Autophagy Negatively Regulates Cell Death by Controlling NPR1-Dependent Salicylic Acid Signaling during Senescence and the Innate Immune Response in Arabidopsis
Autophagy Negatively Regulates Cell Death by Controlling NPR1-Dependent Salicylic Acid Signaling during Senescence and the Innate Immune Response in Arabidopsis
复制标题
DOI：
10.1105/tpc.109.068635
复制
发表时间：
2009-09-01
期刊：
影响因子：
11.6
通讯作者：
Shirasu, Ken
中科院分区：
文献类型：
--
作者：
Yoshimoto, Kohki;Jikumaru, Yusuke;Shirasu, Ken
自噬是一种进化保守的细胞内过程，导致细胞质成分的空泡降解。在高等植物中，无论营养条件如何，自噬缺陷都会导致细胞提前衰老和过度免疫相关的程序性细胞死亡(PCD)；然而，细胞在没有自噬的情况下死亡的机制尚不清楚。在这里，我们证明了在自噬缺陷突变体(ATG突变体)中，这些现象对水杨酸(SA)信号的保守要求。在衰老和免疫过程中，加速PCD的ATG突变表型依赖SA信号，但不需要完整的茉莉酸或乙烯信号通路。SA激动剂的应用诱导了SA缺乏的ATG突变体的衰老/细胞死亡表型，但在ATG npr1植物中不诱导，这表明ATG突变体中的细胞死亡表型依赖于病程相关GENES1的SA信号转导NONEXPRESSOR。我们还表明自噬是由SA激动剂诱导的。这些发现表明，植物自噬运行一个新的负反馈环，调节SA信号，负调控衰老和免疫相关的PCD。
Autophagy is an evolutionarily conserved intracellular process for vacuolar degradation of cytoplasmic components. In higher plants, autophagy defects result in early senescence and excessive immunity-related programmed cell death (PCD) irrespective of nutrient conditions; however, the mechanisms by which cells die in the absence of autophagy have been unclear. Here, we demonstrate a conserved requirement for salicylic acid (SA) signaling for these phenomena in autophagy-defective mutants (atg mutants). The atg mutant phenotypes of accelerated PCD in senescence and immunity are SA signaling dependent but do not require intact jasmonic acid or ethylene signaling pathways. Application of an SA agonist induces the senescence/cell death phenotype in SA-deficient atg mutants but not in atg npr1 plants, suggesting that the cell death phenotypes in the atg mutants are dependent on the SA signal transducer NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1. We also show that autophagy is induced by the SA agonist. These findings imply that plant autophagy operates a novel negative feedback loop modulating SA signaling to negatively regulate senescence and immunity-related PCD.