Favorable Mutations? Help me!!

Itzpapalotl, none of your citations provided even a hint that the mutatated type is more viable than the wild type in a normal envirnonment. For example:

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"Such different evolutionary patterns may be largely due to different functional constraints on the two copies."

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Just becuase one copy is resistant to change compared to the other does not demonstrate that the net effect is positive for the organism in the parent population in a normal environment.

Actually evidence of positive selection does prove the mutated type is more viable than the ancestoral genotype in the environment that it is currently in. That's the whole point of selective neutrality tests.You are right that different functional constraints do not demonstrate a positive effect, neverless there is good evidence that many genes have evolved by duplication that now play essential roles in organisms, which i would argue is a positive effect. Interestingly relaxed functional constraint is what Susumu Ohno suggested as the cause of new function evolution after gene duplication."Moreover, we found some evidence for the action of positive selection on cis-regulatory motifs after gene duplication. These results suggest that the evolution of functional novelty has a substantial role in yeast duplicate gene evolution."

Mr Williams: any comment on posts 11 and 15 of this thread?

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Actually evidence of positive selection does prove the mutated type is more viable than the ancestoral genotype in the environment that it is currently in.

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But that isn’t what I asked. I agree that mutations can have a positive effect on populations in stress environments. This is very well established. What I am asking for is evidence for positive selection where the mutated type is more viable than the parent type in a normal environment. I’ve only seen a handful of examples, and none of them were provocative. The problem is that there should be scores of examples, millions, if evolution is true. We don’t have the evidence; we get essentially a big goose egg. Conclusion? Molecules-to-man evolution has been falsified, or is unfalsifiable, take your pick!

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Most people with hemoglobin C never know it - some have mild anemia, gallstones, or spleen problems.

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ROTFL! Need I say more? Evolution at its finest, folks! Let’s take a poll. How many here wish they would evolve the hemoglobin C type? Come on, don’t be shy!OK, I’ll make this a little easier. Who here will say with a straight face that if given the choice, they would choose to have either Hemoglobin C or sickle-cell if forced to live the rest of your lives in West Africa?

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Is West Africa, with its high incidence of malaria, a "normal environment?"

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NO!Did anyone see Caddyshack? Was the swimming pool with the Baby Ruth in it a normal environment? (pretend the Baby Ruth was the real thing).

Better poll: How many people in West Africa, where the gene is concentrated and malaria is high, would want the hemoglobin C in order to have a better chance of seeing their 16th birthday?Possible spleen and gall bladder problems are nothing compared to contracting malaria.

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Who here will say with a straight face that if given the choice, they would choose to have either Hemoglobin C or sickle-cell if forced to live the rest of your lives in West Africa?

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Me. You see, Fred, unlike you, I'm not too into this whole "dying a horrible death" thing. Perhaps you are.And, BTW, most people in West Africa, even in modern times, do not leave West Africa. Did any country, say, in the middle ages, suddenly have a boatload of west africans show up for a day cruise? The reality is, this is where they have lived throughout most of their existence. This is also where malaria has thrived through its existence. For these people, it might as well cover the whole world - because *their* whole world - their niche - is at high risk of death by malaria. Even in modern times with mosquito controls, 300-500 million people become ill with malaria every year (thankfully, we have brought the death rate down to only a few percent, when before if you caught malaria, odds are you were going to die).Just so you know, when you contract malaria, first there's an incubation period. Then you develop the "cold stage". You shake, and often vomit and have a severe headache. Then you develop the hot stage. You begin to get exhausted and anemic. The sweating stage then takes over. Eventually, the brain and kidneys start to suffer failures and become damaged, leading to coma and death.Please tell me that *you* would rather live in a malaria risk zone (before the advent of modern medicine and controls, which haven't been around for even a tiny fraction of evolutionary history) than have a small chance at getting mild anemia or spleen problems. With a straight face.------------------
"Illuminant light,
illuminate me."

What is a "normal environment"? Has there even been a stable environment in the last 20Ky?Are the bacteria in this study in a normal or abnormal environment?Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11388-93. Related Articles, LinksContribution of individual random mutations to genotype-by-environment interactions in Escherichia coli.Remold SK, Lenski RE.Center for Microbial Ecology, Michigan State University, East Lansing, MI 48824, USA. remold@msu.eduNumerous studies have shown genotype-by-environment (GxE) interactions for traits related to organismal fitness. However, the genetic architecture of the interaction is usually unknown because these studies used genotypes that differ from one another by many unknown mutations. These mutations were also present as standing variation in populations and hence had been subject to prior selection. Based on such studies, it is therefore impossible to say what fraction of new, random mutations contributes to GxE interactions. In this study, we measured the fitness in four environments of 26 genotypes of Escherichia coli, each containing a single random insertion mutation. Fitness was measured relative to their common progenitor, which had evolved on glucose at 37 degrees C for the preceding 10,000 generations. The four assay environments differed in limiting resource and temperature (glucose, 28 degrees C; maltose, 28 degrees C; glucose, 37 degrees C; and maltose, 37 degrees C). A highly significant interaction between mutation and resource was found. In contrast, there was no interaction involving temperature. The resource interaction reflected much higher among mutation variation for fitness in maltose than in glucose. At least 11 mutations (42%) contributed to this GxE interaction through their differential fitness effects across resources. Beneficial mutations are generally thought to be rare but, surprisingly, at least three mutations (12%) significantly improved fitness in maltose, a resource novel to the progenitor. More generally, our findings demonstrate that GxE interactions can be quite common, even for genotypes that differ by only one mutation and in environments differing by only a single factor.

And just where is there a "normal environment" on this planet, then? Luxembourg? Itta Bena, Mississippi? What makes West Africa "abnormal?"

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But that isn’t what I asked. I agree that mutations can have a positive effect on populations in stress environments. This is very well established. What I am asking for is evidence for positive selection where the mutated type is more viable than the parent type in a normal environment.

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Could you list some "normal environments"? Something naturally occurring, please. I'm having great difficulty in thinking of any naturally occurring environments where populations of organisms aren't limited by disease, limited resources or predation. What environments aren't stressed?

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The problem is that there should be scores of examples, millions, if evolution is true. We don’t have the evidence; we get essentially a big goose egg. Conclusion? Molecules-to-man evolution has been falsified, or is unfalsifiable, take your pick!

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Why? Why should there be millions of poorly adapted organisms sitting around, if they have high enough mutation rates for us to observe the beneficial mutations in the few decades we've been looking? Why wouldn't the the vast majority of mutations have already occurred long before?------------------

"The pertinent question to ask is, what evidence exists where the mutated type is more viable than the parent type in a normal environment?" There's hope after all! "Does the nylon example qualify? A quick read of the link and you will see it doesn’t. A huge cost is incurred in efficiency, and thus in a normal environment the mutated strain could not last long (AiG also argues plasmid xfer, but the enzyme effeciency loss alone in the article cited by zephyr is sufficient to dismiss mr. nylon as a hero of the evolutionary faith). Does sickle-cell qualify? Of course not." Of course not! But that part isn't advertised since it doesn't help the 'cause'.I really can’t believe the number of evolutionists who use a DISEASE as evidence of evolution!!! Their choices are few and far between so they gotta go with what they have. It's sort'a like when they're asked for evidence of a 'transitional fossil'. Archaeopteryx has been used so many times that the blasted thing doesn't have any feathers left ... it's been plucked clean! (heheh)

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Joralex[This message has been edited by Joralex, 09-26-2003]

This is a bit of a misnomer. The loss in effeciency comes about when comparing the effeciency of the glycocytic enzymes and the effeciency of the nylonase enzyme. The activity of the nylon enzyme is only 2% that of the glycolytic enzymes which is what you would expect given the amount of time that both enzymes have been subjected to natural selection. Read post 23 in this topic to find examples of enzymes increasing in effeciency due to mutation. Also, nylon as a primary food source was a "normal" environment for the mutant bugs. That's why they were cultured, because bacteria were found growing in an environment they had never been found in before. Do you think mutations that allow an organism to fill and empty niche is a bad thing for the organism? No competition is a very good think IMO. Actually, parasitism (like malaria) is a very strong selective force. Those that can resist the parasite will have more children than those who can not survive the infection. Makes sense to me that evolutionists use it. It's really not that much different than predation, just on a microscopic scale.

Mr Williams: Give me a example or two of "normal environments," and explain, please, without references to Caddyshack, why Burkina Faso is not one.

Name a type of mutation that you want an example of. Nylon is an example of a mutation allowing an organism to use a previously unexploited foodsource. Apparently you don't think that's worth anything. Fine. What type of mutation would *you* consider beneficial? Increase in efficiency in an enzyme? Anything?Name one thing that you could consider beneficial.------------------
"Illuminant light,
illuminate me."

Actually, I will post an example here of beneficial mutations that do not incur a cost or cause a disease yet are fixed or go to high frequency in a bacterial population over timeMicrobiology. 2001 Apr;147(Pt 4):995-1006. Related Articles, LinksRapid phenotypic change and diversification of a soil bacterium during 1000 generations of experimental evolution.Riley MS, Cooper VS, Lenski RE, Forney LJ, Marsh TL.Center for Microbial Ecology, Michigan State University, East Lansing, MI 48824, USA.Evolutionary pathways open to even relatively simple organisms, such as bacteria, may lead to complex and unpredictable phenotypic changes, both adaptive and non-adaptive. The evolutionary pathways taken by 18 populations of Ralstonia strain TFD41 while they evolved in defined environments for 1000 generations were examined. Twelve populations evolved in liquid media, while six others evolved on agar surfaces. Phenotypic analyses of these derived populations identified some changes that were consistent across all populations and others that differed among them. The evolved populations all exhibited morphological changes in their cell envelopes, including reductions of the capsule in each population and reduced prostheca-like surface structures in most populations. Mean cell length increased in most populations (in one case by more than fourfold), although a few populations evolved shorter cells. Carbon utilization profiles were variable among the evolved populations, but two distinct patterns were correlated with genetic markers introduced at the outset of the experiment. Fatty acid methyl ester composition was less variable across populations, but distinct patterns were correlated with the two physical environments. All 18 populations evolved greatly increased sensitivity to bile salts, and all but one had increased adhesion to sand; both patterns consistent with changes in the outer envelope. This phenotypic diversity contrasts with the fairly uniform increases in competitive fitness observed in all populations. This diversity may represent a set of equally probable adaptive solutions to the selective environment; it may also arise from the chance fixation of non-adaptive mutations that hitchhiked with a more limited set of beneficial mutations.and another oneProc Natl Acad Sci U S A. 1999 Mar 30;96(7):3807-12. Related Articles, LinksGenomic evolution during a 10,000-generation experiment with bacteria.Papadopoulos D, Schneider D, Meier-Eiss J, Arber W, Lenski RE, Blot M.Abteilung Mikrobiologie, Biozentrum, CH-4056 Basel, Switzerland.Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.