自噬
下调和上调
细胞生物学
溶酶体
液泡
泛素
蛋白酶体
跨膜蛋白
蛋白质降解
生物
袋3
化学
衰老
脱氮酶
基因敲除
蛋白质稳态
ATG5型
粒体自噬
自噬体
ULK1
内体
程序性细胞死亡
生物化学
基因
酶
细胞凋亡
受体
蛋白激酶A
细胞质
安普克
磷酸化
作者
Yuchen Feng,Aileen Ariosa,Ying Yang,Zehan Hu,Jörn Dengjel,Daniel J. Klionsky
标识
DOI:10.1073/pnas.2005539118
摘要
Macroautophagy/autophagy is a highly conserved eukaryotic molecular process that facilitates the recycling of superfluous cytoplasmic materials, damaged organelles, and invading pathogens, resulting in proper cellular homeostasis and survival during stress conditions. Autophagy is stringently regulated at multiple stages, including control at transcriptional, translational, and posttranslational levels. In this work, we identified a mechanism by which regulation of autophagy is achieved through the posttranslational modification of Atg9. Here, we show that, in order to limit autophagy to a low, basal level during normal conditions, Atg9 is ubiquitinated and subsequently targeted for degradation in a proteasome-dependent manner through the action of the E3 ligase Met30. When cells require increased autophagy flux to respond to nutrient deprivation, the proteolysis of Atg9 is significantly reduced. Overall, this work reveals an additional layer of mechanistic regulation that allows cells to further maintain appropriate levels of autophagy and to rapidly induce this process in response to stress.
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