Uba1 functions in Atg7-and Atg3-independent autophagy

被引:145
作者
Chang, Tsun-Kai [1 ]
Shravage, Bhupendra V. [1 ]
Hayes, Sebastian D. [2 ]
Powers, Christine M. [1 ]
Simin, Rachel T. [1 ]
Harper, J. Wade [2 ]
Baehrecke, Eric H. [1 ]
机构
[1] Univ Massachusetts, Sch Med, Dept Canc Biol, Worcester, MA 01605 USA
[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
关键词
STARVATION-INDUCED AUTOPHAGY; UBIQUITIN-ACTIVATING ENZYME; PROGRAMMED CELL-DEATH; GROWTH ARREST; MUTANTS; E1; DEGRADATION; INDUCTION; CYTOPLASM; REQUIRES;
D O I
10.1038/ncb2804
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Autophagy is a conserved process that delivers components of the cytoplasm to lysosomes for degradation. The E1 and E2 enzymes encoded by Atg7 and Atg3 are thought to be essential for autophagy involving the ubiquitin-like protein Atg8. Here, we describe an Atg7- and Atg3-independent autophagy pathway that facilitates programmed reduction of cell size during intestine cell death. Although multiple components of the core autophagy pathways, including Atg8, are required for autophagy and cells to shrink in the midgut of the intestine, loss of either Atg7 or Atg3 function does not influence these cellular processes. Rather, Uba1, the E1 enzyme used in ubiquitylation, is required for autophagy and reduction of cell size. Our data reveal that distinct autophagy programs are used by different cells within an animal, and disclose an unappreciated role for ubiquitin activation in autophagy.
引用
收藏
页码:1067 / +
页数:21
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