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Abstract:
The biotrophic fungus Ustilago maydis causes the smut disease of maize.
The interaction with its host and induction of characteristic tumors are
governed largely by secreted effectors whose function is mostly unknown.
To identify effectors with a prominent role in virulence, we used RNA
sequencing and found that the gene sta1 is upregulated during early
stages of infection.
We characterized Sta1 by comparative genomics, reverse genetics, protein
localization, stress assays, and microscopy.
sta1 mutants show a dramatic reduction of virulence and show altered
colonization of tissue neighboring the vascular bundles. Functional
orthologues of Sta1 are found in related smut pathogens infecting
monocot and dicot plants. Sta1 is secreted by budding cells but is
attached to the cell wall of filamentous hyphae. Upon constitutive
expression of Sta1, fungal filaments become susceptible to Congo red,
beta-glucanase, and chitinase, suggesting that Sta1 alters the structure
of the fungal cell wall. Constitutive or delayed expression of sta1
during plant colonization negatively impacts on virulence.
Our results suggest that Sta1 is a novel kind of effector, which needs
to modify the hyphal cell wall to allow hyphae to be accommodated in
tissue next to the vascular bundles.
