Both Light-Induced SA Accumulation and ETI Mediators Contribute to the Cell Death Regulated by BAK1 and BKK1.
Both Light-Induced SA Accumulation and ETI Mediators Contribute to the Cell Death Regulated by BAK1 and BKK1.
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光诱导的 SA 积累和 ETI 介质均有助于 BAK1 和 BKK1 调节的细胞死亡
DOI：
10.3389/fpls.2017.00622
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发表时间：
2017
影响因子：
5.6
通讯作者：
He K
中科院分区：
文献类型：
--
作者：
Gao Y;Wu Y;Du J;Zhan Y;Sun D;Zhao J;Zhang S;Li J;He K
受体样激酶BAK 1和BKK 1调节多种细胞过程，包括油菜素类固醇信号传导和PRR介导的拟南芥PTI。我们以前的报道也证明了bak 1 bkk 1双突变体在正常生长条件下表现出自发性细胞死亡表型。由于未知的机制，bak 1 bkk 1中的细胞死亡在黑暗中生长时被显著抑制，但可以被光快速诱导。此外，对BAK 1和BKK 1调节的细胞死亡途径中涉及的内在组分知之甚少。在这项研究中，我们分析了光如何作为细胞死亡的启动子，并确定了ETI组分作为bak 1 bkk 1细胞死亡信号传导的介质。细胞死亡抑制bak 1 bkk 1生长在黑暗条件下复发后外源性处理SA。SA生物合成相关基因SID 2和EDS 5编码叶绿体定位蛋白，在bak 1 -4 bkk 1 -1中高表达。当与bak 1 -3杂交时，bkk 1 -1、bkk 2或eds 5能够有效地抑制细胞死亡。这表明过量产生的SA对于诱导在光下生长的bak 1 bkk 1中的细胞死亡至关重要。值得注意的是，bak 1 -3或bkk 1 -1单突变体显示出更敏感，但bak 1 -3 bkk 1 -1双突变体表现出对细菌病原体的增强的抗性，这表明在bak 1 bkk 1中激活了除PTI之外的免疫信号传导。此外，遗传分析表明，EDS 1或PAD 4（ETI关键介质）的突变显著抑制bak 1 -3 bkk 1 -1中的细胞死亡。在这项研究中，我们发现，光引发的SA积累在诱导bak 1 bkk 1细胞死亡中起主要作用，由ETI组分介导。
Receptor-like kinases BAK1 and BKK1 modulate multiple cellular processes including brassinosteroid signaling and PRR-mediated PTI in Arabidopsis. Our previous reports also demonstrated that bak1 bkk1 double mutants exhibit a spontaneous cell death phenotype under normal growth condition. With an unknown mechanism, the cell death in bak1 bkk1 is significantly suppressed when grown in dark but can be quickly induced by light. Furthermore, little is known about intrinsic components involved in BAK1 and BKK1-regulated cell death pathway. In this study, we analyzed how light functions as an initiator of cell death and identified ETI components to act as mediators of cell death signaling in bak1 bkk1. Cell death suppressed in bak1 bkk1 by growing in dark condition recurred upon exogenously treated SA. SA biosynthesis-related genes SID2 and EDS5, which encode chloroplast-localized proteins, were highly expressed in bak1-4 bkk1-1. When crossed to bak1-3 bkk1-1, sid2 or eds5 was capable of efficiently suppressing the cell death. It suggested that overly produced SA is crucial for inducing cell death in bak1 bkk1 grown in light. Notably, bak1-3 or bkk1-1 single mutant was shown to be more susceptible but bak1-3 bkk1-1 double mutant exhibited enhanced resistance to bacterial pathogen, suggesting immune signaling other than PTI is activated in bak1 bkk1. Moreover, genetic analyses showed that mutation in EDS1 or PAD4, key ETI mediator, significantly suppressed the cell death in bak1-3 bkk1-1. In this study, we revealed that light-triggered SA accumulation plays major role in inducing the cell death in bak1 bkk1, mediated by ETI components.