Abstract
The exocyst complex plays multiple roles via tethering secretory or recycling vesicles to the plasma membrane. Previous studies have demonstrated that the exocyst contains eight components, which possibly have some redundant but distinct functions. It is therefore interesting to investigate the biological function of each component. Here, we found that Sec3, one component of exocyst complex, is involved in Drosophila egg chamber development. Loss of sec3 results in egg chamber fusion through the abolishment of cell differentiation. In addition, loss of sec3 increases cell numbers but decreases cell size. These defects phenocopy Notch pathway inactivation. In line with this, loss of sec3 indeed leads to Notch protein accumulation, suggesting that the loss of Sec3 inhibits the delivery of Notch onto the plasma membrane and accumulates inactive Notch in the cytoplasm. Loss of sec3 also leads to the ectopic expression of two Notch pathway target genes, Cut and FasciclinIII, which should normally be downregulated by Notch. Altogether, our study revealed that Sec3 governs egg chamber development through the regulation of Notch, and provides fresh insights into the regulation of oogenesis.
Highlights
Notch signaling is an evolutionarily conserved pathway that controls various processes, including embryogenesis and cell differentiation (Lai, 2004; Kopan and Ilagan, 2009)
We show that the loss of sec3 phenocopies loss-of-function Notch during Drosophila oogenesis
Loss of sec3 Results in Egg Chamber Fusion sec3GTand sec3PBac are two loss-of-function alleles of Drosophila sec3 which were identified previously (Wan et al, 2013). sec3 mutant follicle cell clones were generated with the Flp/FRT method and egg chambers were stained for the oocyte marker
Summary
Notch signaling is an evolutionarily conserved pathway that controls various processes, including embryogenesis and cell differentiation (Lai, 2004; Kopan and Ilagan, 2009). Vesicle-mediated protein traffic is essential for the transduction of the Notch pathway. The newly synthesized Notch receptor and DSL (Delta/Serrate/LAG-2) ligands are transported through the endoplasmic reticulum (ER) and Golgi apparatus to reach the plasma membrane. The receptors re-enter the cell via endocytosis. These endocytic vesicles from the cell membrane fuse with early endosome. The early endosome works as a sorting center, from which the Notch can be recycled back to the plasma membrane, or to the late endosome for protein degradation (Sorkin and von Zastrow, 2009)
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