Effector FsSCR6 contributes to the virulence of Fusarium sacchari on sugarcane and suppresses plant immunity.
Pokkah Boeng disease caused by Fusarium sacchari seriously threatens the yield and quality of sugarcane worldwide. Effectors play a crucial role in the infection and colonization of pathogens. However, there were few reports on the virulence functions of F. sacchari effectors. To characterize effector functions and unravel the pathogenic mechanisms of F. sacchari, we identified an effector FsSCR6, which was vital for the virulence of F. sacchari. Gene knockout mutants showed no difference in growth rates and colony morphology from wild-type. However, the virulence of knockout mutants was severely impaired. Agrobacterium-mediated transient expression assays in Nicotiana benthamiana showed that FsSCR6 and FsSCR6Δsp (without signal peptide) performed cell death-suppressive activity inside plant cells. 3'3-diaminobenzidine staining and aniline blue staining assays showed that FsSCR6 significantly reduced the accumulation of reactive oxygen species and callose deposition triggered by BCL-2-Associated X protein (BAX) in N. benthamiana leaves. FsSCR6 significantly suppressed the relative expression of the marker genes of the hypersensitive responses and salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene-dependent immunity in N. benthamiana. Overall, FsSCR6 is required for F. sacchari virulence; it performs a function inside plant cells and suppresses the plant immune responses by regulating the SA-, JA- and ethylene-mediated defense pathways. These results clarify the function of this effector from F. sacchari and assist in dissecting the interaction between sugarcane and F. sacchari, ultimately contributing to sugarcane production.