WASH inhibits autophagy through suppression of Beclin 1 ubiquitination.

نویسندگان

  • Pengyan Xia
  • Shuo Wang
  • Ying Du
  • Zhenao Zhao
  • Lei Shi
  • Lei Sun
  • Guanling Huang
  • Buqing Ye
  • Chong Li
  • Zhonghua Dai
  • Ning Hou
  • Xuan Cheng
  • Qingyuan Sun
  • Lei Li
  • Xiao Yang
  • Zusen Fan
چکیده

Autophagy degrades cytoplasmic proteins and organelles to recycle cellular components that are required for cell survival and tissue homeostasis. However, it is not clear how autophagy is regulated in mammalian cells. WASH (Wiskott-Aldrich syndrome protein (WASP) and SCAR homologue) plays an essential role in endosomal sorting through facilitating tubule fission via Arp2/3 activation. Here, we demonstrate a novel function of WASH in modulation of autophagy. We show that WASH deficiency causes early embryonic lethality and extensive autophagy of mouse embryos. WASH inhibits vacuolar protein sorting (Vps)34 kinase activity and autophagy induction. We identified that WASH is a new interactor of Beclin 1. Beclin 1 is ubiquitinated at lysine 437 through lysine 63 linkage in cells undergoing autophagy. Ambra1 is an E3 ligase for lysine 63-linked ubiquitination of Beclin 1 that is required for starvation-induced autophagy. The lysine 437 ubiquitination of Beclin 1 enhances the association with Vps34 to promote Vps34 activity. WASH can suppress Beclin 1 ubiquitination to inactivate Vps34 activity leading to suppression of autophagy.

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عنوان ژورنال:
  • The EMBO journal

دوره 32 20  شماره 

صفحات  -

تاریخ انتشار 2013