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Sea2, a new regulator of metabolism and autophagy, is required for oogenesis in Drosophila

Monday, September 22, 2014 — Poster Session I

12:00 p.m. – 2:00 p.m.

FAES Academic Center




  • W Cai
  • MA Lilly


Our current studies focus on gaining a mechanistic understanding of how components of the SEA/GATOR complex, a newly defined regulator of TORC1, control meiotic progression and growth during oogenesis. Tor functions as a master regulator of metabolism in eukaryotes. Previously, we identified two genes from this complex, missing oocyte(mio) and seh1, required for the maintenance of the meiotic cycle during Drosophila oogenesis. Recently, we have determined that Mio/Seh1 positively regulate TORC1 activity. To further study the function of the SEA/GATOR complex in Drosophila, we identified CG7609 as the homolog of Sea2/WDR24 in yeasts and mammals. We found that Sea2 physically interacts with other SEA/GATOR components. Interestingly, sea2 null mutants are not lethal but female sterile, suggesting an important oogeneic function. However, unlike what is observed in mio and seh1 mutants germline clones of a sea2 null allele are not growth delayed. Additionally ovaries from sea2 null mutants exhibit the accumulation and disorganization of autolysosomes, which is also observed in both mio and seh1 mutants suggesting that these three proteins may act together to influence a pathway that modulates autophagy and lysosomal dynamics. Taken together, our results suggest that a Sea2/Mio/Seh1 associated sub-complex has additional functions beyond TORC1 regulation during oogenesis.

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