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A secreted Ustilago maydis effector promotes virulence by targeting anthocyanin biosynthesis in maize

MPG-Autoren
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Tanaka,  Shigeyuki
Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Brefort,  Thomas
Department of Biogeochemistry, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Neidig,  Nina
Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Djamei,  Armin
Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Kahnt,  Joerg
Department of Ecophysiology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Kahmann,  Regine
Emeriti Molecular Phytopathology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Zitation

Tanaka, S., Brefort, T., Neidig, N., Djamei, A., Kahnt, J., Vermerris, W., et al. (2014). A secreted Ustilago maydis effector promotes virulence by targeting anthocyanin biosynthesis in maize. eLife, 3: e01355. doi:10.7554/elife.01355.


Zitierlink: https://hdl.handle.net/21.11116/0000-0007-BE6D-A
Zusammenfassung
The biotrophic fungus Ustilago maydis causes smut disease in maize with characteristic tumor formation and anthocyanin induction. Here, we show that anthocyanin biosynthesis is induced by the virulence promoting secreted effector protein Tin2. Tin2 protein functions inside plant cells where it interacts with maize protein kinase ZmTTK1. Tin2 masks a ubiquitin-proteasome degradation motif in ZmTTK1, thus stabilizing the active kinase. Active ZmTTK1 controls activation of genes in the anthocyanin biosynthesis pathway. Without Tin2, enhanced lignin biosynthesis is observed in infected tissue and vascular bundles show strong lignification. This is presumably limiting access of fungal hyphae to nutrients needed for massive proliferation. Consistent with this assertion, we observe that maize brown midrib mutants affected in lignin biosynthesis are hypersensitive to U. maydis infection. We speculate that Tin2 rewires metabolites into the anthocyanin pathway to lower their availability for other defense responses.