Wan Ping, Zheng Sumei, Chen Lai, Wang Dou, Liao Ting, Yan Xueming, Wang Xiaoji
School of Life Science, Jiangxi Science and Technology Normal University, Nanchang, China.
Experimental Animal Science and Technology Center, Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Front Physiol. 2019 Mar 29;10:345. doi: 10.3389/fphys.2019.00345. eCollection 2019.
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 egg chamber development. Loss of results in egg chamber fusion through the abolishment of cell differentiation. In addition, loss of increases cell numbers but decreases cell size. These defects phenocopy Notch pathway inactivation. In line with this, loss of 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 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.
外泌体复合体通过将分泌或循环的囊泡拴系到质膜上发挥多种作用。先前的研究表明，外泌体包含八个组分，它们可能具有一些冗余但又不同的功能。因此，研究每个组分的生物学功能很有意思。在这里，我们发现外泌体复合体的一个组分Sec3参与卵室发育。Sec3缺失通过细胞分化的消失导致卵室融合。此外，Sec3缺失会增加细胞数量但减小细胞大小。这些缺陷模拟了Notch信号通路失活。与此一致的是，Sec3缺失确实导致Notch蛋白积累，这表明Sec3缺失抑制了Notch向质膜的转运，并使无活性的Notch在细胞质中积累。Sec3缺失还导致两个Notch信号通路靶基因Cut和FasciclinIII的异位表达，而它们通常应该被Notch下调。总之，我们的研究表明Sec3通过调节Notch来控制卵室发育，并为卵子发生的调控提供了新的见解。
