The Mechanisms Study Of How Xanthomonas Campestris Pv Campestris Effector Protein XopXccN Suppresses Plant Innate Immunity

Xanthomonas campestris pv campestris (Xcc) is a causal agent of black rot diseases on numerous crucifer plants including Brassica and Arabidopsis. Xcc secrete a large repertory of effector proteins into host cells via type III secretion system to modulate host responses, enabling successful infection and multiplication in host tissue. XopXccN is an effector protein of Xcc strain8004, and belongs to the XopN subfamily. Previous studies have shown that XopN contributes to the virulence of Xanthomonas campestris pv vesicatoria (Xcv) in host pepper and tomato plants. XopN interacts with tomato atypical receptor-like kinasel(TARK1) and TFT1, and virulence function of XopN in tomato is TARK1and TFT1dependent. In addition, XopN can inhibit PAMPs induced gene expression and callose deposition in tomato and Arabidopsis tissues, which is TFT1dependent. These results indicated that XopN is a inhibitor of the PAMPs induced immunity(PTI) signaling pathway and probably acts at downstream of PTI. It has been known that XopXccN also mediates virulence function in host Chinese radish, and XopXccN can interfere with photosystems, ROS generation and callose deposition during Xcc8004infection. However, XopN can not replace XopXccN for the virulence of Xcc8004, suggesting that the virulence targets of XopN and XopXccN may different in host plants. In this study, we generated an XopXccN deletion strain (Xcc8004â–³XopXccN) and found that XopXccN is required for Xcc8004full virulence in mesophyll of Arabidopsis. Transient expression of XopXccN in Arabidopsis protoplasts shows that XopXccN can suppress flg22-induced MAPKs activity, and inhibit MAPK activation triggered by the constitutive active MKK5DD, suggesting that XopAccN acts at MAPK cascades to inhibit PTI signaling. In addition, XopXccN can also suppress flg22-induced FRK1:LUC gene expression in Arabidopsis protoplasts. Truncated proteins assay showed that the suppression of FRK1::LUC transcription is dependent on full length of XopXccN. Together our results suggested that XopXccN is a inhibitor of the PTI signaling pathway, and inhibit downstream of MKK5.