Rates of Behavior and Aging Specified by Mitochondrial Function During Development

TLDR

Investigating whether reducing electron transport chain and ATP synthase activity via RNA interference in *Caenorhabditis elegans* affects aging. RNAi-mediated knockdown of ETC and ATP synthase components during development was employed to lower mitochondrial activity. Developmental knockdown of these components decreased body size and behavioral rates, extended lifespan, and these effects could not be reversed by restoring mRNA or by inhibiting the respiratory chain only in adulthood, indicating that early mitochondrial activity sets persistent rates of respiration, behavior, and aging.

Abstract

To explore the role of mitochondrial activity in the aging process, we have lowered the activity of the electron transport chain and adenosine 5′-triphosphate (ATP) synthase with RNA interference (RNAi) in Caenorhabditis elegans. These perturbations reduced body size and behavioral rates and extended adult life-span. Restoring messenger RNA to near-normal levels during adulthood did not elevate ATP levels and did not correct any of these phenotypes. Conversely, inhibiting respiratory-chain components during adulthood only did not reset behavioral rates and did not affect life-span. Thus, the developing animal appears to contain a regulatory system that monitors mitochondrial activity early in life and, in response, establishes rates of respiration, behavior, and aging that persist during adulthood.