Phytophthora sojae Effector PsCRN108 Targets CAMTA2 to Suppress HSP40 Expression and ROS Burst

Author:

Yang Zitong1,Ai Gan1,Lu Xinyu2,Li Yuke1,Miao Jinlu1,Song Wen1,Xu Heng1,Liu Jinding3,Shen Danyu1ORCID,Dou Daolong1ORCID

Affiliation:

1. Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China

2. Institute of Botany, Jiangsu Province and Chinese Academy of Sciences, Nanjing 210014, China

3. Bioinformatics Center, Academy for Advanced Interdisciplinary Studies, Nanjing Agricultural University, Nanjing 210095, China

Abstract

Oomycete pathogens secrete numerous crinkling and necrosis proteins (CRNs) to manipulate plant immunity and promote infection. However, the functional mechanism of CRN effectors is still poorly understood. Previous research has shown that the Phytophthora sojae effector PsCRN108 binds to the promoter of HSP90s and inhibits their expression, resulting in impaired plant immunity. In this study, we found that in addition to HSP90, PsCRN108 also suppressed other Heat Shock Protein ( HSP) family genes, including HSP40. Interestingly, PsCRN108 inhibited the expression of NbHSP40 through its promoter, but did not directly bind to its promoter. Instead, PsCRN108 interacted with NbCAMTA2, a negative regulator of plant immunity. NbCAMTA2 was a negative regulator of NbHSP40 expression, and PsCRN108 could promote such inhibition activity of NbCAMTA2. Our results elucidated the multiple roles of PsCRN108 in the suppression of plant immunity and revealed a new mechanism by which the CRN effector hijacked transcription factors to affect immunity. [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 Natural Science Foundation of China

China Agriculture Research System

Publisher

Scientific Societies

Subject

Agronomy and Crop Science,General Medicine,Physiology

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