Figure 7. A Model for Regulation of XA21-Mediated Innate Immunity by BiP3.

The XA21 LRR domain is responsible for recognition of Xoo strains carrying Ax21 [2], [7], [9]. XA21/Ax21 binding is hypothesized to activate the non-RD kinase domain leading to XA21 autophosphorylation and/or transphosphorylation of downstream target proteins [7], [13], [16]. XA21 transphosphorylates the RING finger ubiquitin ligase XB3, which is required for effective XA21-mediated resistance [16]. XB10 (OsWRKY62) [56] and other WRKY transcription factors either activate or repress PR genes [13], [56]. In plants, pathogen infection upregulates expression of PR genes [13], [57], [58], [59], resulting in increased translations of the corresponding proteins in the ER. The transiently accumulated unfolded and/or misfolded proteins cause ER stress, which, in Arabidopsis, activates BiPs [48]. During systemic acquired resistance, BiP helps to secrete accumulated PRs [22]. Our results suggest that excessive loading of unfolded and/or misfolded proteins during prolonged ER stress attenuates the signal transduction pathway causing the ER stress. In support of this model, BiP3 overexpression drives XA21 proteolysis and down-regulates the XA21-mediated immune response.