Dysregulated metabolism accelerates reduced decision-making and locomotor ability during aging. To identify mechanisms for delaying behavioral decline, we investigated how C. elegans males 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-1 and pck-2, increase in expression during the first 2 days of adulthood. Insufficient PEPCK expression correlates with reduced egl-2-encoded ether-a-go-go K+ channel expression and premature hyper-excitability of copulatory circuits. For copulation, pck-1 is required in neurons, whereas pck-2 is 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.

新陈代谢失调会加速衰老过程中决策能力的降低和运动能力。为了确定延迟行为下降的机制，我们调查了秀丽隐杆线虫男性如何在成年早期到中期维持其交配行为。我们发现，在中年男性中，磷酸烯醇丙酮酸羧激酶（PEPCK）促进的葡萄糖/甘油生成，维持竞争性生殖行为。秀丽隐杆线虫的PEPCK旁系同源物pck-1和pck-2在成年的前两天表达增加。PEPCK表达不足与egl-2编码的ether-a-go-go减少有关钾离子通道表达和交配回路的过早兴奋。对于交配，神经元中需要pck-1，而表皮中需要pck-2。但是，PCK-2更为重要，因为我们发现表皮PCK-2可能会补充燃料来补充交配回路。我们确定了琥珀酸脱氢酶SDHA-1的亚基A作为PEPCK表达的有效调节剂。我们推测，在成年中期，线粒体生理的减少预示着细胞内PEPCK的上调，以维持男性的能量需求。