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

Authors

  • Weihui Xu,

    1. Department of Plant Pathology and Microbiology, Center for Plant Responses to Environmental Stresses, Iowa State University, Ames, IA, USA
    Search for more papers by this author
  • Yan Meng,

    1. Department of Plant Pathology and Microbiology, Center for Plant Responses to Environmental Stresses, Iowa State University, Ames, IA, USA
    Search for more papers by this author
  • Roger P. Wise

    Corresponding author
    1. Department of Plant Pathology and Microbiology, Center for Plant Responses to Environmental Stresses, Iowa State University, Ames, IA, USA
    2. Corn Insects and Crop Genetics Research Unit, US Department of Agriculture-Agricultural Research Service, Iowa State University, Ames, IA, USA
    Search for more papers by this author

Summary

  • Barley (Hordeum vulgare L.) Mildew resistance locus a (Mla) confers allele-specific interactions with natural variants of the ascomycete fungus Blumeria graminis f. sp. hordei (Bgh), the causal agent of powdery mildew disease. Significant reprogramming of Mla-mediated gene expression occurs upon infection by this obligate biotrophic pathogen.
  • We utilized a proteomics-based approach, combined with barley mla, required for Mla12 resistance1 (rar1), and restoration of Mla resistance1 (rom1) mutants, to identify components of Mla-directed signaling.
  • Loss-of-function mutations in Mla and Rar1 both resulted in the reduced accumulation of chloroplast copper/zinc superoxide dismutase 1 (HvSOD1), whereas loss of function in Rom1 re-established HvSOD1 levels. In addition, both Mla and Rom1 negatively regulated hvu-microRNA398 (hvu-miR398), and up-regulation of miR398 was coupled to reduced HvSOD1 expression. Barley stripe mosaic virus (BSMV)-mediated over-expression of both barley and Arabidopsis miR398 repressed accumulation of HvSOD1, and BSMV-induced gene silencing of HvSod1 impeded Mla-triggered H2O2 and hypersensitive reaction (HR) at barley–Bgh interaction sites.
  • These data indicate that Mla- and Rom1-regulated hvu-miR398 represses HvSOD1 accumulation, influencing effector-induced HR in response to the powdery mildew fungus.

Ancillary