Are mutations truly random or are they guided?

When you asked the question, look at some of the early replies you got. People saying that random mutations are just a small part of evolution, and others saying well there is plenty of evidence for it if you just give yourself an education.Well, random mutations aren't a small part of the Theory of Evolution, because without them no evolution takes place, and there isn't plenty of evidence for random mutations causing full scale changes in organisms, because they can't identify a single one. Its part of the common shell game they play here, and I was not trying to derail your thread, I am just pointing this out and trying to curtail the obfuscation. I think it would be great to get rid of the people who say the same two things all the time (1. they are not important anyway, its natural selection's magic that does the changes, and 2. well, there is plenty of evidence, i am just not going to provide any). So far that's all you have got in responses in a nutshell. it is as frustrating to me as perhaps it is to you.I am still waiting for someone to actually discuss your question. Show how they know random mutations guides any evolutionary process that equates to higher complexity. I have seen so many attempts here on this forum to force them to provide better evidence, and the attempts are futile-because of exactly what you are seeing here. Attacks calling people dumb creationists even when that is never brought up, people saying well what is your theory then, can you think of something better, and people complaining that you can't prove your magical God poofed it theory either, so why should we have to prove ours.....and on and on.The fact is they won't address this because they can't. they can't show it in nature, and they can't even show it in a lab. It is a story. Some choose to believe it and some don't.I, like you see plenty examples of animals adapting to their environment. They don't wait for random mutations to change them, they have mechanisms that give them ways to change when it is needed-even if we can't explain what that mechanism is. People in high altitudes develop better lungs. People who climb mountains develop different muscles in their legs. People who live in cold environments have different blood platelets. Put people in the sun and they get darker, put them in the cold and they get lighter. And on and on and on the world goes. we don't have ANY evidence at all that any of this takes places because of random mutations-and yet we are forced to believe its the way-because well the Theory of Evolution is a fact-so if you can't prove it just create a scenario that sounds plausible. " It takes time, you can't see it happening, we are working on it...etc. "And here we also see another favorite diversion-people trying to discuss bacteria resistance and relate that to a ToE which claims that all changes happen this way. Well, a bacteria resistance isn't changing the bacteria, other than making it resistant. Its not making a new kind of bacteria, its not leading to a new type of organism, its simple one small part of all the defense mechanisms we see in nature. Usually once the pathogen that it is developing resistance is removed, the resistance simply disappears. the bacteria is simply still bacteria. So it proves nothing about how life could develop and become more complex.If you are going to say that eyes and ears and breathing and sweating, and copulating, and the entire network of information within a tightly controlled environment of the cell all came about through random mutations-I think you should do better than bacteria resistance to a threat.To me their argument is an argument of incredulity. They can not possibly imagine any other way that it could be-so even if they can't prove it, it still must be this way-and no other way is worth considering, because we don't see how it could be. That is not science, that is faith-their faith. They have no imagination that their might be ways of adapting (a type of neo_Lamarckism as you say) that we simply don't understand yet.But that is absolutely all you are going to get here, along with the requisite insults to creationists, and all the other diversions. If you say what it is you believe, they will pull out the "Lamarck has been proven wrong" card. If you question their dogma they will throw out the "go read a biology book card". Science has proven it over and over they say. Still without addressing your question.So I am with you-SHOW US THE EVIDENCE! I have asked for them to give examples in nature. Bacteria resistance is not an answer to life's complexities. How do complex systems begin if they start from random mutations? What kind of random mutations begin a complex new life system. How do they know they are random and not guided?Answers-NO. Insults-Plenty. Diversions-Plenty. Moderation on the insults-None.I have seen enough people try here-and they get nowhere. I am still waiting for an answer. Good luck.

Hi Balder-dash, still struggling with reality?Note for herebedragons -- see ps at end By random mutation and genetic drift.
By random mutation and natural selection.Evolution is the change in the proportion of hereditary traits in a breeding population from generation to generation in response to the opportunities of their ecology.One of your problems is that you assume that your belief that evolution is wrong is true, and therefore that there cannot be evidence for anything based on evolution. Unfortunately, for you, starting with false assumptions leads to false conclusions.You assumed that this evidence cannot be readily found.Coyote gave you a link to a list of such experiments, but it appears that you have ignored it (or found it too dangerous to read?)With google scholar {"random mutation" evolution} returns some 8,100 hits of journal articles about these two items.One example comes from Coyote's link: https://myxo.css.msu.edu/ecoli/Interesting study, over 20 years of accumulated evolution from a single source, shows a random beneficial mutation arising in one population that is based on a previous neutral mutation.https://myxo.css.msu.edu/ecoli/overview.html

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The inexorable rhythm of the project is as follows:
1. Every day, the cultures are propagated;
2. Every 75 days (500 generations), mixed-population samples are frozen away; and
3. Mean fitness, relative to the ancestor, is estimated using the mixed-population samples.

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Pretty boring stuff eh?https://myxo.css.msu.edu/...ate2008/citrateflasksphotos.html

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Photograph of the long-term evolution experiment taken on 25 June 2008. Each flask harbors one of the 12 evolving populations. The photo was taken about 24 h after the cultures were serially transferred, hence they are at stationary phase. The populations grow in DM25 medium, which contains a relatively low glucose concentration so that the culture is not very turbid. However, one population, designated Ara-3, evolved to use the citrate that is also present in the medium. It has a much greater density of cells than the others, and it is therefore much more turbid, owing to the high concentration of citrate in the medium. (Below) A close-up view showing the Ara-3 population and two others. [Photos courtesy of Brian Baer and Neerja Hajela.]

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Random mutation leads to new ability to use an additional source of nutrition, and this leads to increased growth and reproduction of the cells with the citrate mutation.There's more, here's the peer reviewed journal published article abstract:Just a moment...

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Abstract
The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit+) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. The long-delayed and unique evolution of this function might indicate the involvement of some extremely rare mutation. Alternately, it may involve an ordinary mutation, but one whose physical occurrence or phenotypic expression is contingent on prior mutations in that population. We tested these hypotheses in experiments that replayed evolution from different points in that population's history. We observed no Cit+ mutants among 8.4 1012 ancestral cells, nor among 9 1012 cells from 60 clones sampled in the first 15,000 generations. However, we observed a significantly greater tendency for later clones to evolve Cit+, indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit+ but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection.

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In other words, a neutral mutation arose somewhere between 15,000 and 20,000 generations that was needed as a scaffold for the later beneficial mutation.That's not all:https://myxo.css.msu.edu/ecoli/genomicsdat.html

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Genome sequence of the ancestral strain, REL606, a derivative of E. coli B:
• Complete REL606 genome sequence deposited in GenBank
• First 2009 J Mol Bio paper describing historical derivation of E. coli B
• Second 2009 J Mol Bio paper presenting genome sequence of REL606
• Third 2009 J Mol Bio paper comparing genome sequences of REL606, another B derivative, and E. coli K-12

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They have sequenced the DNA so they can determine where the mutations are for the neutral mutation building block and for the citrate metabolizing mutation.Random mutation and genetic drift -- allows a neutral mutation to propagate in the population.Random mutation and natural selection -- once a beneficial mutation occurs, here for citrate metabolizing, natural selection applies, and the cells with the beneficial mutation grow and reproduce at a much faster rate than the cells without the mutation, leading to a dominant population of cells with the mutation.Evolution -- the change in the proportion of hereditary traits in a breeding population from generation to generation in response to the opportunities of their ecology. There were other results of the study as well, one that showed slowing rates of adaptive mutations being fixed in the populations as they became more adapted to the ecology, then shifting to an increasing rates of neutral mutations as the ecology becomes more limiting to population growth from lack of nutritional resources for additional cells. It was one of these later neutral mutations that led to the rise of the beneficial mutation.This shows the effect of random mutation and natural selection in a population with a dwindling resource/individual ecology, and the stress response to increase the rate of mutation when resources become limiting. Higher mutation rate leads to more neutral mutations and this leads to more opportunity for a beneficial mutation to arise.Evolution is the change in the proportion of hereditary traits in a breeding population from generation to generation in response to the opportunities of their ecology. This is typical of other studies involving mutations and their effect on evolution: they show evolution occurring, that the proportion of hereditary traits in breeding populations from generation to generation changes in response to the opportunities provided by their ecology. So we see that "whenever an experiment is done to test the theory (the real one used by scientists), they end up with results that show that indeed evolution occurs and documents precisely the effects of evolution on the results" is not a "wild claim" but one based on a cornucopia of evidence.You can, of course, actually attempt to falsify the claim by providing an example of an experiment run to test the theory of evolution that does not show that evolution occurs. Good luck with that. Given your response to Coyote's post, however, I expect you to continue to bluster and whine instead of actually doing anything. Yes, everyone knows how much creationists like to be made into beleaguered martyrs, so we let them rattle on post after post regurgitating their institutionalized ignorance before asking them to behave like everyone else, and abide by the rules that everyone else abides by.You poor little thing, being treated as an equal, instead of some awesome superior, must be quite a blow to the dominus ego eh? Such blatant heartless discrimination, oy, such a trial. Perhaps you have not seen evolutionists being cautioned to abide by the rules, because they already do, as a matter of intellectual honesty.Reality is like that.Enjoy.ps - for herebedragons, and the question of whether mutations are random or directed,Consider that if the mutations are directed in the instance cited above involving a neutral mutation followed by a beneficial mutation that allows the carriers to metabolize an additional nutrient, 11 of the 12 populations failed to be directed to do this, and in the one where this occurred it took over 15,000 generations to get around to the neutral mutation that enabled the beneficial mutation, and then another equally large number of generations to finally get to the goal mutation.Statistically unsupportable compared to random mutation.Edited by RAZD, : psEdited by RAZD, : ...

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Hi again, herebedragons, welcome to the rats nest. Yes Bolder-dash is a creationist, and yes, that is one of his favored modus operandi. Another is to repeatedly complain about just about anything. It seems that many creationists use troll tactics because they don't have any real arguments other that denial and misinformation. The result, whether intentional or not, is frequent derailment of topics so that the issues get muddied if anyone else tries to learn anything. One of the problems with discussing cell complexity is what we mean by "complexity." Another is using the product of over 3.5 billion years, rather than the minimum amount of complexity required for life. Of course we do not know how simple an organism can be and still be a viable life form, but there are some prokaryotic cells with very little DNA compared to multicellular life forms. This comes at the abiogenesis question from the other side.Likewise the "vast amount of information" in a modern cell is the product of 3.5 billion years of evolution, and does not constitute the minimum amount of information (and what is this "information"?) needed to form a living cell.When you talk about the ability of a cell to reproduce a whole multicellular organism - " all the tissues, organ and systems" - you are really talking about a large accumulation of "things that work" and the elimination of a lot of "things that don't work" so that the processes that go on inside a cell are not just simply biochemical reactions but the ones that work. Selection does this.Consider a cookbook: you don't need to know squat about chemistry and the way different products interact with the others, if you can read the recipe, measure the ingredients, and follow the correct cooking procedure you should get acceptable results. With a little variation in the ingredients you will get slightly different results, some better than others. Now annotate the recipe with what you did for the better results so you can replicate them next time. This is basically how the system works.Following this process you can make any item in the cookbook. You are, however, limited from making anything that is not in the cookbook, so now consider how recipes are added to the cookbook. Different combinations of ingredients are tried, some work, sort-of, some work well, and some are disasters. The disasters are discarded and the "works well" and "sort-of works" recipes are added. By this process we can get from no recipes to a book with some fabulously delicious recipes and also with some recipes that are less than stellar.The book has no intelligence, and it cannot tell whether one recipe is good or bad.Consider that a cell is continually making every recipe in its"cookbook", modifying the recipes when improvements are discovered among the variations caused by errors in measurement or following the cooking procedure. There is no intelligence in the cookbook, only the accumulated "information" acquired by billions of years of trial and error of "things that work", including the ones that "work well" and the ones that "works sort of". I'd be interested in those instances.Lamarckism - Wikipedia

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Forms of 'soft' or epigenetic inheritance within organisms have been suggested as neo-Lamarckian in nature by such scientists as Eva Jablonka and Marion J. Lamb. In addition to 'hard' or genetic inheritance, involving the duplication of genetic material and its segregation during meiosis, there are other hereditary elements that pass into the germ cells also. These include things like methylation patterns in DNA and chromatin marks, both of which regulate the activity of genes. These are considered "Lamarckian" in the sense that they are responsive to environmental stimuli and can differentially affect gene expression adaptively, with phenotypic results that can persist for many generations in certain organisms. Although the reality of epigenetic inheritance is not doubted (as countless experiments have validated it), its significance to the evolutionary process is uncertain. Most neo-Darwinians consider epigenetic inheritance mechanisms to be little more than a specialized form of phenotypic plasticity, with no potential to introduce evolutionary novelty into a species lineage.[16]

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This seems to be more of interest in the "evo-devo" field than in general biology\evolution.Lamarckism - Wikipedia

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While Lamarckism has been discredited as an evolutionary influence for larger lifeforms, some scientists controversially argue that it can be observed among microorganisms.[17] Whether such mutations are directed or not also remains a point of contention.

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In 1988, John Cairns at the Radcliffe Infirmary in Oxford, England, and a group of other scientists renewed the Lamarckian controversy (which by then had been a dead debate for many years).[18] The group took a mutated strain of E. coli that was unable to consume the sugar lactose and placed it in an environment where lactose was the only food source. They observed over time that mutations occurred within the colony at a rate that suggested the bacteria were overcoming their handicap by altering their own genes. Cairns, among others, dubbed the process adaptive mutation.

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If bacteria that had overcome their own inability to consume lactose passed on this "learned" trait to future generations, it could be argued as a form of Lamarckism; though Cairns later chose to distance himself from such a position.[19] More typically, it might be viewed as a form of ontogenic evolution.

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In microorganisms the details are confused by the possibility of horizontal gene transfer (or single cell sex), where a tidbit of DNA from one cell is injected into a neighbor cell. Thus a mutation in one cell that is beneficial can be spread to other neighboring cells rather than just to descendants.And, of course, any survival or reproductive benefit that is due to a learned behavior (meme), rather than to a hereditary trait, is a acquired trait that is passed to those that learn it. Learned behavior of the organism, though, is not part of what you are considering as going on inside the cell, is it?Enjoy.

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Well, why don't you?

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I have no time for lies and fantasy, and neither should you. Enjoy or die.
-John Lydon

Don't feed the trollish behaviorEdited by RAZD, : .

There is no doubt that there are stress induced mechanisms that increase mutation rates, but there is little or no evidence of the sort of specific targeting that Cairns' model hypothesised.With regard to Herebedragons problem with the availability of the primary literature, one big advantage in recent years to the lay person with an interest is the increasing availability of Open Access publications of high quality research such as PLOS and the BioMedCentral publications. Along with this many traditional journals are now making their articles Open Access after a given period of time.Two examples of open access material dealing with adaptive mutation are a review of various forms of stress induced mutatgenesis (Foster, 2007), and some recent primary research on how a specific form of stress can lead to adaptive mutations when one major element of one of the most common stress induced mutational pathways is knocked out (Stoebel et al., 2009).The Entrez database has a whole collection of searchable Open Access articles known as 'Pubmed Central'. So while access to any specifc article on a topic may be a problem there is certainly a good chance you will be able to find many papers on a topic available under some sort of Open Access.TTFN,WK

If you are having problems with discussion then the proper thread for making those complaints is Report discussion problems here: No.2.Instead of raising moderation issues in this thread, please follow rule 2 of the Forum Guidelines:

2. Please stay on topic for a thread. Open a new thread for new topics.

In this particular case there is no need to open a new thread since there is one already available for discussion issues: Report discussion problems here: No.2Please be specific and accurate in describing the problems. For example, I tried to track down who told you to go read a biology book in the thread, but the first occurrence of the phrase "biology book" is your Message 68.

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--	Percy
	EvC Forum Director

I have a better idea Percy.You can continue to blame all of the creationists for being the one's off topic, continue to allow all the sniping, silly one line posts about trolls and reading biology books, drive away all the people with dissenting opinions like you have already been so successful doing, hand out your little banning and suspension, and continue to allow the bantering and emptyness of the dr. A's and coyotes of the forum, and continue to turn your site into a dull, uninspiring soundboard for all of you evolutionists to brag about how right you all all the time.You asked why your site was better several years ago? You obviously should know the answer-you drove away all the opposing viewpoints. You are not looking for provocative discussion. You want to control what is said. I will argue with you elsewhere, not where you get to hand out your little principal detention slips to the ones you don't agree with.I wasn't the one off topic, I was the one asking for examples. You continue to prove me right. This is what i was warning the newcomers about. Enjoy the circle of pleasure you are advocating.Edited by Bolder-dash, : No reason given.

Because his faith is weak and he is afraid reality will crush it. Rather than acknowledge his god's work as he has revealed it to us in this universe the fool must deny his work to hold onto a cherished fantasy.He has nothing left to fight with in the way of fact or argument so he must rely on denial and bluster.Unfortunately we cannot expect anything better from such delusion.

You need to understand how biologists are approaching the problem. Biologists need an explanation for DIRECTIONAL change. They need an explanation as to why there are more changes in one area of genome than in another. They need to a way of determining which genes are involved in disease, and which are involved in divergent characteristics. The explanation for all of this is selection. No one is saying that the creation of variation is not important. Rather, selection explains the important observations. Several peer reviewed scientific articles have been cited by myself and others. Perhaps you should comment on those. No one is claiming that evolution is guided by random mutations. You are confusing phenotype plasticity with evolution. They are not the same thing. Evolution does not occur to one individual during it's lifetime. Evolution occurs at the level of the population over generations.Also, where are people with gills? Surely populations living along beaches need to be able to swim better, so where are there gills? Can you explain this?Next, can you tell us how achondroplastia (dwarfism) and hemophilia are adaptations? People are born with mutations causing these conditions, and that mutation is not found in either parent. So what niche are these people being guided to? Resistance comes about through random mutation, as I have already shown in the post above (see the plate replica experiment). These mutations occur in the ABSENCE of antibiotics, so this can not be a defense mechanism since there is nothing to defend against when these mutations occur. These bacteria did not exist before the experiment started, and they came about through mutation of their DNA. The scientific literature is loaded with examples of resistance coming about through mutation of DNA. This is exactly the type of evolution that you have asked for, and now you dismiss it.As for the argument "they are still bacteria", it's nothing more than a ploy on your part to lessen the impact of evidence that shoots holes in your argument. The common ancestor of humans and chimps was an ape, and humans and chimps are still apes, so I would guess that you have no problem with humans and chimps sharing a common ancestor, right? Humans and bears are both mammals, as was their common ancestor. Just mammals turning into mammals. No problem, right? Humans and fish are both vertebrates, as was their common ancestor. Just vertebrates turning into vertebrates. You have no problem with this, right? Humans and amoebas are both euakaryotes, as was their common ancestor. Just eukaryotes turning into eukaryotes. Surely you have no problem with this, right?Are you starting to get a sense of why the "they are still bacteria" canard is foolish? What you are playing is the famous "creationist name game". You somehow think that if you can call the parent and daughter species by the same name that evolution didn't occur. What you seem to ignore is that in experiments like the one above new bacteria emerge, bacteria that did not exist at the start of the experiment. This is evolution. It is descent with modification. We are saying that these things came about through random mutation AND selection. You should at least describe our argument correctly before criticizing. This is false. There are experiments that you can run to test whether or not random mutation and selection were responsible for the differences seen between species. One way is to compare the genomes of the two species and to find the ratio of synonymous to non-synonymous mutations (i.e. the ratio of mutations which do not change the amino acid sequence of proteins compared to those that do). What you should find, if random mutations and selection are true, is that the synonymous mutations outnumber the non-synonymous mutations. This is exactly what we see. Instead of whining why don't you focus on the science that has been presented. Why not? Compare the genomes of a simple and complex organism. The differences in DNA are the reason for the difference. Random mutations coupled with selection changes DNA in a way that increases fitness. We know that these mutations are random because of observations such as those in the Luria-Delbruck fluctuation experiment and the Lederbergs' plate replica experiment as I discussed above (and you ignored).

Just to expand on this . . .Cairn wasn't crazy for initially sticking his head out. In the classic lactose experiments these mutants did appear at rates that were inconsistent with known mutation rates. Guided mutations were certainly a possibility, and Cairn could have garnered quite the attention if he turned out to be right. However, further research indicated that the presence of lactose did not induce these mutations. Rather, DNA damage due to starvation induced these mutations through the upregulation of polymerases with lower fidelity (i.e. enzymes that produced more mistakes during replication) and enzymes that increased the rate of recombination. There is one trick that I use often. If you do a search on http://www.pubmed.com look for a small box on the right hand side towards the top. It will have a hyperlink for listing all of the free articles available for that search (e.g. "Free Full Text (17)"). I have found that this is really handy for doing initial research on a topic.

Hi Bolder-dash,I'm removing your posting permissions in this forum. If you'd like to discuss moderation issues, the proper venue is Report discussion problems here: No.2.

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--	Percy
	EvC Forum Director

After losing his posting permissions in this forum, Bolder-dash then went to the Report discussion problems here: No.2 thread and posted his response to this thread over there. He has now been suspended for 4 weeks.

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--	Percy
	EvC Forum Director

Yes, let's.I'll run over the major points. Point #1 : the mechanisms that you envisage do not exist. Yes, the cell is complicated, but scientists have given us a fairly good idea of what each bit of it does. We know what the ribosome does, we know what tRNA does, we know what aminoacyl tRNA synthetase does. Yes, the biological mechanisms are complicated, but biologists understand them. There is no mysterious mechanism left over which might do the thing that you envisage some cellular mechanism doing. Point #2 : the mechanisms that you envisage do not operate. If, for example, you expose bacteria to an antibiotic, then maybe one bacterium in a million will evolve resistance to that antibiotic. Now, if there was some smart mechanism for evolution hidden in the complexity of the cell, then they'd all do this. But they don't. It's a matter of dumb luck. Point #3 : The mechanisms that you envisage are unnecessary. Random variation plus selection does work. I referred you in my previous post to the success of genetic algorithms. I read recently that the boffins at Oak Ridge are using evolutionary methods to produce new designs of nuclear power plants. Are they crazy? No. It works. Random variation plus selection does solve problems. If you threw in your imaginary Lamarckist mechanisms, it might work faster. But boring old Darwinism works anyway. It's slow, but it gets there in the end. We don't need to postulate anything else to explain evolution --- it works just fine already.

"Hand waving", eh?Choose your words with more care. You wish to jump from the proposition that cells are complex to the existence of a cellular mechanism for which there is absolutely no evidence. That is hand-waving.Yes, cells are complicated. But that's no reason to suppose that they are capable of performing any particular complex task that you happen to dream up.