Mla‐ and Rom1 ‐mediated control of microRNA398 and chloroplast copper/zinc superoxide dismutase regulates cell death in response to the barley powdery mildew fungus

Summary Barley ( Hordeum vulgare L.) M ildew resistance locus a ( M la ) confers allele‐specific interactions with natural variants of the ascomycete fungus B lumeria graminis f. sp. hordei ( B gh ), the causal agent of powdery mildew disease. Significant reprogramming of M la ‐mediated gene expression occurs upon infection by this obligate biotrophic pathogen. We utilized a proteomics‐based approach, combined with barley mla, required for M la12 resistance1 ( rar1 ) , and restoration of M la resistance1 ( rom1 ) mutants, to identify components of M la‐ directed signaling. Loss‐of‐function mutations in M la and R ar1 both resulted in the reduced accumulation of chloroplast copper/zinc superoxide dismutase 1 ( H v SOD 1), whereas loss of function in R om1 re‐established H v SOD 1 levels. In addition, both M la and R om1 negatively regulated hvu‐microRNA398 (hvu‐miR398), and up‐regulation of mi R 398 was coupled to reduced H v SOD 1 expression. B arley stripe mosaic virus ( BSMV )‐mediated over‐expression of both barley and A rabidopsis mi R 398 repressed accumulation of H v SOD 1, and BSMV ‐induced gene silencing of H v S od1 impeded M la ‐triggered H 2 O 2 and hypersensitive reaction ( HR ) at barley– B gh interaction sites. These data indicate that M la‐ and R om1 ‐regulated hvu‐mi R 398 represses H v SOD 1 accumulation, influencing effector‐induced HR in response to the powdery mildew fungus.