molecular genetic evidence for a multipurpose genome

Hi Mark, thanks for your patience.

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A bit wasn’t toggled. IT WAS ADDED!!!!!!

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OK, but essentially it’s the same concept. A trigger is either induced, or it is not. I’ll repost it almost verbatim. Note that state 0 = pre-framshift, and state 1 = framshift:1) To keep things simple, let’s assume the change is binary. So there are two states, 0 and 1. The default, or normal setting is 0, which codes for carbohydrate digestion. Setting 1 codes for nylon. In order for there to be new, or increased information, the original state 0 would have to be the unfavorable state. But it is clear that 0 is the favorable state (in general), and the study confirms that this method is a whopping 98% more efficient. So based on this knowledge, we actually lose information when we go from 0 to 1.
2) Was the mutation random? If so, then from 1) above we can again reasonably conclude that a loss of information occurred. What if the mutation was non-random, that is, environmentally induced? This means there was no net gain or loss of information because the information was already present. I haven’t studied the study you provided in-depth, but from the website you posted my bet is this is a non-random mutation. The author states that it’s been observed more than once. What an un-whitting admission he is making here! Given the odds that this specific mutation would be observable more than once certainly raises eyebrows that this may not be a random event. Another reasonable possibility is that certain portions (hot-spots) of the genome have been pre-programmed for hypermutation during environmental stress to toggle bits in an effort to find a possible combination that improves survival in the degraded environment.

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Hot spots are not pre-programmed. Mutations occur with higher frequency at hot spots regardless of environment.

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Do we know this for sure? No. I merely offered it as a reasonable possibility. From a design perspective it is reasonable, in fact the immune system behaves in a somewhat analogous way. But it’s only thinking-out-loud on my part, I’m not claiming I know or can prove this is actually what is going on.

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Furthermore, if you can’t predict where the next mutation is going to occur, then it’s random (in the sense biologists mean it).

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This is false, as I demonstrated to Quetzal in this thread (and I believe he agreed with).

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1/ Let’s get back to the crux of the argument, does evolution require naturally arising new information in the genome? 2/ Does evolution require naturally arising information that never previously existed in the genome? You have tried to say evolution can’t occur because, 1/ can’t occur. If this were actually a physical restraint, you would have a point,

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Apparently you are a theistic evolutionist?

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but since scenario 2/ CAN be true, evolution is safe from information theory.

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Evolution is not safe from info theory because nobody believes evolution has produced life exclusively by using pre-existing genes and rearranging them. If you want to believe this, fine. But observable evidence has already falsified this notion.

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Address the scenarios I mentioned, and I will address yours.

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See post to Quetzal. I'm not interested in wasting time.You made a specific claim. I agreed it would be an example of increased genetic information. Having problems finding your hypothetical example? Why then did you bring it up? All you did was make my case for me. If evolution were true you should be able to produce a myriad of examples, yet you can't produce one.Bye bye evolution. It's a fairytale.

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I believe this tactic is called moving the goal posts. In your original example, you didn’t say anything about benefiting the population as a wholeNow your story is changing such that the allele has to benefit the population as a whole.

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You’re wrong. I have consistently qualified that the benefit must be population- wide. Start here:http://EvC Forum: Give your one best shot - against evolution -->EvC Forum: Give your one best shot - against evolution

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Fred: If the cheetah lost a net sum of ONE useful allele from the parent population then it is patently obvious that its gene pool has LESS genetic information than the parent species. Do you agree or disagree with this?

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Remember, we are not talking about loss of an entire gene to qualify as a loss,

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In this example I was referring to the loss of an allele (gene version) from the entire post-bottleneck cheetah population. However, note that even when a single individual acquires a *new* inheritable deleterious mutation at meiosis, technically the gene pool has lost information, albeit an extremely small loss due to the existence at that loci of all those genes in the population without the mutation. You cannot claim the reciprocal unless the new mutation is beneficial to the population as a whole. This is an important distinction to make. If a superficial mutation such as sickle-cell or Mark’s nylon mutation is not an improvement over the wild type as a whole, then you can’t claim it added information to the gene pool. If anyone here wants to again try to claim sickle-cell is an information gain, please find a single information scientist to agree with you.

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Originally posted by Quetzal:
Fred:

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Quick correction - My response to Moose was intended to imply that there was no correlation between loss of genetic variability in a population and loss of some undefined "information" at the population level. See my post #139 on this thread for why I think the concept is misleading at best - and why your question probably can't be answered, even using your definition. Hope that clarifies what I "think", "imply", "suspect" or any other attribution to me you'd care to make.

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As far as what I "suspect" Mammuthus meant (and I could be wrong), I think he meant that since the population is still extant - IOW there are still cheetahs living in the wild - they can't be considered (in the context of PB's particular assertion), to be "poor". OTOH, I don't think he is implying that they aren't in trouble. However, ASSUMING no new environmental pressures are brought to bear that further degrade their marginal fitness, and ASSUMING they survive in the wild at all, I think he's saying that there's nothing preventing the cheetahs from evolving (or "improving" if you like) like any other species.

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IMO, for what it's worth, I think cheetahs may have already passed the point of no return in a conservation sense, and are more than likely doomed. But that's just my opinion based on what I've read on them concerning infertility, infant mortality, disease susceptibility, continuing habitat degradation/restriction, etc, and has nothing to do with whether or not they DO actually survive - or even thrive. There are enough relictual populations of various organisms running around today that by all rights should have been a historical footnote long ago to make these kinds of predictions pretty speculative.

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Good post. I agree cheetahs may be in error catastrophe, but genomes have proven to be amazingly resilient (due to an incredible design, of course! ) I'll have to search for a paper (I think it's at home), that provides an excellent example of a bottlenecked organism that showed reslience far beyond what was expected; that is, it could not be explained via NDT.BTW, my question can be answered, as I indicated to Page. I'm still waiting for his "example".

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what's the matter Fred, fail out of grad school so your angry at the world

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Actually, I never went to grad school because of all things I wanted to play in a band (which I did for 17 years, then I grew up ). After graduating at 21 years of age with a BSEE (from Univ Missouri-Rolla), I decided that in order to support the expensive hobby of keyboardist, I figured getting a job was a better option than becoming a full-time student! Some people like to go make money and have fun in other ways than staying in school.

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FW:
Even if I totally caved and said I don’t believe non-random mutations occur, your point would still be either bogus or a strawman! M: LOL! duck and bob..duck and bob.....your error was to support non-random mutations and now you have to backpedal by all means possible out of supporting your claims..LOL!

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Baloney. I have not caved on anything, I merely point out that even if I did cave, it doesn’t help your argument on iota. I could admit to martians creating non-random genome or to a flat earth influence on the genome, and your argument would *still* be bogus.

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M: Ah and distortions from Fred..what a surprise...I did not say Monkenstick's post is evidence against non-random mutation There IS NO evidence for non-random mutation. Monkenstick provided evidence FOR random mutation

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Good, now that we got possibility #1 out of the way, this leaves us with possibility #2: a strawman. As I said before, and you seem to be the only one here who doesn’t understand this, your argument is a classic strawman since Peter and I never questioned the existence of random mutations.[This message has been edited by Fred Williams, 11-08-2002]

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Do you accept that the nyl c thymine addition in flavobacterium allowing nylon "digestion", represents information that didn't exist in the previous generation (that never had the extra thymine)? If not, why?

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I have explained this a million times (OK, maybe only 945,657 times). Its either no gain or a loss. Evidence suggests the mutation may be via plasmid xfer. This means no net gain of information in the gene pool. This evidence is not conclusive however, but it doesn’t matter. If it wasn’t due to plasmid xfer, then we have to consider the fact that the new enzyme is no longer specific to its original substrate, which Dr Lee Spetner in ‘Not by Chance’ shows in detail why this type of mutation invariably constitutes a loss of information.I then offered these additional observations:Note that state 0 = pre-framshift, and state 1 = framshift:
1) To keep things simple, let’s assume the change is binary. So there are two states, 0 and 1. The default, or normal setting is 0, which codes for carbohydrate digestion. Setting 1 codes for nylon. In order for there to be new, or increased information, the original state 0 would have to be the unfavorable state. But it is clear that 0 is the favorable state (in general), and the study confirms that this method is a whopping 98% more efficient. So based on this knowledge, we actually lose information when we go from 0 to 1.
2) Was the mutation random? If so, then from 1) above we can again reasonably conclude that a loss of information occurred. What if the mutation was non-random, that is, environmentally induced? This means there was no net gain or loss of information because the information was already present. I haven’t studied the study you provided in-depth, but from the website you posted my bet is this is a non-random mutation. The author states that it’s been observed more than once. What an un-whitting admission he is making here! Given the odds that this specific mutation would be observable more than once certainly raises eyebrows that this may not be a random event. Another reasonable possibility is that certain portions (hot-spots) of the genome have been pre-programmed for hypermutation during environmental stress to toggle bits in an effort to find a possible combination that improves survival in the degraded environment.

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Remembering that you define new information (for genomic purposes, at least) as "the presence of a new algorithm (coding sequence) in the genome that codes for a new useful feature. The algorithm that codes for the nylon digestion is different, & didn't exist in the previous generation, so it makes perfect sense that this gene represents information that didn't previously exist, AND it represents a "new useful feature".

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See #1 above. I again ask, is it a benefit to the organism population as a whole? Clearly it is not. It is a downgrade. It’s like getting sickle-cell. Sure, its just wonderful to be hereozygous if you are exposed to malaria. Wonderful! If it was my choice I would opt not to have the sickle-cell mutation and take my chances with malaria (or get the hell out of there!). Mark, we are beating a dead cheetah. We are repeating ourselves. Unless you have something new to offer, why continue pursuing this? It is OK now and then to agree to disagree and move on. Your nylon-consuming bacteria was a valiant try, it was interesting, but it clearly comes up short.Maybe Scott is ready to shatter the world with the example he implies he has in his hand. Let’s see if he plays the card, or keeps us all in suspense!

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Fred: For example, we know the cheetah has a deteriorated immune system and it is likely it has lost some gene segments...

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M: And your evidence of specific gene losses in the immune system of cheetah' much less any other species?

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I ran across this:http://bowen1.home.mindspring.com/mchs/articles/lorimer.htmNote I said "likely", not "proven".

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What example? Oh yes - an example of a gene duplication and subsequent mutation that conferred a benefit to the population. The series of gene duplications in what we now call the beta globin gene cluster, a group of 5 genes and a pseudogene. Epsilon-globin,

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MEGAROTFL! I must say you are consistent! Perhaps you should let me write your posts for you, I know what you are going to say before you say it!Following is an important question for Scott to answer for the audience.Scott, please tell the audience when you believe this duplication + subsequent mutation event occurred? Thanks!(BTW, your fallacious reasoning, globin and all, was also committed by Richard Dawkins)(Helpful clue for Scott can be found here: Page not found - Nizkor)(I’m swamped, but will try to get to FK’s strawman and other replies tomorrow)

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a gain in function of nylon digestion IS POSSIBLE.

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As I have said over and over again, a gain in function is not necessarily a gain in information. It may be, it may not be. In the case of nylon, since fixing the mutation in the population would be a clear degradation to the organism, it’s a loss of information. You can shout from the mountain tops about your nylon munching bacteria as long as you want, but it won’t change reality.You are on a road to nowhere, the information-less abyss. Scott on the other hand provided a hypothetical example of what I have said all along would constitute a gain in information by most info scientist standards (a substantial improvement over his tree rings = code goofiness). Too bad though that Scott was engaging in his characteristic begging the question fallacy. Anyway, here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO. I’ve spotted you the BING. Just go find the O!

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I am just presenting a scenario that is possible.

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In science, if something is observed countless times over throughout time with no observed exceptions, it qualifies as a Law of Nature. It also means it is justified to declare the opposite is impossible. It is impossible to let go of a rock off a building and not have it drop to the earth. It is also impossible for new information to be created naturalistically.If you guys can produce evidence in the lab of something similar to Scott’s fantasy, then you would have found ONE example of new info in the genome. But you can’t even produce ONE example, despite countless experiments on various rapidly reproducing species. This is a bad sign for evolution. It means evolution of new complex organs and features is impossible.Yet another bad day for evolution.

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FK: That’s one of the silliest assertions I have ever heard. You are making no sense at all. Let’s walk through this. If a single individual is born with a *new* inheritable deleterious mutation, then your assertion is that the gene pool has lost information, despite the fact that the wild type is unaffected in the rest of the population. I guess then if that individual dies without leaving offspring, the population gained the information back? If a horribly mutated individual is born, survives a few minutes, and then dies, was there a loss and then subsequent gain of information when the individual died?

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Technically, yes, albeit incredibly miniscule. Do you have a problem with this?

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FK: On the other hand, if an individual is born with a beneficial mutation, then it is not a gain unless it is beneficial to the population as a whole? What kind of logic is that?

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Sound logic!Sound logic has a way of evaporating strawmen, such as your recent installment here. I never said restored information is not a net gain from the prior state. What I am asking you guys for is *new* information in the genome, such as a new algorithm for sonar, or an algorithm for the avian respiratory system, the origination of feathers, etc, etc.

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To make sure I am clear on your definitions, do you consider sickle-cell to be a loss of information?

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Of course I do!

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Would you accept the opinion of Tom Schneider on the matter? If not, why not?

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On sickle-cell? I don’t need to accept it, he already agrees it’s a loss of information.I have discussed info science with Tom several times in the past. He obviously believes info can increase, because evolution demands it. So he labored putting together a paper explaining how it could happen. The problem is, he only used Shannon statistical probabilities, and he had to jump through hoops just to make it happen (or appear to happen).It was another bad day for evolution! BTW, DR Royal has a good refutation of Schnieder here:http://www.trueorigins.org/schneider.aspPS. I respect Schnieder’s use of Shannon info theory in his work to define and identify binding sites. I hope he stays focused on this instead of wasting time delving into the fantasy world of evolution.

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Originally posted by Itzpapalotl:

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here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO.

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How about this:

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L. Chen, A. L. DeVries, and C. H. Cheng. Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish. Proc.Natl.Acad.Sci.U.S.A 94 (8):3811-3816, 1997.

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Trypsinogen duplicated (clear molecular relics of origin) then mutated to give new benefit (resistance to freezing) to the population of these antarctic fish.

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You might also want to read: M. Long. Evolution of novel genes. Curr.Opin.Genet.Dev. 11 (6):673-680, 2001.

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LOL! Come on guys, you're killing me! Itzpapa, please tell us when this event was observed in the lab. Tanks a bunch!It looks like you missed my helpful hint to Scott:Page not found - NizkorWhat is ironic about your citation is that it is actually evidence for adaptive mutation. Of course the NDT die-hards will dismiss this!"New research shows that fish in the Antarctic and Arctic oceans, at opposite ends of the earth, independently evolved nearly identical antifreeze glycoproteins."

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Gene duplications - even without subsequent mutation - can alter function and phenotype. How does that fit your precious "information theory"? According to other creationist information hawks, duplicating genes does not increase information. And when I have asked them the same questions, they clam up, too.

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Yea, right. O’le Scott shut ‘em up! The truth is, this is a no-brainer. For your answer, why don’t you ask Tom Schnieder if he thinks gene duplications alone represent increased information.

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By the way - if tree rings are not 'coded information', what are they?

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Do you know what a code is? Can you speak tree?

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So is observing something in a lab your new criterion for scientiific validity?

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Most evo here realize I’ve been asking for observed examples. Giving me examples of duplications that allegedly happened millions of years ago is begging the question.We have done countless experiments in the lab over many years on organisms with rapid reproductive cycles, yet we cannot find ONE single example of increased genetic information. If evolution is true, we should be able to produce literally millions of examples. But you guys can’t even produce ONE.

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So, as is a common creationist tactic, you have set up an impossible 'challenge.'

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No, what is a common evolutionist tactic is to handwave away what should be a common observation. IT is hardly an impossible ‘challenge’.

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Apparently, you want something to occur meeting the above criteria in 'real time.' Informed and rational creationists know that this is an unrealistic and therefore fallacious challenge.

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Which creationists are those?

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You can continue to ignore the reality of what experiments have been done as you have persistently done on this board or you can actually learn about the subject and actually adopt an alternative to your ignorance is bliss tactic.
Proc Natl Acad Sci U S A 2001 Sep 25;98(20):11388-93 Related Articles, Links
Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli.
Remold SK, Lenski RE.

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I looked at this paper, and this is hardly an example of new genetic information. It is pretty much no different than Mark’s nylon muncher. Here’s an important passage from your citation (emphasis mine):First, the resource dependence could be caused by recent adaptation in response to the 10,000 generations of selection in minimal glucose medium. During this period of adaptation, fitness increased rapidly for the first 2,000 generations but more slowly thereafter (20). This fitness trajectory suggests that the population is nearing a fitness peak in glucose. Theoretically, the closer a genotype is to the peak, the smaller the number of possible mutations that can be beneficial (36). Moreover, in the absence of selection for performance on maltose, the progenitor may have lost fitness in the maltose environment, leaving more opportunities for improvement in maltose. As a result of both of these effects, more mutations should be beneficial in the un-selected maltose environment than in the glucose environment.What does this all mean? The parent population was near a fitness peak in the glucose environment; in the maltose environment it was in a valley, having lost fitness. The subsequent experiments with the mutant strains only showed selection moving the maltose bacteria back up the maltose peak. There is clearly no new genetic information here.Informed evolutionists who are aware of the information problem propose gene duplication followed by mutation as the mechanism of increasing information in the genome. Fine. Any observed examples? Scott tried "begging the question" by giving a hypoethetical, unobserved example that allegedly occurred millions of years ago, and then protested after his logic was exposed and declared it an impossible challenge. But if evolution is true, there should be plenty of observed examples of this in the literature. Why can’t you give me even one provocative example?Evolution, the "impossible dream".

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I was not saying you believed any specific gene had arisen through duplication just that you were aware of the large amount of research that indicates a high rate of nonsynonymous compared to synonymous mutations in duplicated genes (Kondrashov et al), something which Fred Williams claimed doesn't happen ("gene duplication followed by mutation").

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I never said "gene duplication followed by mutation" doesn't happen. What I did say is that there are no observed examples of "gene duplication followed by mutation" that represent an increase in genetic information. Observed examples often show loss of information since they are associated with some disease.The only examples given for new, useful genetic information for a species (see Page, Mamuthus) are speculative events that allegedly happened millions of years ago. In other words, there is no evidence for increased genetic information - it's all speculation.