Cysteine protease RD21A regulated by E3 ligase SINAT4 is required for drought-induced resistance to Pseudomonas syringae in Arabidopsis
Cysteine protease RD21A regulated by E3 ligase SINAT4 is required for drought-induced resistance to Pseudomonas syringae in Arabidopsis
复制标题
拟南芥干旱诱导的丁香假单胞菌抗性需要受 E3 连接酶 SINAT4 调节的半胱氨酸蛋白酶 RD21A
DOI：
10.1093/jxb/eraa255
复制
发表时间：
2020-09-19
影响因子：
6.9
通讯作者：
Zhao, Bingyu
中科院分区：
文献类型：
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作者：
Liu, Yi;Wang, Kunru;Zhao, Bingyu
植物可以同时暴露在多种压力下。非生物胁迫和生物胁迫的相互作用可能会对植物的发育和健康产生协同或拮抗的影响。短暂的干旱胁迫可以刺激植物的免疫，然而，干旱诱导免疫的分子机制还很不清楚。在这项研究中，我们证明了半胱氨酸蛋白酶RD21A是干旱诱导免疫所必需的。暂时干旱处理的野生型拟南芥植株对细菌病原菌相关分子模式flg22变得更加敏感，触发气孔关闭，从而增加了对紫丁香假单胞菌的抗性。番茄DC3000(PST-DC3000)。Rd21a基因的敲除抑制了flg22触发的气孔关闭，降低了干旱诱导的免疫力。泛素E3连接酶SINAT4与RD21A相互作用，促进其体内降解。SINAT4的过表达也持续抑制干旱诱导的对PST-DC3000的免疫。细菌III型效应物AvrRxo1与SINAT4和RD21A相互作用，增强SINAT4活性，促进RD21A在体内的降解。因此，RD21A可能是干旱诱导免疫的正向调节因子，在致病过程中可能成为病原菌毒力效应分子的靶标。
Plants can be simultaneously exposed to multiple stresses. The interplay of abiotic and biotic stresses may result in synergistic or antagonistic effects on plant development and health. Temporary drought stress can stimulate plant immunity; however, the molecular mechanism of drought-induced immunity is largely unknown. In this study, we demonstrate that cysteine protease RD21A is required for drought-induced immunity. Temporarily drought-treated wild-type Arabidopsis plants became more sensitive to the bacterial pathogen-associated molecular pattern flg22, triggering stomatal closure, which resulted in increased resistance to Pseudomonas syringae pv. tomato DC3000 (Pst-DC3000). Knocking out rd21a inhibited flg22-triggered stomatal closure and compromised the drought-induced immunity. Ubiquitin E3 ligase SINAT4 interacted with RD21A and promoted its degradation in vivo. The overexpression of SINAT4 also consistently compromised the drought-induced immunity to Pst-DC3000. A bacterial type III effector, AvrRxo1, interacted with both SINAT4 and RD21A, enhancing SINAT4 activity and promoting the degradation of RD21A in vivo. Therefore, RD21A could be a positive regulator of drought-induced immunity, which could be targeted by pathogen virulence effectors during pathogenesis.