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The transcription factor Zt107320 affects the dimorphic switch, growth and virulence of the fungal wheat pathogen Zymoseptoria tritici

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Habig,  Michael
Max Planck Fellow Group Environmental Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Bahena-Garrido,  Sharon Marie
Max Planck Fellow Group Environmental Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Barkmann,  Friederike
Max Planck Fellow Group Environmental Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Haueisen,  Janine
Max Planck Fellow Group Environmental Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Stukenbrock,  Eva Holtgrewe
Max Planck Fellow Group Environmental Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Citation

Habig, M., Bahena-Garrido, S. M., Barkmann, F., Haueisen, J., & Stukenbrock, E. H. (2020). The transcription factor Zt107320 affects the dimorphic switch, growth and virulence of the fungal wheat pathogen Zymoseptoria tritici. Molecular Plant Pathology, 21(1), 124-138. doi:10.1111/mpp.12886.


Cite as: https://hdl.handle.net/21.11116/0000-0005-1E76-6
Abstract
Summary Zymoseptoria tritici is a filamentous fungus causing Septoria tritici blotch in wheat. The pathogen has a narrow host range and infections of grasses other than susceptible wheat are blocked early after stomatal penetration. During these abortive infections, the fungus shows a markedly different gene expression pattern. However, the underlying mechanisms causing differential gene expression during host and non-host interactions are largely unknown, but likely include transcriptional regulators responsible for the onset of an infection programme in compatible hosts. MoCOD1, a member of the fungal Zn(II)2Cys6 transcription factor family, has been shown to directly affect pathogenicity in the rice blast pathogen Magnaporthe oryzae. Here, we analyse the role of the putative transcription factor Zt107320, a homologue of MoCOD1, during infection of compatible and incompatible hosts by Z. tritici. We show for the first time that Zt107320 is differentially expressed in host versus non-host infections and that lower expression corresponds to an incompatible infection of non-hosts. Applying reverse genetics approaches, we further show that Zt107320 regulates the dimorphic switch as well as the growth rate of Z. tritici and affects fungal cell wall composition in vitro. Moreover, ∆Zt107320 mutants showed reduced virulence during compatible infections of wheat. We conclude that Zt107320 directly influences pathogen fitness and propose that Zt107320 is involved in the regulation of growth processes and pathogenicity during infection.