A type III effector XopL is vital for Xanthomonas campestris pathovar campestris to regulate plant immunity.

Abstract

Xanthomonas campestris pv. campestris (Xcc) secretes a suite of effectors into host plants via the type III secretion system (T3SS), modulating plant immunity defenses. Strain Xcc8004 causes black rot in brassica plants, including Arabidopsis thaliana, making it a classical model for the study of Xanthomonas pathogenesis. XopL was defined as a T3SS effector (T3SE) since its homologues XopL from Xanthomonas campestris pv. vesicatoria (Xcv85-10) contribute to virulence in host plants. Except for its virulence on Chinese radish plants, little was previously known about the regulation and function of XopL. Here, we tested the role of XopL in the pathogenicity of Xcc8004 on different host plants including Arabidopsis. We found that it was required for full virulence of Xcc8004 in Chinese cabbage. XopL promoted bacterial infection in Arabidopsis and suppressed bacterial flagellin (flg22)-induced FRK1 transcription, reactive oxygen species (ROS) burst, callose deposition, and pathogenesis-related marker gene expression, but it did not affect mitogen-activated protein kinases (MAPKs) cascade. Early and prolonged expression of XopL affected Arabidopsis growth and development. We demonstrated that XopL is a virulence factor and interferes with innate immunity of Arabidopsis by suppressing pathogen-associated molecular pattern-triggered immunity (PTI) signaling, independent of MAPKs.