Cdc14 phosphatase downmodulates ESCRT-0 complex formation on vacuolar membranes and microautophagy after TORC1 inactivation
Cdc14 phosphatase downmodulates ESCRT-0 complex formation on vacuolar membranes and microautophagy after TORC1 inactivation
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TORC1 失活后，Cdc14 磷酸酶下调液泡膜上 ESCRT-0 复合物的形成和微自噬
DOI：
10.1016/j.bbrc.2021.05.021
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发表时间：
2021
影响因子：
3.1
通讯作者：
and Takashi Ushimaru
中科院分区：
文献类型：
--
作者：
Tasnuva Sharmin;Shamsul Morshed;Most Naoshia Tasnin;Tsuneyuki Takuma;and Takashi Ushimaru
由运输所需的内体分选复合体（ESCRT）介导的液泡膜重塑是芽殖酵母诱导微自噬的关键。营养耗竭和雷帕霉素复合物1 （TORC1）蛋白激酶靶蛋白失活可引起ESCRT-0复合物（Vps27-Hse1）在液泡膜上募集，并诱导escrt介导的微自噬。有丝分裂蛋白磷酸酶Cdc14在营养饥饿和TORC1失活后的巨噬诱导中拮抗TORC1介导的磷酸化。在这里，我们报道了在TORC1失活后，Cdc14下调微自噬诱导。在TORC1失活后，Cdc14功能障碍刺激了Hse1的空泡膜募集，而Vps27则没有，从而促进了ESCRT-0复合物的形成。相反，在TORC1失活后，cdc14的过表达会影响空泡膜上Hse1的募集和微自噬的诱导。因此，Cdc14磷酸酶以相反的方向调节两种自噬的通量，即诱导巨噬和减弱微自噬。
Remodeling of vacuolar membranes mediated by endosomal sorting complex required for transport (ESCRT) is critical for microautophagy induction in budding yeast. Nutrient depletion and inactivation of target of rapamycin complex 1 (TORC1) protein kinase elicit recruitment of the ESCRT-0 complex (Vps27–Hse1) onto vacuolar membranes and ESCRT-mediated microautophagy induction. Mitotic protein phosphatase Cdc14 antagonizes TORC1-mediated phosphorylation in macroautophagy induction after nutrient starvation and TORC1 inactivation. Here, we report that Cdc14 downregulates microautophagy induction after TORC1 inactivation. Cdc14 dysfunction stimulated the vacuolar membrane recruitment of Hse1, but not Vps27, after TORC1 inactivation, promoting ESCRT-0 complex formation. Conversely, overexpression ofCDC14compromises Hse1 recruitment on vacuolar membranes and microautophagy induction after TORC1 inactivation. Thus, Cdc14 phosphatase regulates the fluxes of two types of autophagy in the opposite directions, namely, it elicits macroautophagy and attenuates microautophagy.