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BIR2/BIR3 相关的磷酯酶 Dγ1 负调控植物免疫。

The BIR2/BIR3-Associated Phospholipase Dγ1 Negatively Regulates Plant Immunity.

机构信息

Department of Plant Biochemistry, Center for Plant Molecular Biology, University of Tübingen, 72076 Tübingen, Germany.

Swammerdam Institute for Life Sciences, Section Plant Cell Biology, University of Amsterdam, 1098 XH Amsterdam, The Netherlands.

出版信息

Plant Physiol. 2020 May;183(1):371-384. doi: 10.1104/pp.19.01292. Epub 2020 Mar 9.

DOI:10.1104/pp.19.01292
PMID:32152212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7210654/
Abstract

Plants have evolved effective strategies to defend themselves against pathogen invasion. Starting from the plasma membrane with the recognition of microbe-associated molecular patterns (MAMPs) via pattern recognition receptors, internal cellular signaling pathways are induced to ultimately fend off the attack. Phospholipase D (PLD) hydrolyzes membrane phospholipids to produce phosphatidic acid (PA), which has been proposed to play a second messenger role in immunity. The Arabidopsis () PLD family consists of 12 members, and for some of these, a specific function in resistance toward a subset of pathogens has been shown. We demonstrate here that Arabidopsis PLDγ1, but not its close homologs PLDγ2 and PLDγ3, is specifically involved in plant immunity. Genetic inactivation of resulted in increased resistance toward the virulent bacterium pv. DC3000 and the necrotrophic fungus As mutant plants responded with elevated levels of reactive oxygen species to MAMP treatment, a negative regulatory function for this PLD isoform is proposed. Importantly, PA levels in mutants were not affected compared to stressed wild-type plants, suggesting that alterations in PA levels are not likely the cause for the enhanced immunity in the line. Instead, the plasma-membrane-attached PLDγ1 protein colocalized and associated with the BAK1-INTERACTING RECEPTOR-LIKE KINASES BIR2 and BIR3, which are known negative regulators of pattern-triggered immunity. Moreover, complex formation of PLDγ1 and BIR2 was further promoted upon MAMP treatment. Hence, we propose that PLDγ1 acts as a negative regulator of plant immune responses in complex with immunity-related proteins BIR2 and BIR3.

摘要

植物已经进化出有效的策略来抵御病原体的入侵。从质膜开始,通过模式识别受体识别微生物相关分子模式 (MAMPs),内部细胞信号通路被诱导,最终抵御攻击。磷脂酶 D (PLD) 水解膜磷脂产生磷脂酸 (PA),PA 被认为在免疫中发挥第二信使的作用。拟南芥中的 PLD 家族由 12 个成员组成,其中一些成员在抵抗某些病原体方面具有特定的功能。我们在这里证明,拟南芥 PLDγ1,而不是其密切同源物 PLDγ2 和 PLDγ3,特异性参与植物免疫。PLDγ1 的基因失活导致对毒性细菌 pv. DC3000 和坏死真菌 的抗性增加。与野生型对照相比,突变体植物对 MAMP 处理表现出更高水平的活性氧,因此推测该 PLD 同工型具有负调节功能。重要的是,与应激野生型植物相比,突变体中的 PA 水平没有受到影响,这表明 PA 水平的改变不太可能是 突变体增强免疫的原因。相反,质膜附着的 PLDγ1 蛋白与 BAK1-INTERACTING RECEPTOR-LIKE KINASES BIR2 和 BIR3 共定位和关联,BIR2 和 BIR3 是模式触发免疫的已知负调节剂。此外,MAMP 处理进一步促进了 PLDγ1 和 BIR2 的复合物形成。因此,我们提出 PLDγ1 与免疫相关蛋白 BIR2 和 BIR3 形成复合物,作为植物免疫反应的负调节剂。

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