Posted on 06/17/2003 7:05:07 PM PDT by Pharmboy
H. E. Hoekstra
Evolution has allowed some rock pocket mice,
pictured on light and dark rocks, to produce
distinct fur that helps disguise them.
In the deserts of the Southwest, among the towering saguaros and the spiny cholla cactuses, rock pocket mice hop and dash in search of a meal of seeds. But while these mice may seem to scamper haphazardly across the desert floor, their arrangement in nature is strikingly orderly.
Nearly everywhere these mice are sandy-colored, well camouflaged as they scurry across beige-colored outcrops. But in some areas, ancient lava flows have left behind swaths of blackened rock. There the same species of rock pocket mouse has only dark coats, having evolved an entirely distinct and, for their surroundings, equally well-disguised pelage.
Now, in a recent study in The Proceedings of the National Academy of Sciences, researchers report identifying the gene responsible for the evolution of dark coat coloration in these mice, pinpointing the DNA sequence changes that underlie this classic story of evolutionary change, the cute and furry counterpart to the famous case of the peppered moth.
Researchers say the study is the first documentation of the genetic changes underlying an adaptive change where the evolutionary forces were natural. Scientists point out that other well-known cases involve evolution caused by humans; some have suggested that those changes may be atypical of natural evolutionary change, since they have typically involved intense, directed pressures destroying most of a population, like the spraying of pesticides or the application of antibiotics.
"This work is very important," said Dr. Mike Majerus, an evolutionary geneticist at Cambridge University, who was not part of the study. "Here man is just not involved. The sandy and lava flow substrates are entirely natural phenomena."
Other well-studied examples of human-driven adaptive change include the evolution of pesticide resistance in insects after widespread spraying and the increase in the numbers of dark-winged forms compared with light-winged forms of the peppered moth in the United States and England after industrialization turned air sooty and polluted.
Dr. Michael W. Nachman, a population geneticist, along with colleagues at the University of Arizona, Dr. Hopi E. Hoekstra and Susan L. D'Agostino, studied mice living on Arizona's Pinacate lava flow in Arizona and on light-colored rocks nearby. The researchers were able to take advantage of decades of meticulous work in which other scientists identified some 80 genes that affected coat color in laboratory mice.
On close examination, the light-colored rock pocket mice could be seen to have a type of hair coloration similar to standard, sandy-colored laboratory mice. In this pattern, known as agouti, the hair is black at the base, yellow in the middle and black again at the tip. The dark-colored rock pocket mice had completely dark hairs.
Researchers knew that mutations in a few well-known coat coloration genes in laboratory mice could cause such complete darkening of the hair, and they began by looking at two genes known as agouti and Mc1r. When they looked at DNA sequences in light and dark mice, changes in the agouti gene did not appear to be associated with light-colored fur versus dark-colored. Still, the researchers found that a certain cluster of mutations at Mc1r could be found in every dark-colored mouse.
"It's a textbook story," Dr. Nachman said. "Now we have all the pieces of the puzzle together in a natural setting."
Dr. Nachman noted that while the new study points to the Mc1r gene as the key to turning mice dark on the Pinacate lava flow, the team also found that dark mice on another lava flow in New Mexico did not share those mutations.
"So the same dark color has evolved independently in the two different populations," he said, "through different genetic solutions to the same evolutionary problem." Dr. Nachman said changes in another gene, perhaps the agouti gene, could be responsible for dark coloration in the New Mexico's Pedro Armendaris lava flow.
One could easily imagine that coloration would be of no consequence to the rock pocket mice, as they are nocturnal, darting about under the desert night sky. But researchers, working early in the last century, released light and dark mice on light and dark backgrounds in an enclosure at night and found that owls, a major predator of mice, could easily spot a mouse on a mismatched background.
Dr. Nachman noted, however, that these early researchers did not use rock pocket mice in their study, but instead used a species in which the dark and light forms were actually much less distinct.
As a result, he said, "we think the owls are discriminating even more strongly in our species." He said tiny bits of rock pocket mouse were often found in pellets at owl roosts.
Dr. Majerus said many kinds of animals showed light and dark forms, from deer mice to squirrels and chipmunks. There are even black ladybugs.
"A lot of the dark forms show an association with a particular type of substrate they're on, or the frequency of burning and charring of the trees in the woodlands," he said, noting that it would be interesting to do genetic studies in other animals, to see how many genetic solutions these other animals have come up with to turn dark.
But while many dark forms are abundant and can be studied at scientists' leisure, Dr. Majerus said that of the peppered moth was slowly disappearing.
So while there is nearly unanimous praise for the increasingly clean air in industrialized regions of the United States and Britain, there may be, at least for some scientists, a downside. "We've got about 15 or 16 years," Dr. Majerus said, "before those black forms, if they continue to disappear at the current rate, disappear completely."
Ah, Uriel. Yes, I remember you!
You keep conflating atheist Objectivist libertarians with atheist Socialists. I know it's hard for many people to keep the distinctions between theist/atheist and socialist/libertarian separate, but you, being a christian libertarian, should know better!
Just one observation: It's the better-educated people generally who have fewer children. I suspect that welfare queens have more children than working people. Us first-worlders, who live in an industrialized society, have fewer children than third-world peasants. Hispanics have many more children than American Jews. I suspect priests also have fewer children, on average, than pro-life athiests like myself. I guess the Long March of Evolutionary Progress must be favoring the ignorant third world Hispanic peasant welfare-queen Presbyterians over the educated first-world libertarian Catholics & Jews. (I don't know if that's a good or a bad thing.)
the Apo-AIM Mutation is associated with a decreased risk of arteriosclerosis (clogged arteries), heart attack, and stroke -- diseases generally associated with the Elderly, at least 90%+ of the time, if not more.
Haven't you heard of America's obesity epidemic? Heart disease affects middle-aged people too, and even some young people. If it weren't for the Atkins Diet, the American population would be devastated by heart disease. Even with Atkins, I think that any Milano who wanted to marry an American would increase his/her chances by advertising the fact that they have the Apo-M mutation so their prospective partners would know that their babies were much more likely to survive long enough to have healthy grandchildren.
I got these figures for 2000 from the CDC (combining all races & both sexes):
Ages Heart disease
as % of all deaths1-4 3.6 5-9 3.3 10-14 4.0 15-19 3.0 20-24 3.5 25-34 7.3 35-44 14.7 45-54 22.1 55-64 26.3 65-74 27.7 75-84 31.4 85-over 38.2
Well, it would be a bad ethical argument, but in fact it's a demographic argument. OK, it's also a bad demographic argument. (You were expecting what, maybe?)
If my statement in 214 is idiotic a genius like you should have been able to refute it. So who is the idiot?
"It would appear that the questioner is under the mistaken impression that beneficial mutations are a problem for creationists. Some creationists make this unfortunate error. The mutations Q&A section of our Web site clearly teaches that the issue is not whether the mutation is beneficial but if it adds new genetic information (specified complexity). So it would have been clear that the A-I Milano mutation is not evidence for microbe-to-man evolution."
Yes, regardless of whether it is beneficial or not, it is not evidence for evolution. Regardless whether it is a mutation or not, it is still not evidence of evolution.
Let's continue. They question now is whether the variation is beneficial or not. To this AIG's DR. Don Batten responds:
"Now in gaining an anti-oxidant activity, the enzyme has lost a lot of activity for making HDLs. So the mutant enzyme has sacrificed specificity. Since antioxidant activity is not a very specific activity (a great variety of simple chemicals will act as antioxidants), it would seem that the result of this mutation has been a net loss of specificity, or, in other words, information. This is exactly as we would expect with a random change.
... Of course it remains to be seen if this mutation is completely beneficial. The fact that the persons with it are unable to produce normal levels of HDLs, which are known to perform a valuable role in moving bad cholesterol, suggests that there could be a health down side to this mutation"
Both quotes from: Answers In Genesis
The lame response to the doctor's statement above from the three nobodies at TalkOrigins is that the url's given of press releases do not say what the doctor says! Well, did these folk bother to read the study - like the doctor did and cites at the bottom of the article? If they did, then they are indulging in dishonest tactics. If they did not, then they should not be attacking the doctor's statements.
Guess that thugs like you cannot read. Here it is again and maybe someone can read it to you:
" Actually the principle is quite simple. The biological diversity of 1,000,000 individuals will always be larger than that of 100,000 of its members. When you split a group you therefore get less biological diversity any way you cut it. If in addition the cut off group has been selected for a specific trait then the traits being selected against will be lost. Such traits might have been useful at a future time when circumstances change again (as they always do). "
Yeah but then after a few tough generations the 100,000 that have survived natural selection start to really prosper in their new home & grow into a population of 1,000,000 of their own & now you've got 2,000,000 individuals in all, doubling your own measure of "biological diversity".
If in addition the cut off group has been selected for a specific trait then the traits being selected against will be lost. Such traits might have been useful at a future time when circumstances change again (as they always do).
Yeah but then the new generations of the breakaway group of 1,000,000 builds up their own set of new mutations, and now you've got 2,000,000 separate genetic experiments going on where before you only had 1,000,000. So again, by your own metric, you end up with more diversity.
Do you realize what you are implying about the King Jenny?
I think I should've said OP was sacrificing his Queen (the human mind, which is what makes old people valuable and the good life possible) for his Bishop (his religious dogma, which says creationism must be true at all costs). His King would be his belief in the God of the Bible.
Is that clearer? (Or am I just being pedantic? :-)
"Now in gaining an anti-oxidant activity, the enzyme has lost a lot of activity for making HDLs. So the mutant enzyme has sacrificed specificity. Since antioxidant activity is not a very specific activity (a great variety of simple chemicals will act as antioxidants), it would seem that the result of this mutation has been a net loss of specificity, or, in other words, information. This is exactly as we would expect with a random change.
... Of course it remains to be seen if this mutation is completely beneficial. The fact that the persons with it are unable to produce normal levels of HDLs, which are known to perform a valuable role in moving bad cholesterol, suggests that there could be a health down side to this mutation"
Both quotes from: Answers In Genesis
Both these objections were handled clearly in the T.O. article. You should read it sometime when your Morton's Demon is asleep. (Yeah, I know, he never sleeps. :-)
The ol' "everybody does it" excuse again.
Just to clarify--all scientists are engaged in leveraging the work of others, and, lately, in breakneck races to be first to major milestones in the process of said leveraging, so as to get the credit, and the resulting academic cheese.
Darwin was cudgled by his friends into publishing before he really intended to, because another avid collector with enough of a scientific background to make his way to the principles of evolution through variation and selection, was hot on his tail, and he was substantially preceeded in in the neighborhood of his speculations by some of the leading lights of the previous generation of scientists.
Like any good Popperian, Darwin was solving a problem with a rather detailed pedagree that had already been voiced by the scientists that preceeded him.
At least you agree he didn't ORIGINate the idea.
Indeed not--he only solved a problem set, whose solution would have been published, probably within the year, by someone else with a less compulsive need to gather up the devastating evidence quite so encyclopeiacly.
You are making an assumption which is not valid. You are assuming that the variations in the gene pool that existed before will be recaptured. This is not the case. First of all if the reason for the split was that the variations were selected against due to the current environment they will continue to be suppressed for as long as the current environment remains pretty much the same. In which case when it changes again the variations will no longer be there to enable the species to survive.
Second, the variations in a species - even under evolutionist assumptions to which I do not subscribe - are a function of both time and number of individuals so even if you multiply the population within a short time you still will not regain all that was lost.
Thirdly, and here we finally get to reality is the question of whether the gene pool of a species once cut off can be regained. Scientists by and large do not think so. That is why when trying to save an endangered species they try to get as many possible individuals to become part of the breeding group as they can find and the preference is for individuals from as far away as they can get because they are more likely to have different alleles the farther apart physically that they are.
Nope, it does not deal with it, it circumvents what was said. Dr. Don Batten did not say as TO claims he said that:
Apo-AIM has not lost the ability to make HDLs, so it has not sacrificed specificity.
Dr. Don Batten said:
"Now in gaining an anti-oxidant activity, the enzyme has lost a lot of activity for making HDLs."
In short they are arguing against what was not said.
Further as to the question whether a person having both alleles with the mutation is beneficial or not, the argument in TO is faulty. Since the variation has only been found in individuals in one small town, it is obvious that this town is pretty inbred so one would expect to find individuals with both alleles if it is as beneficial as TO claims, but we do not. Secondly the comparison to mice who have been given both alleles is not valid in this case because the diet of humans and mice is different (and I really do not want to know what they eat) - especially lab mice.
Further, I need to strenuosly object to the rhetoric in the TO article with its constant references to some press releases as the sole source of information on this. This is a clearly dishonest implication by the TO writers that Dr. Bennett has only consulted these articles when he clearly did not. He went to the source. In fact the whole implication by the TO article that Dr. Don Batten was uninformed about this is completely false as the AIG article shows:
For the original paper, see: Bielicki, J.K., Oda, M.N., Apolipoprotein A-I(Milano) and apolipoprotein A-I(Paris) exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I, Biochemistry 41(6):2089-96, 2002.
Note: the original posting of this response was modified following interaction with a Dr Steven Pirie-Shepherd, an evolutionist. We started out publishing Dr Pirie-Shepherds objections with Dr Battens responses, but he was clearly not happy with our publishing his letters after we had demonstrated the flaws in them; he kept coming back for more, continually changing his point of contention. If we had persisted with publishing this interaction as the back-and-forth continued it would have become quite tedious to follow. Also, it became clear that Dr Pirie-Shepherd was willing to concede nothing and was using the opportunity merely to develop a propaganda piece to be published on a web site given to opposing Biblical Creation. Consequently, our answer was modified in response to Pirie-Shepherds claims, but his words were not included.
Dr Pirie-Shepherd has contributed his name to Project Steve of the National Center for Science Education, an organization founded and still run by secular humanists (atheists)NOT to promote real science such as physics, chemistry and experimental biology, but solely to oppose Biblical Creation and promote evolution from goo-to-you-via-the-zoo (see How Religiously Neutral are the Anti-Creationist Organizations?).
So unlike what the TO writers say, AIG did seek review by those disagreeing with them - something which the TO writers themselves did not do.
The implication that Darwin's book was a rush job is totally ridiculous - it took him 20 years to put it to paper. Secondly, the rushing was not done by his friends, it was a result of Wallace publishing a similar (nay, almost identical) thesis.
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