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CaPti1-CaERF3 模块通过增强免疫和耐旱性来正向调控辣椒对青枯病的抗性。

The CaPti1-CaERF3 module positively regulates resistance of Capsicum annuum to bacterial wilt disease by coupling enhanced immunity and dehydration tolerance.

机构信息

Key Laboratory of Applied Genetics of Universities in Fujian Province, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.

Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.

出版信息

Plant J. 2022 Jul;111(1):250-268. doi: 10.1111/tpj.15790. Epub 2022 May 13.

Abstract

Bacterial wilt, a severe disease involving vascular system blockade, is caused by Ralstonia solanacearum. Although both plant immunity and dehydration tolerance might contribute to disease resistance, whether and how they are related remains unclear. Herein, we showed that immunity against R. solanacearum and dehydration tolerance are coupled and regulated by the CaPti1-CaERF3 module. CaPti1 and CaERF3 are members of the serine/threonine protein kinase and ethylene-responsive factor families, respectively. Expression profiling revealed that CaPti1 and CaERF3 were upregulated by R. solanacearum inoculation, dehydration stress, and exogenously applied abscisic acid (ABA). They in turn phenocopied each other in promoting resistance of pepper (Capsicum annuum) to bacterial wilt not only by activating salicylic acid-dependent CaPR1, but also by activating dehydration tolerance-related CaOSM1 and CaOSR1 and inducing stomatal closure to reduce water loss in an ABA signaling-dependent manner. Our yeast two hybrid assay showed that CaERF3 interacted with CaPti1, which was confirmed using co-immunoprecipitation, bimolecular fluorescence complementation, and pull-down assays. Chromatin immunoprecipitation and electrophoretic mobility shift assays showed that upon R. solanacearum inoculation, CaPR1, CaOSM1, and CaOSR1 were directly targeted and positively regulated by CaERF3 and potentiated by CaPti1. Additionally, our data indicated that the CaPti1-CaERF3 complex might act downstream of ABA signaling, as exogenously applied ABA did not alter regulation of stomatal aperture by the CaPti1-CaERF3 module. Importantly, the CaPti1-CaERF3 module positively affected pepper growth and the response to dehydration stress. Collectively, the results suggested that immunity and dehydration tolerance are coupled and positively regulated by CaPti1-CaERF3 in pepper plants to enhance resistance against R. solanacearum.

摘要

青枯病是一种严重的血管阻塞性疾病,由青枯雷尔氏菌引起。尽管植物免疫和脱水耐性都可能有助于抗病性,但它们之间的关系及其相互作用机制尚不清楚。在此,我们表明,青枯雷尔氏菌的免疫反应和脱水耐性是相关的,并受 CaPti1-CaERF3 模块的调控。CaPti1 和 CaERF3 分别是丝氨酸/苏氨酸蛋白激酶和乙烯响应因子家族的成员。表达谱分析表明,CaPti1 和 CaERF3 被青枯雷尔氏菌接种、脱水胁迫和外源施加脱落酸(ABA)上调。它们通过激活水杨酸依赖性 CaPR1,以及激活与脱水耐性相关的 CaOSM1 和 CaOSR1 来促进辣椒对青枯病的抗性,从而彼此表型模拟,同时通过 ABA 信号依赖的方式诱导气孔关闭来减少水分损失。我们的酵母双杂交实验表明,CaERF3 与 CaPti1 相互作用,该相互作用通过共免疫沉淀、双分子荧光互补和下拉实验得到了证实。染色质免疫沉淀和电泳迁移率变动分析表明,接种青枯雷尔氏菌后,CaPR1、CaOSM1 和 CaOSR1 被 CaERF3 直接靶向并正向调控,且受 CaPti1 增强。此外,我们的数据表明,CaPti1-CaERF3 复合物可能作用于 ABA 信号下游,因为外源施加的 ABA 不会改变 CaPti1-CaERF3 模块对气孔开度的调控。重要的是,CaPti1-CaERF3 模块对辣椒生长和对脱水胁迫的响应具有正向影响。总的来说,这些结果表明,在辣椒植物中,CaPti1-CaERF3 模块正向调控免疫和脱水耐性的耦联,以增强对青枯雷尔氏菌的抗性。

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