摘要：SummaryDysregulated metabolism accelerates reduced decision-making and locomotor ability during aging. To identify mechanisms for delaying behavioral decline, we investigated howC. elegansmales sustain their copulatory behavior during early to mid-adulthood. We found that in mid-aged males, gluco-/glyceroneogenesis, promoted by phosphoenolpyruvate carboxykinase (PEPCK), sustains competitive reproductive behavior.C. elegans'PEPCK paralogs,pck-1andpck-2,increase in expression during the first 2 days of adulthood. Insufficient PEPCK expression correlates with reducedegl-2-encodedether-a-go-goK+ channel expression and premature hyper-excitability of copulatory circuits. For copulation,pck-1is required in neurons, whereaspck-2is required in the epidermis. However, PCK-2 is more essential, because we found that epidermal PCK-2 likely supplements the copulation circuitry with fuel. We identified the subunit A of succinate dehydrogenase SDHA-1 as a potent modulator of PEPCK expression. We postulate that during mid-adulthood, reduction in mitochondrial physiology signals the upregulation of cytosolic PEPCK to sustain the male's energy demands.Graphical AbstractDisplay OmittedHighlights•C. elegansupregulatespck-1-andpck-2-encoded PEPCK during early adulthood•Loss of PEPCK causes premature male copulatory behavior decline•Epidermal PEPCK is required to sustain the copulatory fitness•Subunit A of succinate dehydrogenase antagonizes PEPCK expressionBiological Sciences; Animal Physiology; Behavior Genetics
