The IRE1-bZIP60 branch of Unfolded Protein Response is required for Arabidopsis immune response to B. cinerea

The Unfolded Protein Response (UPR) is a retrograde signalling pathway which is activated when endoplasmic reticulum (ER) proteostasis is disturbed. Here, we have investigated by reverse genetics the contribution of such pathway in Arabidopsis thaliana response to two necrotrophic fungi of agricultural importance, Botrytis cinerea which is responsible for the development of grey mold disease, and Alternaria brassicicola which triggers black spot disease. We found that the branch of UPR dependent on the INOSITOL-REQUIRING ENZYME 1 (IRE1) and the transcription factor (TF) bZIP60 is required to restrict foliar necrotic symptoms induced by both fungi. Accordingly, focussing on B. cinerea, we provided evidence for the production of the active bZIP60 form during infection. This activation was accompanied by an increased expression of UPR-responsive genes coding for ER-localized chaperones and co-chaperones that belong to the ER-Quality Control (ER-QC) system, and mutants deficient for two ER-QC components were also more susceptible to infection. By contrast, investigating the involvement of CELL DIVISION CYCLE 48 (CDC48) AAA+-ATPAses that assist ER-Associated Degradation (ERAD) pathway for disposal of luminal unfolded proteins, we showed that a series of mutants and transgenics are more resistant to grey mold disease. Seeking for molecular insights into how the ER could shape Arabidopsis immune response to B. cinerea, we quantified the expression of defence gene and cell death markers in single bzip60 and double ire1 mutants. However, none of those genes were mis-regulated in mutant genetic backgrounds, indicating that IRE1-bZIP60 branch of UPR modulates the Arabidopsis response to B. cinerea by a yet-to-be-identified mechanism. Interestingly, we identified the NAC053/NTL4 TF as a potential actor of this unknown mechanism, linking the UPR and proteasome stress regulon. ### Competing Interest Statement The authors have declared no competing interest.