Single Gene Leads to Longer Lifespan Across Species

By Becky Lang | May 22, 2013 12:27 pm

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.

And fascinatingly, the same mechanism may be behind the touted longevity benefits of red wine and other foods. Rapamycin and resveratrol, two compounds known to play a role in longevity, also activated the mitochondrial unfolded protein response in the worms, the authors report in Nature.

These results thus tie mitochondrial translation and metabolism to natural lifespan regulation across species. The fact that similar mechanisms drive longevity in mice opens the door to investigations of the genes in human longevity, though at the moment most known mitochondrial mutations shorten human life rather than extending it. Still, if the cellular fountain of youth is to be found, this study indicates the mitochondria remains the place to look for it.

MORE ABOUT: lifespan, longevity, youth
  • Will Baird

    That’s interesting. My family has a history of very long life…but its patrilineal. That would preclude the mitochondria being the source.

    • SixSixSix

      It would preclude the mitochondria gene being the source, but not that it might involve mitochondria interaction with nuclear genes. The nucleus genetic material and mitochondria live in an uneasy balance. The faster the metabolism, the closer the compatibility is required to be. In hummingbirds it is quite close with relatively little deviation, in rats its correspondingly wider with more deviation within members of the species. In fact the difficulty of matching mitochondria and nucleic genes may be why one one gender only contributes the mitochondria.

  • Jerry Hodge

    In mammals, nuclear genes, such as mrps-5, code for mitochondrial ribosomal proteins. Since nuclear genes are passed equally from both parents, longevity due to the mrps-5 could be due to patrilineal effects.

    • jovyxafeseda

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  • stargene

    And how they got C. elegans to drink that red winein the first place is an oenological mystery indeed.


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