasitic organisms have lost their independence and become obligate parasites. If you mean is it documented as a whole as in have we actively observed every step of such a degradation in a laboratory then the answer is no, these things take a long time to occur. But neither is it mere speculation as there is compelling genetic evidence showing the derived nature of several obligate parasites from independent ancestors. Again without some clearly identified system agreed to be IC this is virtually impossible to answer and similarly without some functional definition of what constitutes genetic information this statement is impossible to address. Once again the nature of the information you mean is unclear. Do you mean perhaps that there must be a minimum amount of genetic information, and specific information that performs a particular purpose, before a genome can reproduce itself? There are a number of pre-cellular and pseudo cellular genetic systems which are possible and truly cellular life itself is usually considered a subsequent development. This is more an abiogenesis question than an IC question, unless the contention is that life itself is fundamentally IC. I may just have misunderstood the question. I think that neither of these things is neccessarily true depending on your understanding of information. For the first point we can see entire genomes duplicate as one 'mutation'. While I agree that this deosn't neccessarily produce any novel information there are any number of informational metrics where such an event would represent a doubling in the informational content, and higher ploidy numbers are also commonly associated with increases in size, which may well represent a beneficial trait in some situations.The second point, that a random positive mutation requires an increase in information, is definitely not true. In many cases it is beneficial for an organism to lose something it no longer needs, those reduced obligate parasites would be a prime example. In a permissive environment an organism that loses a feature which requires energy to produce or maintain but which is superfluous in its current environment has a beneficial increase in its available energy in that environment. Beneficial mutations need not represent an increase in genetic information. I can't tell if it is accurate or not, though I suspect not, or answer the rest of this query without a robust definiton of what you mean by genetic information. Spetner doesn't have to be lying, he might just be wrong. As far as I can tell the paper Spetner published in 1964 was in the 'Journal of Theoretical Biology', which as its name suggests focusses on theoretical speculations. This is just plain wrong. Most mutations are neutral. There is certainly a higher frequency of detrimental than beneficial ones though, as far as we have been able to determine. It is also worthwhile recalling that this is not occurring in individuals in isolation but in populations. While a particular gene may be compromised by mutation in an individual the original form will still be extant in the population. This is one reason why natural selection is considered such an important factor as it reduces the spread of such compromised alleles though the population, or in many cases they are so deleterious as to preclude their being passed on such as mutation which are lethal at the early stages of embryonic development.Not all 'detrimental' mutations need be so lethal however and organisms could easily carry a substantial burden of such genes in a population provided the environment was not too severe. Without more information on how he gets to his conclusion whether this in anyway precludes evolution from fitting into current timeframes is hard to say. 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'. What are you? A Raelian? The chances of an individual getting some mutation are very high, almost every generation will introduce several mutations into a relatively large genome simply because copying during DNA synthesis while very good is not perfect. Most humans are though to have around 20-30 novel mutations, of some kind, compared to their parent. The chances of any particular mutation occurring are very small, although some are more likely than other, such as chromosomal abnormalities which crop up infrequently but with regularity. Very low, but 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. depending on what one considers to constitute the environment I might be tempted to say it plays the whole role, if one were to allow the genetic environment of the cell and the other organisms in the individual's population to be considered environmental factors.There are a myriad of factors which contribute to natural selection and as I suggest any one could be considered environmental. I think it would be hard to dispute the existence of such mutations given the numerous experimental studies on factors such as antibiotic resistance in bacteria. Not anything particularly significant and Spetner's precis of Fisher is also correct, but do not forget that it applies equally to detrimental and neutral mutations. 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, as I pointed out before the genetic bases of reproductive isolation are highly variable. but even taking 500 as a fixed number then why is it of neccessity a problem, we would need to have both that figure and the calculated probability for mutations arising and being fixed to determine that. It also seems to assume that the contributing fixed mutations would necessarily be beneficial which need not be the case. 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. Well point mutations don't show 'true randomness' in the sense of all being equiprobable, the probability of a particular mutation is highly affected by the particular base involved the surrounding genetic sequence and the surrounding higher order structure of the chromosome. This would seem to limit the applicability of his conclusions right from the get go. It also make a potentially unwarranted assumption that the most frequent type of mutation, the single base substitution, is also the most important type of mutation. 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. 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 certainly can't answer this question especially, as I already pointed out, since beneficial mutations can be caused by a loss of information, by most informational metrics. Reproductive isolation can be of several kinds, if it is the result of geographic isolation then it can often be reversed if the two populations are allowed to mix again. However given a long enough period of geographic isolation sufficient genetic changes, either influencing behaviour or directly affecting the biology of reproduction, may accrue that when reintroduced the two species cannot reintegrate. Some people use an even more stringent requirement that behavioural isolation is insufficient and that even in-vitro fertilisations should not produce fertile offspring.I think the most common conception of speciation is that from the biological species concept, this includes geographical isolation as a suitable isolating factor except in flying species. I personally would ted to be a bit more stringent and want to see evidence of some reproductive isolation if the two potential species are reintegrated. Again I can't answer this until you tell me how you personally are measuring such information since there are several possible metrics. Well the examples I am thinking of are cases where for one reason for another a particular gene fails to be expressed but a related gene compensates for its loss, this is sometimes even associated with an unusual spread of the expression domain of the second gene. This naturally principally occurs in embryos, although I imagine you might see similar effect in cell cultures, but I don't suppose that is what you meant. They may also persist into adulthood but that is a lot harder to study. I don't see any particular barrier to it, but its hard to tell without proper deftions of several of the key terms, i.e. IC and information. Certainly there are, including the very popular sickle cell related mutations. There are sickle cell types which both illustrate the highly context sensitive nature of the concept of beneficial, i.e. Hbs providing an advantage to heterozygotes in areas where malaria is endemic, and ones which show that different mutations can perform the same function, the Hbc allele which shows a much reduced severity of sickle cell symptoms although not in conjunction with Hbs. That is the smallest possible change. Well in the case of cancers many of the studies have been on tissues taken from 'nature' i.e. clinical samples an we can get a pretty good idea of the pre-cancerous genetic makeup based on the patients non-cancerous cells.'Prior information' is obviously important as it is the raw material novel mutations work with. As we have both agreed new things are rarely likely to appear from nowhere. The closest to such a deus ex machina would be examples where new proteins are thought to have originated from frame shift mutations, such as the nylon degrading protein nylb see [thread=-9415]. I don't understand the issue. Are you wondering if the temporary benefits of resistance are outweighed by long term effects on the population? Evolution doesn't operate like that, if the resistant ones live and the non-resistant ones die then thats the important thing. 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.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 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. You might be surprised what a lone voice yours is on that matter.TTFN,WKEdited by Wounded King, : fixed link to nylon bug thread

This is old stuff. At the Dover "ID" trial Behe admitted that there were no known IC mechanisms that could not be explained.There was a thread discussing the trial that had links to the transcripts and quotes from it.Also see (Dr) Ken Miller's website:
http://www.millerandlevine.com/km/evol/DI/AcidTest.htmlAnd Irreducible Complexity, Information Loss and Barry Hall's experiments

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... the definition Michael Behe used when he made the term up ("Darwin's Black Box: The Biochemical Challenge to Evolution." - p 39):

By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution.

The conclusion made by Behe and others is that IF evolution cannot produce them, THEN they must have been made, designed, created.

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How did this arch form by natural processes:

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The Bridge of Ross is situated in County Clare in the west of Ireland. Photo by Ray Millar.

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Is that a clue maybe? Then he is telling you falsehoods. Mutations can add nucleotides so there is no limit. Every time the limit for the existing number of nucleotides is reached you can add another base pair and start again. ... not likely to bear any relationship to reality. Especially when they are calculated by someone feeding you false information on how many possibilities there are ...Enjoy.

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First, tell us how you're measuring how much "information" there is in the genome. That's more or less right. No ... not really.The difference between a beneficial and a harmful mutation is like the difference between a guy with one lottery ticket and one with 10,000 lottery tickets. Neither of them is likely to win, but the odds overwhelmingly favor the guy with 10,00 tickets over the guy with one. The odds are slim for any particular mutation to achieve fixation. But there are a lot of mutations. Transposition is a copying error. It would be nice if any of that meant anything, but I'm afraid that it doesn't. See my remarks about "information".What you mean by "how many copying errors would it take to produce an active cumulative evolution" I cannot guess. "Information", again. Yes. Yes. Yes. I think you'll find that evolution is to be credited for evolution, and that adaptation is evolution. That would depend on the degree of evidence for the unobserved phenomena. I, for example, am not skeptical of electrons, though they are unobserved, but I am skeptical of flying pigs (also unobserved). ... have yet to be produced.

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: 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. This is, from what I can gather, Spetner's best definition of information storage as relating to the genotype. Edward O. Wilson is quoted as saying,

quote:

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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.

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{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:

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All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not to increase it.

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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. 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. 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. 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? sry about that, should put on the ol' spectacles from time to time... 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? 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? Sorry, I originally took that WAY out of context. Thanks for the answer anywho. 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. 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 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... 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. 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 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.

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

Hello TW
I'll jump in for a moment to keep things moving if that is ok. There is this quote you supplied. It is all by itself obviously wrong.First note that your source has defined information in DNA in a way that seems (as far as you quote) to be compatible with C. Shannon's definition. Let's say for now that it is.Second do you know what a point mutation is? It is a change in one of the base pairs in the DNA. Let's say somewhere in your DNA there is a string AAGCATGG. Now let's say that there is a point mutation and the next generation gets AAGCATGA instead. Now let's say that Spetner is correct and this point mutation is a reduction in information. (it isn't by the Shannon definition by the way. In fact, I am guessing that a careful calculation will show it is a tiny increase )Now we have the string AAGCATGA somewhere in some genome (maybe your grandkids). Now a point mutation occurs and we get AAGCATGG in the next generation. If the first point mutation caused a reduction information this one must be causing an increase. Do you get that?Now, we need to understand what he is saying. Clearly he can not be saying that point mutations can not increase this "information" (which isn't yet carefully enough defined -- for one thing we don't know how to calculate the amount of it yet -- for "information" as it is used most of the time we do). So the only thing he can be saying is that the ones we have studied don't increase information.But this seems enormously unlikely. For example: If you had a string in your DNA that went AAAAAAAAAAAAAAAA then it contains only (about - I'm not doing the calc.) 6 bits of information. (2 bits to pick the letter out of 4 and 4 more bits to give the number of repeats). If however there is a point mutation that puts a T in place of the 8th A we now have ( I think) 15 bits of information (2 bits for the first letter, 3 bits for it's repeat length then 2 more for the T, 1 bit for it's repeat, 2 more for the next A and 3 more for it's repeat length).So we'd need Spetner's method of calculating information to check out what he says. But it sure looks wrong.

Rather than take your post apart piece by piece, I suggest you take a good, long look at this:Information Theory and Creationism: Spetner and Biological InformationIt destroys Spetner.If you need more info, go here ...Search the Talk.Origins Archive... and search "Spetner".There are over 30 pages devoted to Spetner, including a page of personal correspondence between the PhD who wrote the link above (Dr. Max) and Dr. Spetner.

So selection of some BRAND NEW traits involved compromise on some others. Is this a problem? If we consider this in the context of natural selection instead of artificial, then the selection FOR the trait will mean it has net benefit to the organism that compensates for the loss in the compromised element. Start with this precept: The concept of information (increase\decrease\whatever) either does not apply to evolutionary systems OR the concept that it cannot increase is invalidated.http://EvC Forum: Irreducible Complexity, Information Loss and Barry Hall's experiments -->EvC Forum: Irreducible Complexity, Information Loss and Barry Hall's experimentsEnjoy.

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I'm familiar with Spetner's arguments. The problem in bried is that he offers a measure of information, but only uses part of it and keeps changing how he calculates the information change so that he gets the result. For instance in one case he measueres specificity against one compound. In another he finds that doing that doesn't give the result he wants and insistes on using three compounds - without explaining why or how the extra two were chosen, why one was good enough in the previous example or why three is enough this time. In another case he uses an entirely different and arbitrary measure (based on the size of sets) instead of looking at specificity at all.Really it looks to me as if his main concern is to get the results he wants. He doesn't do a full measure of information by his own list - only an incomplete calculation of one aspect (and in one case not even that) and isn't even consistent in how he does that.(And since you've got his book I'll mention that some years ago I got involved in a discussion of his argument about the probability of speciation - where he made a big mathematical blunder).

That's what we asked you. Trouble is, it includes the word "information". And it does not tell us how to quantify it. Because the ID crowd throw the word about without telling us how to quantify it. Still doesn't tell us how to quantify it. Right, that's Shannon information. In which case any mutation which increases the size of the genome increases the amount of information in it; and any point mutation leaves the amount of information constant. In which case the creationist stuff about mutations and information is false. Have a look at this experiment. But why should the degrees of similarity be exactly in line with the predictions of evolution? This article may help to clarify the issues. This is exactly why scientists distinguish between analogy and homology. The difference is that the observations supporting evolution are reproducible. We can go and look at the fossils or the DNA or the morphology of living creatures again and again and again, it's not like someone saying "I saw a flying saucer but it's gone now." It didn't. Natural selection was also involved. It is. It's also the greatest evidence for the Earth being flat. Here is Claude Shannon's original paper on the subject --- this is where it all starts.