good news for worms

Gene tweaking safely doubles lifespan

A US team has doubled the lifespan of the nematode worm with no apparent physiological side effects. The key to what appears to be uncompromised longevity is to silence a gene involved in ageing at just the right point in a worm's life cycle.

In previous work involving interfering with the gene, longer life was only achieved at the cost of a loss of ability to reproduce in C. elegans. "But knocking down the gene after the worms reach adulthood increases their life span without affecting their reproduction," says Cynthia Kenyon at the University of California, San Francisco, who led the research.

The gene, called daf-2, is also found in fruit flies and mice, and Kenyon thinks it is possible that it is present in humans. Interfering with this gene in a similar way might also safely extend the human lifespan, she says.

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But Tom Kirkwood, an expert on ageing at Newcastle University, UK, warns that the apparent absence of reproductive problems in the worms "does not mean longevity has come for free - the trade-off could be more subtle than this. When one looks for evidence of trade-offs, fertility is one of the things involved, but it's not the only one."

Independent pathways

Evolutionary biologists have long predicted that lifespan cannot be lengthened without a reproductive trade off. And in 1993, Kenyon discovered that knocking out the gene, called daf-2, at the point of hatching doubled the worm's normal two-week lifespan. But they were unable to reproduce.

But now her team has shown that if daf-2 is switched off at the onset of adulthood, about four days after birth, the worms live twice as long as normal but reproduce normally.

What is more, if daf-2 is switched off when the worms hatch, then switched back on when they reach adulthood, the worms' life span is not altered but the onset of their fertile period is delayed.

This shows that the daf-2 gene controls reproduction during the worm's developmental phase and lifespan during its adult life. Since the two pathways are independent, there need not be a trade off between them at all, Kenyon argues.

Mario de Bono, who works with nematode worms at the MRC Laboratory of Molecular Biology in Cambridge, UK, welcomes the new findings. "The original daf-2 mutants were fine apart from their inhibited reproduction. If you can rescue this reproductive delay there's no reason why the worms should exhibit other problems," he says.

Journal reference: Science (vol 289, p 830)

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2 Responses:

  1. deus_x says:

    Nice LJ-cut tag, man. I almost missed it, until I remembered I was reading this in a web browser. :)