CBL-interacting protein kinase 31 regulates rice resistance to blast disease by modulating cellular potassium levels.

Rice blast disease caused by infection with Magnaporthe oryzae , a hemibiotrophic fungal pathogen, significantly reduces the yield production. However, the rice defense mechanism against blast disease remains elusive. To identify the genes involved in the regulation of rice defense to blast disease, dissociation (Ds) transposon tagging mutant lines were analyzed in terms of their response to M. oryzae isolate Guy11. Among them, CBL-interacting protein kinase 3 1 (CIPK 31) mutants were more susceptible than wild-type plants to blast. The CIPK31 transcript was found to be insensitive to Guy11 infection, and the CIPK31-GFP was localized to the cytosol and nucleus. Overexpression of CIPK31 promoted rice defense to blast. Further analysis indicated that CIPK31 interacts with Calcineurin B-like 2 (CBL2) and CBL6 at the plasma membrane, and cbl2 mutants are more susceptible to blast compared with wild-type plants, suggesting that calcium signaling might partially through the CBL2-CIPK31 signaling regulate rice defense. Yeast two-hybrid results showed that AKT1-like (AKT1L), a potential potassium (K+) channel protein, interacted with CIPK31, and the K+ level was significantly lower in the cipk31 mutants than in the wild-type control. In addition, exogenous potassium application increased rice resistance to blast, suggesting that CIPK31 might interact with AKT1L to increase K+ uptake, thereby promoting resistance to blast. Taken together, the results presented here demonstrate that CBL2-CIPK31-AKT1L is a new signaling pathway that regulates rice defense to blast disease. • CIPK31 positively regulates rice resistance to blast. • CBL2 interacts with CIPK31 and positively regulates blast resistance in rice. • CIPK31 interacts with AKT1L to control cellular K+ level. • Exogenous application of K+ enhances rice resistance to blast. • CBL2-CIPK31-AKT1L is a new signaling pathway that regulates rice defense to blast. [ABSTRACT FROM AUTHOR]