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一种钙依赖蛋白激酶调节……中的防御反应。

A Calcium-Dependent Protein Kinase Regulates the Defense Response in .

作者信息

Zhang Jinghan, Sun Lifan, Wang Yu, Li Baiyang, Li Xiangguo, Ye Ziqin, Zhang Jie

机构信息

State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.

School of Life Sciences, Hebei University, Baoding, Hebei 071002, China.

出版信息

Mol Plant Microbe Interact. 2024 May;37(5):459-466. doi: 10.1094/MPMI-12-23-0208-R. Epub 2024 May 28.

Abstract

Citrus Huanglongbing (HLB), which is caused by ' Liberibacter asiaticus' (CLas), is one of the most destructive citrus diseases worldwide, and defense-related gene resources remain largely unexplored. Calcium signaling plays an important role in diverse biological processes. In plants, a few calcium-dependent protein kinases (CDPKs/CPKs) have been shown to contribute to defense against pathogenic microbes. The genome of encodes dozens of CPKs. In this study, the role of calcium-dependent protein kinases (CsCPKs) in defense was investigated. Silencing of compromised the induction of defense-related genes in . Expression of a constitutively active form of CsCPK6 (CsCPK6) triggered the activation of defense-related genes in . Complementation of CsCPK6 rescued the defense-related gene induction in an mutant, indicating that CsCPK6 carries CPK activity and is capable of functioning as a CPK in . Moreover, an effector derived from CLas inhibits defense induced by the expression of and autophosphorylation of CsCPK6, which suggests the involvement of CsCPK6 and calcium signaling in defense. These results support a positive role for CsCPK6 in defense against CLas, and the autoinhibitory regulation of CsCPK6 provides a potential genome-editing target for improving defense. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

摘要

柑橘黄龙病(HLB)由亚洲韧皮杆菌(CLas)引起,是全球最具毁灭性的柑橘病害之一,与防御相关的基因资源在很大程度上仍未被探索。钙信号在多种生物学过程中发挥着重要作用。在植物中,一些钙依赖蛋白激酶(CDPKs/CPKs)已被证明有助于抵御病原微生物。[植物名称]的基因组编码数十种CPKs。在本研究中,研究了钙依赖蛋白激酶(CsCPKs)在[植物名称]防御中的作用。[植物名称]中[基因名称]的沉默削弱了防御相关基因的诱导。组成型活性形式的CsCPK6(CsCPK6)的表达触发了[植物名称]中防御相关基因的激活。CsCPK6的互补挽救了[突变体名称]突变体中防御相关基因的诱导,表明CsCPK6具有CPK活性,并且能够在[植物名称]中作为CPK发挥作用。此外,一种源自CLas的效应物抑制了[植物名称]表达诱导的防御以及CsCPK6的自磷酸化,这表明CsCPK6和钙信号参与了防御。这些结果支持CsCPK6在[植物名称]抵御CLas中的积极作用,并且CsCPK6的自抑制调节为改善[植物名称]防御提供了一个潜在的基因组编辑靶点。[公式:见正文] 版权所有© 2024作者。这是一篇根据知识共享署名 - 非商业性使用 - 禁止演绎4.0国际许可协议分发的开放获取文章。

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