Genetic Analyses of the Arabidopsis ATG1 Kinase Complex Reveal Both Kinase-Dependent and Independent Autophagic Routes during Fixed-Carbon Starvation
Genetic Analyses of the Arabidopsis ATG1 Kinase Complex Reveal Both Kinase-Dependent and Independent Autophagic Routes during Fixed-Carbon Starvation
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拟南芥 ATG1 激酶复合物的遗传分析揭示了固定碳饥饿期间激酶依赖性和独立的自噬途径
DOI：
10.1105/tpc.19.00066
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发表时间：
2019-12-01
期刊：
影响因子：
11.6
通讯作者：
Li, Faqiang
中科院分区：
文献类型：
--
作者：
Huang, Xiao;Zheng, Chunyan;Li, Faqiang
在营养和能量有限的条件下，植物上调复杂的分解代谢途径，如自噬，以重新调动营养物质和恢复能量稳态。在这些情况下，自噬通量通过AutophaGy相关1（ATG 1）激酶复合物进行严格调节，该激酶复合物将上游营养和能量信号传递给驱动自噬的下游组分。在这里，我们调查的作用（S）的拟南芥（拟南芥）ATG 1激酶在自噬过程中，通过分析的四个突变体缺陷的所有四个ATG 1亚型。这些异构体似乎冗余地起作用，包括植物特异性的截短的ATG 1 t变体，并且像其他充分表征的atg突变体一样，纯合atg 1abct四重突变体显示早期叶片衰老和对氮和固定碳饥饿的超敏反应。尽管ATG 1激酶在氮剥夺和短期碳饥饿下上调自噬是必不可少的，但它在长期碳饥饿下不刺激自噬。相反，一种不依赖于ATG 1的反应需要磷脂酰肌醇-3-磷酸激酶（PI 3 K）和蔗糖非发酵1相关蛋白激酶1（SnRK 1），这可能是通过SnRK 1的催化性KIN 10亚基磷酸化PI 3 K复合物内的ATG 6亚基实现的。总之，我们的数据将ATG 1激酶与自噬联系起来，并揭示了植物在营养胁迫期间参与多种途径来激活自噬，其中包括ATG 1途径以及需要SnRK 1和ATG 6信号传导的替代途径。
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-related1 (ATG1) 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 (Arabidopsis thaliana) 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 quadruple mutants display early leaf senescence and hypersensitivity to nitrogen and fixed-carbon starvations. Although 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 phosphatidylinositol-3-phosphate kinase (PI3K) and SUCROSE NONFERMENTING1-RELATED PROTEIN KINASE1 (SnRK1), possibly through phosphorylation of the ATG6 subunit within the PI3K complex by the catalytic KIN10 subunit of SnRK1. Together, our data connect 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.