Genetic Analyses of the Arabidopsis ATG1 Kinase Complex Reveal Both Kinase-Dependent and Independent Autophagic Routes during Fixed-Carbon Starvation

编号 040021603

推送时间 20191209

研究领域 森林培育 

年份 2019 

类型 期刊 

语种 英语

标题 Genetic Analyses of the Arabidopsis ATG1 Kinase Complex Reveal Both Kinase-Dependent and Independent Autophagic Routes during Fixed-Carbon Starvation

来源期刊 The Plant Cell

期 第216期

发表时间 20191015

关键词 autophagy;  ATG1 kinase complex;  nitrogen starvation;  fixed-carbon starvation; 
SnRK1;  vacuole;  Arabidopsis; 

摘要 Under nutrient and energy-limiting conditions, plants up-regulate sophisticated catabolic pathways such as autophagy to remobilize nutrients and restore energy homeostasis. Autophagic flux is tightly regulated under these circumstances through the autophagy-related (ATG)-1 kinase complex, which relays upstream nutrient and energy signals to the downstream components that drive autophagy. Here, we investigated the role(s) of the Arabidopsis ATG1 kinase during autophagy through an analysis of a quadruple mutant deficient in all four ATG1 isoforms. These isoforms appear to act redundantly, including the plant-specific, truncated ATG1t variant, and like other well-characterized atg mutants, homozygous atg1abct plants display early leaf senescence and hypersensitivity to nitrogen and fixed-carbon starvation. Although the ATG1 kinase is essential for up-regulating autophagy under nitrogen deprivation and short-term carbon starvation, it did not stimulate autophagy under prolonged carbon starvation. Instead, an ATG1-independent response arose requiring the phosphatidylinositol-3-phosphate (PI3K) and Sucrose-Non-Fermenting Kinase (SnRK)-1 kinases, possibly through phosphorylation of the ATG6 subunit within the PI3K complex by the catalytic KIN10 subunit of SnRK1. Together, our data connect the ATG1 kinase to autophagy, and reveal that plants engage multiple pathways to activate autophagy during nutrient stress, which include the ATG1 route as well as an alternative route requiring SnRK1 and ATG6 signaling.

服务人员 孙小满

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