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In the shadow of the crisis in Crimea, Ukrainian legislators are weighing a pair of science and education bills that...
Researchers dependent on government funding would face a flat future under the White House's $3.9 trillion budget...
Reservoirs of cells that harbor HIV DNA woven into human chromosomes have become the bane of researchers trying to cure...
Geochemists have now incorporated in their models some details of the way naturally acidic rainwater dissolves rock...
Schizophrenia is a devastating mental disorder that afflicts about 1% of the world's population at one time or another...
Surface tension is a force to be reckoned with, especially if you are small. It enables a water strider to skate along...
- 13 March 2014 11:08 am , Vol. 343 , #6176
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Mutation Slows Aging in Mice
18 November 1999 7:00 pm
A single mutation in a gene can lengthen a mouse's life by nearly a third without any noticeable harm, according to a study in today's Nature. The mutation changes the way the animals deal with toxic chemicals that damage DNA, the authors say.
A group led by oncologist Pier Guiseppe Pelicci of the European Institute of Oncology in Milan, Italy, had been studying a gene that can make any of three proteins, two of which are activated by growth factors. Wondering why the third protein, an enzyme called p66, was not, despite being very similar to the other two, Pelicci's team knocked out the piece of the gene that enabled it to code for p66, in order to make mice and mouse embryonic cells that lacked p66.
They found that without p66, cells were only half as likely to die when exposed to hydrogen peroxide (H2O2), a corrosive compound, or to ultraviolet light, both of which can oxidize and damage DNA. Apparently, p66 retards the cell's ability to deal with these stresses and instead causes damaged cells to die, Pelicci says. The team found a similar effect in whole mice lacking the enzyme. Because oxidative stress is thought to promote aging, the team also measured the mutant mice's life span. They found that the mutants lived 36 months, instead of the normal 28.
"It's a very important study because it provides further support for the idea that oxidative stress plays a role in aging," says Tomas Prolla, a geneticist at the University of Wisconsin, Madison. However, he says, "it's unclear if the rate of aging itself is retarded," as proof of that requires that the maximum life span be extended. But Pelicci hopes he's on the right track, and he is now working with gerontologists to see whether people who reach the century mark happen to lack p66.