All mother's fault! - exploring why males die younger and are less fertile
29 May 2014
One clue to why males die earlier and are less fertile than females across many species, including humans, has been explored by a study led by the University of Sydney.
The study, just published in Philosophical Transactions of the Royal Society provides an explanation: it is all mother's fault!
Professor Madeleine Beekman, from the University of Sydney's School of Biological Sciences and her colleagues from Monash University and Netherland's Wageningen reviewed the role mitochondria, our cells 'powerhouses' play in affecting male health, fertility and longevity.
"We weren't the first to come up with this idea but this is the first time that all the studies to date have been collated that address sex-specific effects," said Professor Beekman.
"We found evidence for mitochondrial effects in particular on male fertility and longevity. We think that similar effects on other components of male life history are likely to be present. We found an effect on male longevity in experiments on fruit flies, but we suspect that a similar effect can be found in other organisms."
The harming effects of mitochondria on male fertility are also known from plants, again suggesting that the phenomenon is widespread.
Mitochondria are tiny structures that supply most of the cell's chemical energy as well as having a major role in the cell's development and death. Mitochondria are inherited from one parent, in the vast majority of organisms through the female.
"Males don't matter to the tiny powerhouses of our cells because mitochondria are never transmitted via the male line. Therefore, in evolutionary terms, mitochondria couldn't care less about their effect in males, even if that means their presence harms males," said Professor Beekman.
Natural selection is basically 'blind' to mitochondria when present in males. As a result, any mutation in the mitochondrial genome (as mitochondria have their own genome) that is harmful to males, will be maintained provided it has no negative effect in females.
"The situation becomes even more interesting when a mutation has a positive effect in females but is negative in males. If this is the case such a mutation will spread despite harming males," said Professor Beekman.
"We had also hoped to find evidence in the medical literature for sex-biases in mitochondrial diseases, but it appears that medical researchers have not separated the prevalence and severity of mitochondrial diseases on males and females. It will certainly be interesting to see if males are indeed more likely to suffer from mitochondrial diseases than females," said Professor Beekman.
Contact: Verity Leatherdale
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