Abstract
The biotrophic pathogen Ustilago maydis, the causative agent of corn smut disease, infects one of the most important crops worldwide – Zea mays. To successfully colonize its host, U. maydis secretes proteins, known as effectors, that suppress plant defense responses and facilitate the establishment of biotrophy. In this work, we describe the U. maydis effector protein Cce1. Cce1 is essential for virulence and is upregulated during infection. Through microscopic analysis and in vitro assays, we show that Cce1 is secreted from hyphae during filamentous growth of the fungus. Strikingly, Δcce1 mutants are blocked at early stages of infection and induce callose deposition as a plant defense response. Cce1 is highly conserved among smut fungi and the Ustilago bromivora ortholog complemented the virulence defect of the SG200Δcce1 deletion strain. These data indicate that Cce1 is a core effector with apoplastic localization that is essential for U. maydis to infect its host.
Highlights
The primary goal of plant pathogenic fungi is to proliferate using the host as a source of nutrients, shelter, and a structure from which to distribute spores
Many putative effectors have been previously found in clusters in the U. maydis genome, we focused on highly conserved genes encoding putative effectors outside of these clusters
Prediction of apoplastic localization was tested using ApoplastP (Sperschneider et al, 2017), which showed that Cce1 has a 57% probability of being localized to the apoplast (Table 1)
Summary
The primary goal of plant pathogenic fungi is to proliferate using the host as a source of nutrients, shelter, and a structure from which to distribute spores. Biotrophic fungi depend on a living host, which has led to the evolution of sophisticated strategies for suppressing host defense and redirecting its metabolic flux. The gall inducing, biotrophic fungus Ustilago maydis grows with intra- and extracellular hyphae after appressoria-mediated penetration of the maize epidermis. The intracellular hyphae are encased by the host membrane, forming the biotrophic interface where the exchange of nutrients as well as defense and defense suppression molecules occurs (Brefort et al, 2009; Jones and Dangl, 2006). The maize response includes apoplastic H2O2 production, directed secretion of papilla material like callose to block fungal penetration, and induction of defense genes (Cook et al, 2015; Oliveira-Garcia and Deising, 2016)
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