Is mrps-5 the Longevity Gene?

Mitochondria are the cell’s workhorse, transforming the calories we eat into useable energy. They have also been the subject of lots of scrutiny over longevity, since lifespan is intimately tied up with metabolism. Now a new study reports that mitochondrial malfunction may actually be the key to extending life.

Although loss of mitochondrial function has been associated with increased lifespan in a number of species, the reasons behind this effect have been poorly understood. It’s also been known that low levels of stress within a cell—for instance, running on low energy—can increase an animal’s lifespan. Most of these studies have however been done in flies, worms and yeast. Thus a Swiss research team led by Riekelt Houtkooper decided to examine stress and longevity in mice, as well as the worm C. elegans.

In mice, they analyzed a set of related mouse strains that have lots of natural variation in lifespan—they live anywhere from 1 to 2 1/2 years. With genetic tests the researchers were able to pin down three specific genes that seemed to be the key determinants of the mouse’s lifespan. Mice with lower activity in these genes lived up to 2.5 times longer than those with high activity.

Then, in worms, the researchers artificially damped down the activity of the equivalent genes and observed how long they lived. One gene stuck out as most important: Worms with a dampened mrps-5 gene lived 60 percent longer than normal.

The key, the researchers say, appears to be that loss of mrps-5 causes the mitochondria to send a kind of cellular SOS to the nucleus. The nucleus’s response, called the “mitochondrial unfolded protein response,” is to send out protective proteins.

 This is interesting.   It also runs contrary to the family history.  We have very long lived folks in the family, but its in the patrilineal side of things.  The men live fairly long, often inspite of their lifestyles rather than because of them.  That would seem to preclude the source of longevity being a mitochondria based source.  Rather it would argue to be a y linked trait.  Interesting if we might be carrying something else.  What happens if you combine them (assuming we haven't just been lucky).