In 2009, it was shown by the Spanish National Cancer
Research Center under Óscar Fernández-Capetillo that mice age faster with low
levels of ATR protein, an essential protein for the repair of damaged DNA,
Stopping the premature ageing of these mice and doubling their life span has
been achieved by introducing a mutation capable of increasing the body's
capacity to produce nucleotides available in the cell.
This was originally tested in yeast, Saccharomyces
cerevisiae, where it proved to be true and has since been tested on mice.
The mice were given two genetic alterations with the first being the original
ATR gene mutation that led to premature aging and the second which was the
animals had multiple copies of Rrm2, the key gene for nucleotide synthesis. The
results showed the aging process to be significantly slowed in these mice,
taking their life span from 24 weeks to 50 weeks.
Every genome has weak or fragile sections which break
spontaneously. These fragile sections have been shown to be involved in human
diseases like cancer. The research paper showed that those mice with additional
copies of Rrm2 suffered less DNA breaks in these fragile areas. "The question we are asking
ourselves now is whether an increase in the capacity to produce nucleotides
could also lengthen life expectancy in normal animals without premature
ageing," says Fernández-Capetillo.
I found this article very interesting due to the research of
prolonging and increasing the life span of animals. Although it is not said in
the article I think it goes without saying that the obvious implications of a
study like this is to eventually see if causing these same mutations in humans
could lead to longer and healthier life spans.
