Sunday, August 5, 2012

Genetic Clue Discovered For Why Women Outlive Men - Medical News Today

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Main Category: Seniors / Aging
Also Included In: Men's Health;  Biology / Biochemistry;  Genetics
Article Date: 03 Aug 2012 - 2:00 PDT

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DNA Clue To Women's Longevity Found In Fruit Flies


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A new study of mitochondrial DNA in fruit flies offers a number of clues that might explain why females tend to outlive males across much of the animal kingdom, including humans.

Researchers from Monash University in Australia and Lancaster University in the UK, write about their work in the 2 August online issue of Current Biology.

They found male fruit flies appear to have mutations in their mitochondrial DNA that affect how fast they age and how long they live.

Scientists use fruit flies as models for studies in genes and aging because their biological processes are remarkably similar to that of other animals, such as humans, and with a lifespan of about a month, it doesn't take too long to investigate generational effects.

Senior author Damian Dowling, a research fellow in the Monash School of Biological Sciences, told the press:

"All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male aging across the animal kingdom."

"Intriguingly, these same mutations have no effects on patterns of aging in females. They only affect males," he added.

Mitochondria are special subunits of cells, about the same size as bacteria, that provide the energy for life. They combine sugar and oxygen into adenosine triphosphate or ATP, molecular packets of energy that are usable by cells.

Mitochondria have their own DNA that is quite separate from the cellular DNA in the nucleus of the cell.

And, unlike cellular DNA, which is inherited from the sperm and egg that fuse to make the new individual, mitochondrial DNA comes only from the egg.

Thus, as mitochondrial DNA is passed down from generation to generation, the process of natural selection has no opportunity to "screen out" mutations in mitochondrial DNA that might be harmful to males. The researchers refer to this as a "sex-specific selective sieve".

For their study, Dowling and colleagues looked at differences in longevity and biological aging in male and female fruit flies whose mitochondria came from different origins.

They found genetic variations in both male and female mitochondrial DNA, but only the male ones could be linked to life expectancy. There weren't just a few mutations in one place, there were several, spread all over the mitochondrial genome:

"... our results indicate that the mitochondrial mutation loads affecting male aging generally comprise numerous mutations over multiple sites," they write.

The researchers suggest the mutations are entirely due to the way mitochondrial DNA is passed down through the female line.

"If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed," Dowling explained.

In an earlier study that looked at the effect of mitochondria being passed down the female line, the team had also discovered a link with male infertility.

Dowling said combining this latest study with their earlier work suggests mitochondria are "hotspots" for mutations that influece male health.

"What we seek to do now is investigate the genetic mechanisms that males might arm themselves with to nullify the effects of these harmful mutations and remain healthy," said Dowling.

Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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"Mitochondria, Maternal Inheritance, and Male Aging "; M. Florencia Camus, David J. Clancy, Damian K. Dowling; Current Biology, 02 August 2012; DOI: 10.1016/j.cub.2012.07.018; Link to Abstract.
Additional source: Monash University.
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