Abstract
The preservation of female fertility under unfavorable conditions is essential for animal reproduction. Inhibition of the target of rapamycin complex 1 (TORC1) is indispensable for Drosophila young egg chamber maintenance under nutrient starvation. Here, we show that knockdown of RagA results in young egg chamber death independent of TORC1 hyperactivity. RagA RNAi ovaries have autolysosomal acidification and degradation defects, which make the young egg chambers sensitive to autophagosome augmentation. Meanwhile, RagA RNAi ovaries have nuclear-localized Mitf, which promotes autophagic degradation and protects young egg chambers under stress. Interestingly, GDP-bound RagA rescues autolysosome defects, while GTP-bound RagA rescues Mitf nuclear localization in RagA RNAi young egg chambers. Moreover, Rag GTPase activity, rather than TORC1 activity, controls Mitf cellular localization in the Drosophila germ line. Our work suggests that RagA separately controls autolysosomal acidification and Mitf activity in the Drosophila young egg chambers.
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