The role of the wheat Reduced height (Rht)-DELLA mutants and associated hormones in infection by Claviceps purpurea, the causal agent of ergot.

Abstract

Partial resistance to the biotrophic fungal pathogen Claviceps purpurea, causal agent of ergot, has been found that co-locates with mutant alleles of the wheat Reduced height (Rht) loci on chromosomes 4B and 4D. These Rht loci represent the wheat orthologues of the Arabidopsis Della genes. To investigate the role of the Rht mutant DELLA proteins in ergot resistance we assessed C. purpurea infection in wheat near-isogenic lines (NILs) carrying the gibberellic acid (GA)-insensitive semi-dwarf alleles Rht-B1b and Rht-D1b and the severe dwarf alleles Rht-B1c and Rht-D1c. NILs of the GA-sensitive alleles Rht8 (chromosome 2D) and Rht12 (chromosome 5A) were also included. A general trend towards increased resistance to C. purpurea, with smaller and lighter sclerotia, was observed on the NILs Rht-B1b, Rht-D1b, Rht-B1c and Rht-D1c, but also on Rht8. Levels of the bioactive GA4 and the auxin indole-3-acetic acid (IAA) increased following inoculation with C. purpurea, following similar patterns and implicating a potential auxin-mediated induction of GA biosynthesis. In contrast, jasmonic acid (JA) levels fell in the parental lines Mercia and Maris Huntsman following inoculation with C. purpurea, but increased in all the Rht-mutant NILs. Inoculation with C. purpurea did not show any informative changes in the levels of salicylic acid. Our results suggest that GA-mediated degradation of the DELLA proteins and down-regulation of JA-signalling pathways supports infection of wheat by C. purpurea. As these responses are generally associated with necrotrophic fungal pathogens, we propose that the biotroph C. purpurea may have a necrotrophic growth stage.