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Stress Can Increase the Mutation Rate in Fruit Flies
The Mutation Rate Depends on the Health of the Mother in Fruit Flies
February 29, 2008
A new study out shows that female fruit flies that are under stress have kids with more mutations. This means that mutation rates are not necessarily constant which has implications for evolution.
And these mutations might not be a bad thing. Some of these mutated offspring may be able to better survive than they otherwise could.
Mutations and Natural Selection
Mutations sound scary but they aren't necessarily bad. They are simply small changes in DNA. And they happen to all of us.
These changes can be good, bad or neutral. They can have big effects or none at all.
Mutations can sometimes cause cancer. And sometimes give rise to new traits like lighter skin or the ability to drink milk as an adult.
In fact, most of the differences we see around us came about because of previous mutations of one kind or another. These differences are the raw material of natural selection.
Natural selection simply means that the creature best suited to its environment will do best. So a finch with a pointy beak will do better in wet weather than one with a broad beak. The pointy-beaked finch will get more food and so go on to have many more offspring.
This finch has a pointy beak because of its DNA. So as these finches do better, their DNA will come to dominate the species in that particular environment.
But when the environment changes, which creatures are best suited will change too. When the weather turns dry, broad-beaked finches will now do better. And so that DNA will become more common.
What can the pointy-beaked finches do now in their new dry environment? One possible solution would be to increase the number of mutations in their kids in the hope that one will make a chick with a broader beak. This is a desperate hope since most mutations are bad for an organism. But if it is going to die anyway
We don't know if birds can do this sort of thing (or people or petunias either). But data from a new study suggests that fruit flies just might.
A stressed fruit fly mom has offspring with more mutations. Perhaps this is a survival mechanism of last resort for an animal that is being out-competed.
Whatever the reason, these results show that the mutation rate is not constant (at least in fruit flies). Stressed creatures can have significantly higher mutation rates. Which means that there may be times when evolution could proceed more quickly since mutations are the raw material of evolution.
Past mutations have led to the differences between people, plants, and animals.
The experiment the researchers did was to zap male flies with a chemical that mutates DNA and then mix these males with stressed or unstressed females. The chemical mutated the DNA of the males including the DNA in their sperm.
The researchers then compared the offspring to see which group had more mutations. The result was that the offspring from unstressed females had fewer mutations than did the offspring from stressed females.
The reason the researchers mutated the males has to do with how DNA is fixed in male and female fruit flies. There is almost no DNA repair in sperm. But the egg can repair DNA in any sperm that fertilizes it.
So the researchers were basically asking how much of the mutated DNA from the male could slip through the repair processes in the egg. The answer was that eggs from stressed females let a lot more mutations through.
Why would stressed female eggs not fix DNA as well? Probably because fixing DNA perfectly costs lots of energy. And these stressed females may not have had enough energy to spare.
There are two different kinds of DNA repair out there. The one that fixes the DNA perfectly costs a lot of energy. The other kind gets rid of any gross problems but leaves errors behind. This costs less energy but leads to more mutations.
The idea is that stressed females can't afford to use the perfect DNA repair system. So they use the other one. Their kids survive but they have more mutations.
Testing for Mutations in Fruit Flies
This kind of experiment would be tough in other animals. This is because the researchers had to look at a whole lot of fliesover 78,000 of them in all. That is way too many flies to study by looking at their DNA.
So how did the researchers check for mutations? By looking for dead grandsons. Basically what the researchers were testing was how often the flies had lethal mutations on their X chromosome.
Flies are like people in that the females have two X chromosomes and the males have an X and a Y. This means that males have one copy of all of the genes on the X while females have two. So if a male inherits an X chromosome with a lethal mutation, he won't have another gene copy around to compensate. And so he will die.
So the researchers took 4-10 daughters from each of the matings. They had these females mate with normal male flies and then looked at their kids.
The researchers needed a way to trace where each fly's X chromosome came from. They used something called a balancer chromosome.
A balancer chromosome usually has a gene on it so that a researcher can tell it is there. In this case, the researchers used something called Bar eye. The other advantage of this chromosome is that it won't mix and match (recombine) with another X chromosome. So it passes virtually unchanged from generation to generation.
The results were that there were many fewer surviving males with Bar eye if mom was stressed. Another way to say this is that stressed moms had fewer surviving grandsons that had grandpa's X chromosome. Stressed moms let more mutations through.
So stressed fruit fly moms have offspring with more mutations because she can't fix DNA mistakes as well. It will be interesting to see if this sort of thing translates to other animals. And so might help us understand more about how evolution works.
Stressed moms had offspring with more mutations.
The researchers studies over 78,000 flies and so could not use equipment like this to study the flies' DNA directly.
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This project was supported by the Department of Genetics, Stanford School of Medicine. Its content is solely the responsibility of the authors and does not necessarily represent the official views of Stanford University or the Department of Genetics.