PUB4, a CERK1-Interacting Ubiquitin Ligase, Positively Regulates MAMP-Triggered Immunity in Arabidopsis

PUB4, a CERK1-Interacting Ubiquitin Ligase, Positively Regulates MAMP-Triggered Immunity in Arabidopsis
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DOI:
10.1093/pcp/pcz151
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发表时间:
2019-11-01
影响因子:
4.9
通讯作者:
Shibuya, Naoto
Shibuya, Naoto
中科院分区:
生物学2区
文献类型:
--
作者:
Desaki, Yoshitake;Takahashi, Shohei;Shibuya, Naoto

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赖氨酸基序 (LysM) 受体样激酶 CERK1 是针对碳水化合物微生物相关分子模式 (MAMP) 的植物免疫反应所必需的辅助受体。关于 CERK1 的直接下游信号传导成分,据报道 PBL27 等受体样细胞质激酶和其他 RLCK VII 成员可以积极调节免疫反应。在这项研究中,我们报道了一种新型的 CERK1 相互作用 E3 泛素连接酶 PUB4,也参与 MAMP 触发的免疫反应的调节。 PUB4 的敲除导致几丁质诱导的防御反应的改变,表明 PUB4 正向调节活性氧的产生和胼胝质沉积,但负向调节 MAPK 激活和防御基因表达。另一方面,对水杨酸(SA)合成途径突变体pub4和sid2双敲除突变体的详细分析表明,pub4突变体的矛盾表型实际上是由该突变体中SA的异常积累引起的,而PUB4是免疫反应的正调节因子。目前和最近关于 PUB4 作用的发现表明,PUB4 是一种独特的 E3 泛素连接酶,参与植物免疫和生长/发育的调节。
Lysin motif (LysM) receptor-like kinase CERK1 is a co-receptor essential for plant immune responses against carbohydrate microbe-associated molecular patterns (MAMPs). Concerning the immediate downstream signaling components of CERK1, receptor-like cytoplasmic kinases such as PBL27 and other RLCK VII members have been reported to regulate immune responses positively. In this study, we report that a novel CERK1-interacting E3 ubiquitin ligase, PUB4, is also involved in the regulation of MAMP-triggered immune responses. Knockout of PUB4 resulted in the alteration of chitin-induced defense responses, indicating that PUB4 positively regulates reactive oxygen species generation and callose deposition but negatively regulates MAPK activation and defense gene expression. On the other hand, detailed analyses of a double knockout mutant of pub4 and sid2, a mutant of salicylic acid (SA) synthesis pathway, showed that the contradictory phenotype of the pub4 mutant was actually caused by abnormal accumulation of SA in this mutant and that PUB4 is a positive regulator of immune responses. The present and recent findings on the role of PUB4 indicate that PUB4 is a unique E3 ubiquitin ligase involved in the regulation of both plant immunity and growth/development.