Octopamine-MAPK-SKN-1 signaling suppresses mating-induced oxidative stress in gonads to protect fertility.

Sexual conflict over mating is costly to female physiology. hermaphrodites generally produce self-progeny, but they can produce cross-progeny upon successfully mating with a male. We have uncovered that hermaphrodites experience sexual conflict over mating, resulting in severe costs in terms of their fertility and longevity. We show that reactive oxygen species (ROS) accumulate on the apical surfaces of spermathecal bag cells after successful mating and induce cell damage, leading to ovulation defects and fertility suppression. To counteract these negative impacts, hermaphrodites deploy the octopamine (OA) regulatory pathway to enhance glutathione (GSH) biosynthesis and protect spermathecae from mating-induced ROS. We show that the SER-3 receptor and mitogen-activated protein kinase (MAPK) KGB-1 cascade transduce the OA signal to transcription factor SKN-1/Nrf2 in the spermatheca to upregulate GSH biosynthesis.