SABRE is required not only for growth but also for osmotic tolerance and suppression of cell death in Arabidopsis thaliana

Acquired osmotolerance induced after salt stress is widespread across Arabidopsis thaliana accessions, and is conferred by disruption of an NLR gene, designated ACQOS, whose derepression under osmotic stress causes detrimental autoimmunity via EDS1/PAD4. However, it remains unclear how the tolerance is established. To reveal the mechanism of acquired osmotolerance, we performed a forward genetic screening and isolated acquired osmotolerance defective10 (aod10) from ion-beam-mutagenized Bu-5 seeds. The aod10 displayed growth retardation with short roots and osmo-sensitive phenotype. Even under normal growth conditions, pathogenesis-related genes were strongly induced in aod10 but not in wild type. The osmo-sensitive phenotype of aod10 was suppressed by high temperature of 28°C, at which compromised immune responses through TIR-NLR and EDS1/PAD4. It suggests that the detrimental autoimmunity renders aod10 sensitive to osmotic stress. As results of genetic analyses, we found a 45 bp deletion in SABRE within the causal region of aod10. The sabre_Bu-5 generated by editing of SABRE gene in Bu-5 using the CRISPR/Cas9 system exhibited osmo-sensitive phenotype and enhancement of cell death and autoimmunity as well as aod10. These findings suggest that SABRE is the causal gene of aod10. Taken together, AOD10/SABRE is required not only for growth but also for osmotic tolerance and suppression of cell death in Arabidopsis.