Phosphorylation of CPR5 by the receptor-like kinase FLR2 promotes mRNA poly(A) tail processing and immunity to Magnaporthe oryzae in rice.

Regulation of RNA metabolism is crucial for the modulation of gene expression in plants exposed to external stresses. However, the mechanism by which plant membrane receptors transmit external signals to regulate RNA metabolism has not been determined. In this study, we show that FERONIA-like receptor 2 (FLR2) modulates innate immunity in rice by inducing the translation of the immune regulator OsEIL1, thereby promoting resistance to Magnaporthe oryzae. FLR2 interacts with and phosphorylates the mRNA processing factor CONSTITUTIVE EXPRESSER OF PATHOGENESIS-RELATED GENES 5 (CPR5), leading to modulation of OsEIL1 poly(A) tail length and translation in response to M. oryzae infection. Like the flr2 loss-of-function mutant, the cpr5 mutant exhibited increased resistance to M. oryzae, induced reactive oxygen species generation, and activated the MAPK cascade. Furthermore, the phospho-dead cpr5 mutant (cpr5(mut5A)), in which the FLR2 phosphorylation sites are altered, could not rescue the cpr5 phenotype and resulted in longer OsEIL1 poly(A) tails than in the wild type. Conversely, the phospho-mimic cpr5(mut5D) restored both the wild-type phenotype and OsEIL1 poly(A) tail length in the cpr5 mutant background. These findings suggest that FLR2 perceives external stressors and regulates RNA metabolism via CPR5, revealing a novel posttranscriptional regulatory pathway in rice.