We're still learning, and we always shall be. Hopefully!

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By Viviane Callier

Aging can seem like an unregulated process: As time marches along, our cells and bodies inevitably accumulate dings and dents that cause dysfunctions, failures and ultimately death. However, in 1993 a discovery upended that interpretation of events. Researchers found a mutation in a single gene that doubled a worm’s life span; subsequent work showed that related genes, all involved in the response to insulin, are key regulators of aging in a host of animals, from worms and flies to humans. The discovery suggested that aging is not a random process — indeed, specific genes regulate it — and opened the door to further research into how aging proceeds at a molecular level.

Recently, a set of papers documented a new biochemical pathway that regulates aging, one based on signals passed between mitochondria, the organelles best known as the powerhouse of the cell. Working with worms, the researchers found that damage to mitochondria in brain cells triggered a repair response that was then amplified, setting off similar reactions in mitochondria throughout the worm’s body. The effect of this repair activity was to extend the organism’s life span: The worms with repaired mitochondrial damage lived 50% longer.

What’s more, cells in the germline — the cells that produce eggs and sperm — were central to this anti-aging communication system. It’s a finding that adds new dimensions to the fertility concerns implied when people talk about aging and their “biological clock.” Some of the findings were reported in Science Advances and others were posted on the scientific preprint server biorxiv.org in the fall.
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The research builds on a recent body of work that suggests that mitochondria are social organelles that can talk to one another even when they are in different tissues. In essence, the mitochondria function as cellular walkie-talkies, sending messages throughout the body that influence the survival and life span of the entire organism.

“The important thing here is that in addition to genetic programs, there is also a very important factor to regulate aging, which is the communication between tissues,” said David Vilchez, who studies aging at the University of Cologne and was not involved in the new research.

The cell biologist Andrew Dillin discovered the first hints of this novel pathway that regulates life span about a decade ago. He was hunting for life-extending genes in Caenorhabditis elegans worms when he found that genetically damaging the mitochondria extended the worms’ lives by 50%.

That was unexpected. Dillin had assumed that defective mitochondria would hasten death rather than prolong life — after all, mitochondria are central to cell functioning. Yet for some reason, gumming up the smooth functioning of the mitochondria compelled the worms to live longer.

More intriguing was the fact that damaged mitochondria in the worms’ nervous system seemed to be driving the effect. “It really says that some mitochondria are more important than others,” said Dillin, who is now a professor at the University of California, Berkeley. “The neurons dictate this over the rest of the organism, and that was really surprising.”