More on CLK-1 and the Retrograde Response

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You might recall that the gene CLK-1 can influence longevity in a range of species:

CLK-1 - or clock-1 - is a gene that affects lifespan, most likely through its influence on mitochondrial activity. It's the standard story, or at least appears to be: anything that can lower the rate at which mitochondria damage themselves will extend life in flies, mice, and so forth.

Here's more on CLK-1 in yeast and worms; an open access PLoS Genetics paper:

Mitochondrial respiration generates energy in the form of adenosine triphospate (ATP), a molecule that powers many cellular processes. When respiration is inhibited in C. elegans, rates of behavior and growth are slowed and, interestingly, lifespan is extended.
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We find that inhibiting respiration increases the expression of genes predicted to protect and metabolically remodel the animal. This pattern of gene expression is reminiscent of the expression profile of long-lived respiration-defective yeast, suggesting ancient evolutionary conservation. Mutations in clk-1, which inhibit the synthesis of the respiratory-chain factor ubiquinone, produce gene expression, longevity, and behavioral phenotypes similar to those produced by inhibiting components of the respiratory chain.

We find that knocking down the activities of two similar genes - fsrt-1 and fstr-2- accelerates the behaviors and aging rates of clk-1 mutants ... Thus, fstr-1/2, which encode potential signaling proteins, appear to be part of a mechanism that actively slows rates of growth, behavior, and aging in response to altered ubiquinone synthesis. Unexpectedly, fsrt-1/2 are not required for the longevity and behavioral phenotypes produced by inhibiting the gene isp-1, which encodes a different component of the respiratory chain. Our findings suggest that different types of mitochondrial perturbations activate distinct pathways that converge on similar downstream processes to slow behavioral rates and extend lifespan.

Our mitochondria appear to be the crux of a great many evolved mechanisms of longevity, which continues to point them out as a good place place to start when trying to prevent or reverse the damage of aging.