An effector SsCVNH promotes the virulence of Sclerotinia sclerotiorum through targeting class III peroxidase AtPRX71

Authors: MA, MING - Huazhong Agricultural University; TANG, LIQUANG - Huazhong Agricultural University; SUN, RUI - Huazhong Agricultural University; LYU, XUELIANG - Huazhong Agricultural University; XIE, JIATAO - Huazhong Agricultural University; FU, YANGPING - Huazhong Agricultural University; LI, BO - Huazhong Agricultural University; CHEN, TAO - Huazhong Agricultural University; LIN, YANG - Huazhong Agricultural University; YU, XIAO - Huazhong Agricultural University; Chen, Weidong; JIANG, DAOHONG - Huazhong Agricultural University; CHENG, JIASEN - Huazhong Agricultural University

Submitted to: Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/17/2024
Publication Date: 5/2/2024
Citation: Ma, M., Tang, L., Sun, R., Lyu, X., Xie, J., Fu, Y., Li, B., Chen, T., Lin, Y., Yu, X., Chen, W., Jiang, D., Cheng, J. 2024. An effector SsCVNH promotes the virulence of Sclerotinia sclerotiorum through targeting class III peroxidase AtPRX71. Molecular Plant Pathology. 25(5): e13464. https://doi.org/10.1111/mpp.13464.
DOI: https://doi.org/10.1111/mpp.13464

Interpretive Summary: A good understanding of pathogenesis mechanisms is necessary to device effective strategies for controlling plant fiseases. Our knowledge of the pathogenic mechanisms for many plant diseases is insufficient. An example is Sclerotinia whit mold caused by Sclerotinia sclerotiorum. This pathogen secrets numerous effector proteins that interact with and manipulate host plant to lower plant immunity. This study investigated an effector protein called SsCVNH which contains the highly conserved CyanoVirin-N Homology (CVNH) domain. Cyanovirin-N (CV-N) protein was originally reported from a cyanobacterium and is very effective against human viruses including AIDS. In Sclerotinia, it is significantly upregulated during plant infection and required for full virulence. Deletion of SsCVNH lead to reduced virulence and heterologous expression of SsCVNH in Arabidopsis enhanced pathogen infection, inhibited plant pattern triggered immunity response and increased plant susceptibility to S. sclerotiorum. SsCVNH interacted with class ' peroxidase AtPRX71, a positive regulator of innate immunity against plant pathogens. This study reveals a new infection strategy employed by S. sclerotiorum in which the fungus suppresses the function of class ' peroxidases, the major component of plant defense system, advancing our understanding mechanisms of Sclerotinia pathogenesis.

Technical Abstract: To combat plants, many pathogens secrete effector proteins into the host to suppress host immunity and facilitate pathogen colonization. The necrotrophic pathogen Sclerotinia sclerotiorum causes severe plant diseases and results in enormous economic losses, in which secreted proteins play a crucial role. SsCVNH was previously reported as a secretory protein, and its expression was significantly upregulated at 3 hours after inoculation on the host plant. Here, we further demonstrated that deletion of SsCVNH leads to attenuated virulence. Heterologous expression of SsCVNH in Arabidopsis enhanced pathogen infection, inhibited the host PTI response and increased plant susceptibility to S. sclerotiorum. Further study showed that SsCVNH interacted with class ' peroxidase AtPRX71, a positive regulator of innate immunity against plant pathogens. In addition, SsCVNH could also interact with other class ' peroxidases, thus reducing peroxidase activity and suppressing plant immunity. Our results reveal a new S. sclerotiorum infection strategy employed by S. sclerotiorum in which the fungus suppresses the function of class ' peroxidases, the major component of PTI to promote its own infection.