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Rhizoctonia solani , one of the most detrimental necrotrophic pathogens, causes rice sheath blight and poses a severe threat to production. Focus on the function of effectors secreted by necrotrophic pathogens during infection has grown rapidly in recent years. However, little is known about the virulence and mechanisms of these proteins. In this study, we performed functional studies on putative effectors in R. solani and revealed that AGLIP1 out of 13 putative effectors induced cell death in Nicotiana benthamiana. AGLIP1 was also demonstrated to trigger cell death in rice protoplasts. The predicted lipase active sites and signal peptide (SP) of this protein were required for the cell death-inducing ability. AGLIP1 was greatly induced during R. solani infection in rice sheath. The AGLIP1's virulence function was further demonstrated by transgenic technology. The pathogenesis-related genes induced by pathogen-associated molecular pattern and bacteria were remarkably inhibited in AGLIP1-expressing transgenic Arabidopsis lines. Ectopic expression of AGLIP1 strongly facilitated disease progression in Arabidopsis caused by the type III secretion system-defective mutant from Pseudomonas syringae pv. tomato DC3000. Collectively, these results indicate that AGLIP1 is a possible effector that plays a significant role in pathogen virulence through inhibiting basal defenses and promoting disease development in plants. [ABSTRACT FROM AUTHOR]

Ustilaginoidea virens , the causal agent of rice false smut (RFS), has become one of the most devastating rice pathogens worldwide. As a group of essential virulence factors, the effectors in the filamentous fungus might play central roles in the interaction between plants and pathogens. However, little is known about the roles of individual effectors in U. virens virulence. In this study, we identified and characterized a small secreted cysteine-rich effector, SCRE2, in U. virens. SCRE2 was first confirmed as an effector through yeast secretion, protein localization and translocation assays, as well as its expression pattern during U. virens infection. Transient expression of SCRE2 in Nicotiana benthamiana suppressed necrosis-like defense symptoms triggered by the mammalian BAX and oomycete elicitin INF1 proteins. The ability of SCRE2 to inhibit immunity-associated responses in N. benthamiana , including elicitor-triggered cell death and oxidative burst, is further defined to a small peptide region SCRE268-85 through expressing a series of truncated proteins. Convincingly, ectopic expression of SCRE2 in the transgenic rice cells significantly inhibited pathogen-associated molecular pattern-triggered immunity including flg22- and chitin-induced defense gene expression and oxidative burst. Furthermore, the scre2 knockout mutant generated by the CRISPR/Cas9 system greatly attenuated in U. virens virulence to rice. Collectively, this study indicates that the effector SCRE2 is able to inhibit plant immunity and is required for full virulence of U. virens. [ABSTRACT FROM AUTHOR]