An exposition of ejaculate senescence and its inhibition in Drosophila

Résumé fourni par la source

Abstract Declining male ejaculate performance with age (ejaculate senescence) is thought to be a widespread phenomenon, and a major contributor to the current ‘male fertility crisis’ in humans. However, the mechanistic basis of ejaculate senescence is poorly understood. Here, we show that, in Drosophila, ejaculate senescence arises via distinct changes to both sperm and seminal fluid proteins (Sfps). Sperm production declines with age, while repeated mating depletes sperm reserves and reduces sperm viability. In contrast, Sfps accumulate over time in sexually abstinent males, resulting in compositional change in the seminal proteome, which is associated with reduced Sfp transfer. We also find evidence of age-related qualitative changes in several functionally important Sfps. Finally, we reveal that ablation of insulin-like peptide-producing cells in males can ameliorate declines in fertility and other aspects of ejaculate senescence, suggesting that anti-ageing interventions could be co-opted to promote healthy male reproductive ageing. One sentence summary Ejaculate senescence arises from mating-dependent sperm and seminal protein quality and quantity loss, but it can be delayed

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