A Calcium-Dependent Protein Kinase Regulates the Defense Response in Citrus sinensis

Author:

Zhang Jinghan12,Sun Lifan1,Wang Yu1,Li Baiyang1,Li Xiangguo13,Ye Ziqin1,Zhang Jie1ORCID

Affiliation:

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

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

3. College of Agronomy, Shanxi Agricultural University, Taigu 030801, China

Abstract

Citrus Huanglongbing (HLB), which is caused by ‘ Candidatus Liberibacter asiaticus’ (CLas), is one of the most destructive citrus diseases worldwide, and defense-related Citrus sinensis 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 C. sinensis encodes dozens of CPKs. In this study, the role of C. sinensis calcium-dependent protein kinases (CsCPKs) in C. sinensis defense was investigated. Silencing of CsCPK6 compromised the induction of defense-related genes in C. sinensis. Expression of a constitutively active form of CsCPK6 (CsCPK6CA) triggered the activation of defense-related genes in C. sinensis. Complementation of CsCPK6 rescued the defense-related gene induction in an Arabidopsis thaliana cpk4/11 mutant, indicating that CsCPK6 carries CPK activity and is capable of functioning as a CPK in Arabidopsis. Moreover, an effector derived from CLas inhibits defense induced by the expression of CsCPK6CA and autophosphorylation of CsCPK6, which suggests the involvement of CsCPK6 and calcium signaling in defense. These results support a positive role for CsCPK6 in C. sinensis defense against CLas, and the autoinhibitory regulation of CsCPK6 provides a potential genome-editing target for improving C. sinensis 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 .

Funder

National Key Research and Development Program of China

National Natural Science Foundation of China

Youth Innovation Promotion Association of the Chinese Academy of Sciences

Publisher

Scientific Societies

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