Perception of unrelated microbe-associated molecular patterns triggers conserved yet variable physiological and transcriptional changes in Brassica rapa ssp.pekinensis

Pattern-triggered immunity(PTI)includes the different transcriptional and physiological responses that enable plants to ward off microbial invasion.Surface-localized pattern-recognition receptors(PRRs)recognize conserved microbeassociated molecular patterns(MAMPs)and initiate a branched signaling cascade that culminate in an effective restriction of pathogen growth.In the model species Arabidopsis thaliana,early PTI events triggered by different PRRs are broadly conserved although their nature or intensity is dependent on the origin and features of the detected MAMP.In order to provide a functional basis for disease resistance in leafy vegetable crops,we surveyed the conservation of PTI events in Brassica rapa ssp.pekinensis.We identified the PRR homologs present in B.rapa genome and found that only one of the two copies of the bacterial Elongation factor-Tu receptor(EFR)might function.We also characterized the extent and unexpected specificity of the transcriptional changes occurring when B.rapa seedlings are treated with two unrelated MAMPs,the bacterial flagellin flg22 peptide and the fungal cell wall component chitin.Finally,using a MAMP-induced protection assay,we could show that bacterial and fungal MAMPs elicit a robust immunity in B.rapa,despite significant differences in the kinetic and amplitude of the early signaling events.Our data support the relevance of PTI for crop protection and highlight specific functional target for disease resistance breeding in Brassica crops.

Direct acetylation of a conserved threonine of RIN4 by the bacterial effector HopZ5 or AvrBsT activates RPM1-dependent immunity in Arabidopsis

Plant pathogenic bacteria deliver effectors into plant cells to suppress immunity and promote pathogen survival;however, these effectors can be recognised by plant disease resistance (R) proteins to activate innate immunity. The bacterial acetyltransferase effectors HopZ5 and AvrBsT trigger immunity in Arabidopsis thaliana genotypes lacking SUPPRESSOR OF AVRBST-ELICITED RESISTANCE 1 (SOBER1). Using an Arabidopsis accession, Tscha-1, that naturally lacks functional SOBER1 but is unable to recognise HopZ5, we demonstrate that RESISTANCE TO P. SYRINGAE PV MACULICOLA 1 (RPM1) and RPM1-INTERACTING PROTEIN 4 (RIN4) are indispensable for HopZ5- or AvrBsT-triggered immunity. Remarkably, T166 of RIN4, the phosphorylation of which is induced by AvrB and AvrRpm1, was directly acetylated by HopZ5 and AvrBsT. Furthermore, we demonstrate that the acetylation of RIN4 T166 is required and sufficient for HopZ5- or AvrBsT-triggered RPM1-dependent defence activation. Finally, we show that SOBER1 interferes with HopZ5- or AvrBsT-triggered immunity by deacetylating RIN4 T166. We have thus elucidated detailed molecular mechanisms underlying the activation and suppression of plant innate immunity triggered by two bacterial acetyltransferases, HopZ5 and AvrBsT from different bacterial pathogens.