Phytohormone sensing in the biotrophic fungus Ustilago maydis – the dual role of the transcription factor Rss1. Issue 2 (8th August 2016)

• Record Type: Journal Article
• Authors: Rabe, Franziska; Seitner, Denise; Bauer, Lisa; Navarrete, Fernando; Czedik‐Eysenberg, Angelika; Rabanal, Fernando A.; Djamei, Armin
• Is Part Of: Molecular microbiology. Volume 102:Issue 2(2016)
• Page Start: 290
• Page End: 305
• Publication Date: 2016-08-08
• Subjects: Molecular microbiology -- Periodicals; 572.829
• DOI: 10.1111/mmi.13460
• Languages: English
• ISSNs: 0950-382X

Abstract

Summary: The 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. Abstract : The biotrophic plant pathogenic fungus Ustilago maydis senses salicylic acid (SA), a major phytohormone. Here we identified one factor important for this process – the binuclear zinc cluster transcription factor Rss1. Rss1 is activated by SA and anthranilic acid and it regulates genes for SA as well as tryptophan degradation during biotrophic growth. However, Rss1 seems to be dispensable for virulence. Our data suggests the presence of redundant pathways that regulate SA‐responsive genes during pathogenic development.