Meeting Abstract
Lactation in tsetse flies requires a dramatic increase in the expression and synthesis of milk proteins to nourish developing intrauterine progeny. In the recovery period following progeny birth, tsetse cease milk production and the milk gland undergoes involution within 24 hours. In this study, we examined the role that autophagy plays during milk gland involution. Autophagy genes show elevated expression in the milk gland immediately before or within two hours post-parturition, which decline within 24-48h post-parturition. This expression pattern is inversely correlated with that of the milk gland proteins (lactation-specific protein coding genes) and the autophagy inhibitor FK506-bp1. Increased expression of Drosophila inhibitor of apoptosis 1, diap1, was observed in the milk gland during involution, which likely prevents apoptosis o.f milk gland cells. RNAi-mediated knockdown of autophagy related gene 8a (atg8a) prevented rapid milk gland autophagy during involution, which prolongs gestation and reduces fecundity in the subsequent gonotrophic cycle. In addition, atg8a knockdown reduced the recovery of stored lipids during the non-lactating periods by 15-20%. Population modeling revealed that a delay in involution due to the suppression of autophagy yields a negative population growth rate. This study indicates that periods of autophagy in the milk gland during involution are critical to restore nutrient reserves and allow efficient lactation in subsequent pregnancy cycles.
