Abstract Colletotrichum viniferum, the causal agent of grape ripe rot and leaf spot, poses a serious threat to grape yield and fruit quality. Like many phytopathogens, C. viniferum secretes effector proteins; however, the molecular mechanisms by which these effectors manipulate host immune responses remain poorly understood. In this study, we functionally characterized a candidate effector, CvA10999. CvA10999 suppressed INF1 (infestans 1, P. infestans PAMP elicitor) triggered cell death in Nicotiana benthamiana and was significantly upregulated during C. viniferum infection of susceptible grape V. vinifera cv. Thompson Seedless (TS) leaves. Targeted deletion of CvA10999 resulted in reduced sporulation, abnormal appressorium formation, and attenuated virulence on TS leaves. Further analysis revealed that CvA10999 interacts with the grape protein β-subunit of sucrose non-fermenting 1-related protein kinase (VvSnRKb1). Transient overexpression of VvSnRKb1 in TS leaves, as well as stable transgenic grapevines overexpressing VvSnRKb1, conferred enhanced resistance to C. viniferum. Mechanistically, CvA10999 bound to VvSnRKb1, disrupting its interaction with nonexpressor of pathogenesis-related genes 1 (VvNPR1) and interfering with VvNPR1 phosphorylation. This likely impaired the transcriptional activator function of VvNPR1 and downregulated salicylic acid (SA)-responsive pathogenesis-related (PR) genes. Collectively, these findings demonstrate that CvA10999 targets VvSnRKb1 to subvert host immunity and promote C. viniferum infection.
Dou et al. (Thu,) studied this question.