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Endoplasmic Reticulum Glucosidase II Is Required for Pathogenicity of Ustilago maydis.

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Schirawski,  Jan
Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

Boehnert,  Heidi
Max Planck Society;

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Steinberg,  Gero
Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Adamikova,  Lubica
Max Planck Research Group Evolutionary Biochemistry, 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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引用

Schirawski, J., Boehnert, H., Steinberg, G., Snetselaar, K., Adamikova, L., & Kahmann, R. (2005). Endoplasmic Reticulum Glucosidase II Is Required for Pathogenicity of Ustilago maydis. The Plant Cell, 17, 3532-3543. doi:10.1105/tpc.105.036285.


引用: https://hdl.handle.net/21.11116/0000-0007-C7D7-6
要旨
We identified a nonpathogenic strain of Ustilago maydis by tagging mutagenesis. The affected gene, glucosidase1 (gas1), displays similarity to catalytic alpha-subunits of endoplasmic reticulum (ER) glucosidase II. We have shown that Gas1 localizes to the ER and complements the temperature-sensitive phenotype of a Saccharomyces cerevisiae mutant lacking ER glucosidase II. gas1 deletion mutants were normal in growth and mating but were more sensitive to calcofluor and tunicamycin. Mutant infection hyphae displayed significant alterations in the distribution of cell wall material and were able to form appressoria and penetrate the plant surface but arrested growth in the epidermal cell layer. Electron microscopy analysis revealed that the plant-fungal interface between mutant hyphae and the plant plasma membrane was altered compared with the interface of penetrating wild-type hyphae. This may indicate that gas1 mutants provoke a plant response.