Sec61β Deficiency Disrupts Drosophila Oogenesis Through UPR-Mediated Defects in Germ Cell Proliferation and Differentiation
TL;DR
It is found that knockdown of Sec61β in either germ cells or somatic cells of ovaries causes complete female sterility, with a small size of ovaries from larval to adult stages, significant reduction in germ cell numbers beginning in the late third-instar larval stage and a complete absence of germ cells in pupal and adult ovaries.
Abstract
Sec61β encodes one of the subunits of the Sec61 translocon, which is essential for translocation of the nascent polypeptides to the endoplasmic reticulum (ER). Knockdown of Sec61β in the testis leads to male sterility in Drosophila melanogaster. Although Sec61β is expressed in both testes and ovaries, its role in female reproduction remains unclear. In this study, we found that knockdown of Sec61β in either germ cells or somatic cells of ovaries causes complete female sterility, with a small size of ovaries from larval to adult stages, significant reduction in germ cell numbers beginning in the late third-instar larval stage and a complete absence of germ cells in pupal and adult ovaries. Overexpression of Sec61β efficiently rescues these defects. Furthermore, we observed that Sec61β knockdown in the germline triggers the unfolded-protein response (UPR), which not only non-autonomously activates JAK/STAT signaling in adjacent somatic cells to inhibit Bam expression but also autonomously impedes the G1/S phase progression of germ cells. These effects collectively impact cell proliferation and differentiation. Our results suggest that Sec61β is essential for germ cell maintenance via UPR-mediated cell-autonomous proliferation control and non-autonomous JAK/STAT signaling in Drosophila ovaries.