Abstract
SummaryThe phenolic compound salicylic acid (SA) is a key signalling molecule regulating local and systemic plant defense responses, mainly against biotrophs. Many microbial organisms, including pathogens, share the ability to degrade SA. However, the mechanism by which they perceive SA is unknown. Here we show that Ustilago maydis, the causal agent of corn smut disease, employs a so far uncharacterized SA sensing mechanism. We identified and characterized the novel SA sensing regulator, Rss1, a binuclear zinc cluster protein with dual functions as putative SA receptor and transcriptional activator regulating genes important for SA and tryptophan degradation. Rss1 represents a major component in the identified SA sensing pathway during the fungus’ saprophytic stage. However, Rss1 does not have a detectable impact on virulence. The data presented in this work indicate that alternative or redundant sensing cascades exist that regulate the expression of SA‐responsive genes in U. maydis during its pathogenic development.
Highlights
Salicylic acid (SA, 2-hydroxybenzoic acid) belongs to the class of phenolic compounds and is composed of an aromatic ring with a carboxyl- and hydroxyl group
We show that Ustilago maydis, the causal agent of corn smut disease, employs a so far uncharacterized salicylic acid (SA) sensing mechanism
We identified and characterized the novel SA sensing regulator, Rss1, a binuclear zinc cluster protein with dual functions as putative SA receptor and transcriptional activator regulating genes important for SA and tryptophan degradation
Summary
Salicylic acid (SA, 2-hydroxybenzoic acid) belongs to the class of phenolic compounds and is composed of an aromatic ring with a carboxyl- and hydroxyl group. SA serves as building block for siderophore biosynthesis or as siderophore itself (Visca et al, 1993) In plants, it was identified as important hormone regulating diverse processes, including seed germination, cell growth, respiration, and most prominently defense responses to biotrophic pathogens (Vlot et al, 2009). To limit the spread of biotrophic pathogens that rely on the living host for proliferation (Glazebrook, 2005), SA regulates a complex network of diverse signalling components. Upon pathogen attack, this network activates defense responses which can culminate in hypersensitive cell death at the site of infection (Vlot et al, 2009). SA is involved in systemic acquired resistance in distal, non-infected parts of the plant resulting in broad-spectrum resistance to diverse pathogens and an immune memory that primes the plant for secondary infections (Fu and Dong, 2013)
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