| 35762 | Q7K2X8 | SEH1_DROME | Nucleoporin seh1 (GATOR complex protein seh1) (Nucleoporin complex protein 44A) | DISRUPTION PHENOTYPE | Adults develop normally, however females display ovarian defects and reduced fertility likely due to the significant decrease in TORC1 activity within the germline cells (PubMed:21521741, PubMed:25512509). Ovarian defects include adherent cyst divisions due to mitotic delay, accumulation of autolysosomes resulting in reduced number of egg chambers and reduced number of eggs laid per female per day (PubMed:21521741, PubMed:25512509). Spindle defects and mitotic delay results in egg chambers often containing 16 polyploid nurse cells and no oocyte because the oocyte enters the endocycle and develops as a polyploid nurse cell (PubMed:21521741). In early meiotic germline cells, the nucleoporin Mtor is displaced from the nuclear envelope to the nucleoplasm, most notably as cysts enter the meiotic cycle beginning in R2a of the germarium (PubMed:21521741). However, there is no effect on the recruitment of Mtor or other nucleoporins (Nup107, Nup153, Mtor and FG-containing nucleoporins) to the nuclear pore complex (PubMed:21521741). In contrast, somatic tissues do not display any obvious developmental defects; there is no decrease in TORC1 activity and no accumulation of autolysosomes in the larval fat body (PubMed:25512509, PubMed:21521741, PubMed:27166823). Increasing TORC1 activity in the mutant female germline via RNAi-mediated knockdown of the GATOR1 subcomplex members Nprl2, Nprl3, Iml1 or knockdown of Tsc1 rescues the ovarian defects (PubMed:25512509). However, knockdown of Nprl2 or Nprl3 does not rescue the accumulation of autolysosomes (PubMed:27166823). {ECO:0000269|PubMed:21521741, ECO:0000269|PubMed:25512509, ECO:0000269|PubMed:27166823}. |