The SsSmk1-SsSom1-SsMsb2 Pathway Regulates Infection Cushion Formation and Pathogenicity in Sclerotinia sclerotiorum

Sclerotinia sclerotiorum causes Sclerotinia stem rot on economically important plants, posing serious threats to food security worldwide. Host-induced gene silencing (HIGS) was reported as a promising strategy for preventing infections caused by S. sclerotiorum; however, highly effective HIGS gene targets are limited. During infection, transmembrane proteins sense cell surface signals to induce infection cushion differentiation. The regulatory pathways governing intracellular signal transduction and the expression patterns of these transmembrane proteins remain unclear. Here, we demonstrated that the transcription factor SsSom1 interacted with the mitogen-activated protein kinase SsSmk1. Deletion of SsSom1 abolished sclerotia formation, regulated infection cushions development and reduced pathogenicity of S. sclerotiorum. Biochemical analysis demonstrated that SsSom1 could bind to the promoter of SsMSB2 and the SsMsb2 protein interacts with SsSte50 to activate the SsSmk1-MAPK pathway, thereby driving infection cushion differentiation of S. sclerotiorum. Furthermore, ChIP-qPCR analysis demonstrated that in the presence of SsSmk1, SsSom1 significantly enhanced the transcriptional activity of SsMSB2 under infection cushion-induced conditions. Moreover, we infiltrated HIGS constructs targeting SsSOM1 in Nicotiana benthamiana, which reduced the virulence of S. sclerotiorum. Taken together, this study elucidated the SsSmk1-SsSom1-SsMsb2 regulated infection cushions formation and the pathogenicity of S. sclerotiorum, identifying SsSom1 as a potential HIGS target for Sclerotinia stem rot control.