I’m not an expert in the feild of evolution, but I’ve read my fair share. To use the moths as an example, there would have been mutations of white moths having grey offspring all the time, but because the trees were white, these grey offspring were eaten rather quickly. when the trees started to change color, the mutations didn’t increase, the mutated offspring just survived better than their white counter-parts.
so, in answer to your question, no, the rate of mutation doesn’t (nesisarily) increase in the face of a changing environment, but the mutated offspring (might) survive better to pass on their mutated genes.
whether it’s gradual or punctuated, it’s still evolution
Phobos:
you’re right… now, I don’t know much about the whole thing, but perhaps Scylla meant to title this “Scylla strikes a blow against Natural Selection?”
“Scylla strikes a blow against the generally accepted and commonly understood aspect of evolution known as natural selection in specific circumstances pertaining to fruit flies and bacteria in instances of punctuated equilibrium,” just doesn’t have the same ring to it.
Scylla: Did the paper you referred to in the OP state that this was an example of a change in the genome? Or was it a hormonal change, as I postulated? If it was the latter, then unfortunately no blow has been struck 
Besides, the fruit-fly example shows changes under laboratory conditions; I don’t know how natural we can call the selection in that case (if, indeed, this is a change in actual mutation rates).
Mauve Dog:
From my OP:
“Hormones can effect gene expression, and the commonly accepted theory is that all fruit flies have the gene for cold-weather survival. A new generation will only express it if it’s needed. the parents experience codes for cold weather adaptation if it’s needed, and it’s expressed in the genome of their offspring (kind of, I don’t really understand so maybe somebody’ll help me out. I’m a finance guy not a geneticist, Dammit!)”
I think that says pretty clearly that the gene is assumed to already be there. Nobody thinks they evolve it in a single generation in response to cold.
My understanding was that neither was it natural selection. The fruit flies had an adaptation that turned on the cold-weather gene in their offspring, though they themselves did not adapt.
The whole point of the paragraph was not about fruit flies, but rather as an example that hormones can affect gene expresion, and that perhaps as exhibited in both fruit fly and bacterial populations mutation rates can be shown to dramatically increase versus control groups under certain circumstances, most notably environmental stress which is where one would expect new mutations to be needed. Instead of a few major mostly unviable mutations (which is what is expected,) we see a plethora of minor seemingly innocuous and random mutations. The new idea is that these mutations may combine synergistically in a very rapid and efficient manner to produce the specific adaptation necessary to overcome the environmental obstacle in question.
In other words, it seems that in some circumstances something in a population of organisms (seemingly deliberately)produces minor mutations in order to adapt when presented with change.
This idea is of course at odds with the slow random mutations theory by which evolution is beleived to work, but fits in quite well with the observed punctuated equilibrium model.
Thanks for the response, Scylla 
However, I don’t think that:
a) hormonal regulation of genes (or genetic regulation of hormones) is anything new (one can, for example, get three-toed horses and chickens with teeth by messing with hormones during development);
b) this counts as a mutation, per se. I guess it depends on what researchers choose to label a mutation. The genes themselves do not appear to be changing, merely their expression (differing phenotypes for a given genotype).
I guess the point that I am trying to get across here is that this (“hormones can affect gene expression”) is certainly an example of adaptation, but it does not seem to explain the pattern of speciation seen in the fossil record (which is what punctuated equilibrium is all about), since we are not seeing ‘true’ mutations. At least I think that’s my point…I’m not sure anymore…
Regarding Lamarkism:wasn’t there a biologist named Paul Kammerer (in Austria, ca 1920’s) who claimed to have illustrated Lamarkian changes of a species? As I recall his work was denounced as fraudulent, and he shot himself.
Did anybody critique his research?
A cold environment causing fruit flies to produce hormones that express genes for cold-hardiness has nothing to do w/ mutation, punc. e., etc.
Think of frogs–temperature affects whether the eggs laid turn out to be male or female. This has nothing to do with genetic mutation. Just a biological change instigated by environmental conditions. Yes, genes are involved, but so what? They’re involved with most everything.
Now that I finally understand what your post was about, I’m not sure why you posted it.
Your point is well taken Mauve-dog, but the implication of all this is that perhaps hormones can affect expression in sex-cells, maybe even affect mutation rate as well, directing an organism to evolve when it is needed.
This is significantly different from the accepted model of natural selection where the rate of mutations remains static, they are mostly unviable and overwhelmingly detrimental. Once in a blue moon a beneficial one occurs and natural selection implements it in the population.
Instead, environmental changes stimulate a variety of minor mutations initiated by the organism, of which the beneficial ones coalesce to provide a useful adaptation.
Well, then someone should run the DNA of the pre cold and post cold flies and see if there is any above normal mutation between the generations due to the hormonal shift as a result of the temperate change.
If yes, then Scylla is right.
Otherwise, the hormones are only expressing genes which are already there.
Or, the body simply adapts in a non-genetic way, much as I’ve adapted to typing on a keyboard.
The experiment seems to have been half-assed if the original researchers drew any conclusions without a follow-up DNA comparison.
Joel
I think I have an explanation. Mutations within a large population appear at a constant rate over a long period of time. Most of these genes remained dormant, not expressed, because the genetic diversity within the population is quite large and individuals mate with other individuals that are quite geneticly different. Some of these mutated genes are beneficial in the current environment and these will gradually spread throughout the population. Some of these mutated genes will be beneficial after some major environmental change. Because these genes are not beneficial now, they do not increase in number within the population.
Now comes the major envrionmental change.
The population dwindles in size and as a result becomes much less diverse. By chance, a large precentage of surviving individuals are carriers of the mutated new environment genes. After a few generations their offspring begin expressing these genes. They benefit from them and become more prolific. This whole episode may take centuries to occur but it may make it appear that millions of years of evolution happened within a short time frame. One might hypothesize that the genetic mutations all occured very quickly and the major climatic change caused the mutations. It is more likely that the change concentrated the mutations in a few individuals who had aquired the mutations before the change. This is called Genetic Drift. This is considered a primary means of evolution.
Organisms take great care in avoiding mutations, because most of them are bad for the organism. It is general rule that organisms will desire not to mutate. As usual there are exceptions. Smeghead gives one. However it is a mistake to generalize what a few baceria do to all organisms. Bateria often face rapidly changing environments, and need to evolve quickly. And within a bateria colony an individual is not paricularly important. So if a colony of a thousand decides to mutate rapidly and the mutatations kill nine hundred, don’t benefit ninety-nine, and help one the colony can be back to full strength in less than half a day. This is not a viable option for most multicellular organisms. It is important to stress that the intentional mutation don’t mutate in any direction. That is to say they are random and the bateria hope that a couple are successful.
As for hormones, Mauve Dog is correct. Hormones affect gene expression, that is how most hormones work. This is not evolution. The fruit flies were already adapted to the cold before they were introduced into the environment. Sometime in the past, the flies ancestors were exposed to the cold. The cold resistant genes then evolved and modern flies have the ability to switch them on in respose to cold weather.
Smeghead wrote:
There was an article in Scientific American a few years later, which dealt with this experiment. The author was of the opinion that although the E. Coli could indeed increase their mutation rate in response to stress, the mutations were still random. It only looked like there were more “good” mutations than “bad” mutations because the E. Coli with the “bad” mutations died off too quickly to be counted.
I’m sitting in a room completely surrounded by Drosophila melanogaster in vials and bottles. Millions of them. Mutants of all types, that grow eyes on their wings and their antennae and all types of freakshow stuff.
My first grad school rotation was in the lab of Susan M Rosenberg, the queen of “adaptive evolution.” It is interesting, really. If you stick E. coli in an environment on which they starve, they tend to downregulate some of their DNA repair genes (mismatch repair system). This tends to let them accumulate mutation in their genome (they become hypermutable). This is interesting, but it is not really Lamarck – Lamarck’s theories imply directed change, where the bacteria really just take a shotgun approach by become hypermutable.
But, it is still cool.
I won’t add anything to the fruit fly argument, because most of the comments have been valid. Change occuring in a population without permanent genetic change is not evolution.
tracer, not having read the SciAm article, I’m guessing here, but I think we’re talking about different things. I suspect the article you’re talking about is in regards to what’s known as the SOS response in E. coli. When an E. coli cell is in serious trouble, it drastically changes the way it does business as kind of a last ditch effort to somehow make it through. One component of this response is that proofreading in DNA replication is pretty much turned off, resulting in error-prone replication. This, in turn, has two effects. Firstly, the daughter cells will have a lot of mutations, maybe even just the one they need to survive the changed environment. Secondly, replication can happen more quickly and with less energy. Anyway, the net effect is that a stressed cell will have a higher mutation rate - but the mutations will all still be random.
The article I mentioned describes a different type of experiment. It’s been a few years since I’ve read it, so forgive me if I’m a little hazy on the details. They raised two populations of cells. The first was raised from the start in a medium where an essential amino acid was scarce. The other was raised without the scarcity. They were looking for mutations that allowed the cells to manufacture the needed amino acid. If the mutations were totally random, you’d expect the same number of healthy colonies in each population. After correcting for different growth rates in the different media etc etc, they showed that although the overall mutation rate was the same (or nearly so) for both populations, the cells raised with the shortage had a disproportionate number of advantageous mutations - in other words, their mutations were directed. To be fair, the difference wasn’t huge, and before everyone gets in a tizzy, I even dimly recall an outline for a possible mechanism for doing this.
Hope that clears things up a little.
I don’t know why were stuck on this, I must not be making my point clearly.
Modern evolutionary theory says that an organism cannot pass on an acquired trait to its young. For example, no matter how much you bench press, it won’t help your kid get bigger muscles.
The idea that this could occur is generally associated with Lamarck, and sometimes called Lamarckian evolution, or a Lamarckian mechanism, and is generally scoffed at.
There are good reasons why this can’t occur from a microbiology standpoint. Basically, you can’t get any new information that an organism acquires into its DNA. (Don’t get persnickety with viruses or mutations during replication, ok?)
Ok so far?
Evolutionary theory says that change occurs through random mutation. The rare beneficial mutation gets the nod from natural selection and perpetuates. THe negative ones do not.
Their is currently evidence that runs counter to both these ideas, and it is significant.
Fruit flies not adapted to cold may suffer and die quickly. Their offspring may be born adapted to cold and thrive. THe fruit flies experience affected the genome of their offspring. The theory is, that the prodigious fruit fly has encoded within its DNA a host of potentially useful adaptations. If it encounters a situation where one of those might be needed, hormones are activated which cause the adaptation to occur IN THE NEXT GENERATION. While no knew information has been encoded within the genome, the existing information was reshuffled to “deliberately” produce a cold adpated fly.
Fruit flies are masters of evolution, and adapt to thrive under myriad environments, and they do so very quickly. Their mutation rate is very high, and any population of fruit flies will produce the odd one with the white head, the extra set of legs, etc. etc. Some are viable, some are not.
Under controlled conditions, both bacteria and fruit flies will raise their mutation rate to combat environmental stress. It’s as if something in the genome “knows” that the population has encountered a roadblock, and decides to increase the rate of random mutations in order to overcome it. THis is a pretty revolutionary idea in evolutionary theory.
So, we have two interesting examples. In one, a population encounters a “known” obstacle and alters its DNA to specifically provide a certain adaptation to overcome it.
In the second, a population encounters an “unknown” obstacle and produces small random mutations in the hopes that they will combine synergistically to overcome the obstacle.
In either case the organism is not a passive participant waiting for luck and natural selection to speed it down the evolutionary path. It is actively seeking adaptations. It’s making its own luck.
This new theory as I’ve probably badly explained it, has an advantage to existing theory. The slow gradual change of an organism through natural selection over millions of years of random mutation as a theory, is at odds with the observed phenomenom of punctuated equilibrium.
THe slow random change of evolution as we know it with the addition of an onslaught of random mutations at crucial times of change to speed up the process and promote adaptation fits the observed reality better.
The articles that I have read, are beyond me. I was hoping that somebody who knew about this might show up and explain it better, and correct some of my errors.
An excellent article on fruit flies, evolution, and disease appears in the January 1998 issue of New Scientist. I understand about a fifth of it.
Edwino posted while I was still writing my last post, so I bow down before his experience.
It is very cool, and I envy you (sitting in your room surrounded by mutant flies.)
I would beg you to tell me more about adaptive mutation. Up to a week ago, the idea that an organism would actually try to evolve to overcome environmental stress seemed impossible to me. I’m a babe in the woods.
Failing your willingness to provide an online lecture, do you have any cool links on this sort of thin?
You seem to see this as a challenge to standard evolutionary theory. I don’t. Over time, through natural selection, these flies have developed an arsenal of genes that are useful under different conditions. There’s nothing magical about different genes being expressed under different conditions. It happens all the time. Every gene in any organism’s body is under some control. Flies with this type of arsenal are better able to survive, or at least produce viable offspring, than those without.
Well, no, not really. These types of mechanisms have been known for years. Again, they’re just other survival mechanisms that have developed over the years and have proven beneficial in some way.
Again, I have to disagree here. I realize that the directed adaptation experiment I mentioned before looks that way. I wish I could remember the mechanism they proposed - I do remember that it takes away a lot of the mystery, which is one reason why it never made much of a splash in the scientific community.
Realize that with the SOS response I talked about, we’re dealing with a last-ditch effort to somehow survive. If an increased mutation rate was really a good thing, they’d be reproducing that way all the time. The cell isn’t “actively seeking adaptations” or “making its own luck,” it’s dying. If we want to anthropomorphize that much, we could say that in its death throes, it flails about frantically looking for hope. Or we could explain away the whole thing as merely an attempt to reproduce faster, with the increased mutation rate as an unfortunate side effect.
Correct
Not correct. The existing information is there in its original form in both the adapted and unadapted flies. In the unadaped flies the simply don’t express the gene. Why don’t the unadapted flies express the gene right away an avoid death? Maybe because the gene in question is only switched on or off during the developmental stages of the flies. When it is a larva or a pupa. Gene control is very important in not yet adult organisms because the changes the expressed genes cause must be done in a specific order. Maybe when the larva develop in the cold, the cold adapting gene is then turned on? The point is that the genes aren’t changed from one case to the other, it is merely an example of turning a gene on or off.
Where do you get this from? I saw citations of experiments involving bacteria increasing their mutation rate in response to environmental stress, but not fruit flies. Please explain.
Nothing of the sort occurs. No DNA is altered, in the fruit fly case. Only one (or more) genes was simply unexpressed in the unadapted case and expressed in the adapted case.
It may explain puntuated equilibrium better, but as far as I can tell, it isn’t supported by the evidence in most cases.
I must apologize Scylla, I didn’t read the OP carefully. In my last post I described what you already said in the OP as the commonly accepted theory. You were offering what you read in Evolution Magazine as a challange to this theory. Sorry about that. However, your description of the article is quite cryptic.
I’m confused by this. What do you mean by changes? Changes as in genetic mutations? From later posts you seem to suggest this. What do you mean by seeking a favorable adaptation? Were there more positive changes than negative ones, as apparently there were in Smeg’s example? Or was it an SOS response as in tracer’s example? Is there anyway people who don’t have access to the magazine can get the article, is there a web address? Sorry about blowing you off in earlier posts, I assumed right away that you had misinterpreted the article. That was very stupid of me. Now you got me as intrigued as you are about this article!