Abstract
Cytospora chrysosperma is the main causal agent of poplar canker disease in China, especially in some areas with poor site conditions. Pathogens secrete a large number of effectors to interfere the plant immunity and promote their infection and colonization. Nevertheless, the roles of effectors in C. chrysosperma remain poorly understood. In this study, we identified and functionally characterized a candidate effector CcSp84 from C. chrysosperma, which contained a nuclear localization signal motif at the C-terminal and was highly induced during infection stages. Transient expression of CcSp84 in Nicotiana benthamiana leaves could trigger cell death. Additionally, deletion of CcSp84 significantly reduced fungal virulence to the polar twigs, while no obvious defects were observed in fungal growth and sensitivity to H2O2. Confocal microscopy revealed that CcSp84 labeled with a green fluorescent protein (GFP) was mainly accumulated in the plant nucleus. Further analysis revealed that the plant nucleus localization of CcSp84 was necessary to trigger plant immune responses, including ROS accumulation, callose deposition, and induced expression of jasmonic acid and ethylene defense-related genes. Collectively, our results suggest that CcSp84 is a virulence-related effector, and plant nucleus localization is required for its functions.
Highlights
Cytospora chrysosperma is a necrotrophic fungal pathogen that causes stem canker in a broad range of hosts [1,2]
In Phytophthora infestans, RXLR effector Pi04314 could be active in the host nucleus to reduce the expression of jasmonic and salicylic acid-related defense genes and induce the relocation of three host protein phosphatase 1 catalytic isoforms from the nucleolus to nucleoplasm during infection to enhance leaf colonization [23]
The results showed that CcSp84 was required for the fungal pathogenicity and could trigger plant cell death in N. benthamiana leaves, while CcSp31 deletion mutants displayed no obvious defects compared to the wild type, and it could not trigger cell death or suppress the INF1-induced cell death in N. benthamiana
Summary
Cytospora chrysosperma is a necrotrophic fungal pathogen that causes stem canker in a broad range of hosts [1,2]. The transcription factor CcSge, belonging to the Gti1/Pac family, was essential to the hyphal radial growth, conidiation, and fungal virulence Both CcSge and CcPmk positively regulated the expression of the putative effector gene CcCAP1 in C. chrysosperma [10]. In Phytophthora infestans, RXLR effector Pi04314 could be active in the host nucleus to reduce the expression of jasmonic and salicylic acid-related defense genes and induce the relocation of three host protein phosphatase 1 catalytic isoforms from the nucleolus to nucleoplasm during infection to enhance leaf colonization [23]. PvAVH53 located in the plant nucleus and could interact with tobacco importin-α genes, NbImp-α1 and NbImp-α2, which were essential to induce cell death in N. benthamiana leaves. Further analyses suggest that the plant nucleus localization of CcSp84 was important for its activation functions
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