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钙依赖性 ABA 信号通过调节保卫细胞中快速的 SA 反应来参与气孔免疫。

Calcium-dependent ABA signaling functions in stomatal immunity by regulating rapid SA responses in guard cells.

机构信息

Gansu Key Laboratory of Protection and Utilization for Biological Resources and Ecological Restoration, College of Life Sciences and Technology, Longdong University, Qingyang, Gansu Province, 745000, China.

College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang Province, 310058, China.

出版信息

J Plant Physiol. 2022 Jan;268:153585. doi: 10.1016/j.jplph.2021.153585. Epub 2021 Dec 4.

DOI:10.1016/j.jplph.2021.153585
PMID:34894596
Abstract

Stomatal immunity is mediated by ABA, an osmotic stress-responsive phytohormone that closes stomata via calcium-dependent and -independent signaling pathways. However, the functional involvement of ABA signal transducers in stomatal immunity remains poorly understood. Here, we demonstrate that stomatal immunity was compromised in mutants of the ABA signaling core. We also found that it is a subset of calcium-dependent protein kinases (CPK4/5/6), but not the calcium-independent kinase OST1, that relay the stomatal immune signaling. Surface-inoculated bacteria caused an endogenous ABA-dependent induction of local SA responses, whilst expression of the ABA biosynthetic genes and the ABA levels were not affected in leaf epidermis. Furthermore, flg22-elicited ROS burst was attenuated by mutations in CPK4 and CPK5, and pathogen-induced SA production in leaf epidermis was compromised in cpk4, cpk5, and cpk6 mutants. Our results suggest that CPKs function in stomatal immunity through fine-tuning apoplastic ROS levels as well as reinforcing the localized SA signal in guard cells. It is also envisioned that ABA mediates stomatal responses to biotic and abiotic stresses via two distinct but partially overlapping signaling modules.

摘要

气孔免疫是由 ABA 介导的,ABA 是一种渗透胁迫响应的植物激素,通过钙依赖和非依赖的信号通路关闭气孔。然而,ABA 信号转导物在气孔免疫中的功能参与仍知之甚少。在这里,我们证明了 ABA 信号核心突变体的气孔免疫受损。我们还发现,是钙依赖性蛋白激酶(CPK4/5/6)的一个亚类,而不是钙非依赖性激酶 OST1,传递气孔免疫信号。表面接种的细菌引起局部 SA 反应的内源性 ABA 依赖性诱导,而叶片表皮中的 ABA 生物合成基因表达和 ABA 水平不受影响。此外,在 CPK4 和 CPK5 突变体中,flg22 诱导的 ROS 爆发减弱,而在 cpk4、cpk5 和 cpk6 突变体中,叶片表皮中病原体诱导的 SA 产生受损。我们的结果表明,CPKs 通过微调质外体 ROS 水平以及增强保卫细胞中局部 SA 信号来发挥作用。人们还设想 ABA 通过两个不同但部分重叠的信号模块介导气孔对生物和非生物胁迫的反应。

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