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The Gbeta-Subunit-Encoding Gene bpp1 Controls Cyclic-AMP Signaling in Ustilago maydis.

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

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Teunissen,  Hedwich
Department of Organismic Interactions, Alumni, 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

Mueller, P., Leibbrandt, A., Teunissen, H., Cubasch, S., Aichinger, C., & Kahmann, R. (2004). The Gbeta-Subunit-Encoding Gene bpp1 Controls Cyclic-AMP Signaling in Ustilago maydis. Eukaryotic Cell, 3(3), 806-814. doi:10.1128/ec.3.3.806-814.2004.


Zitierlink: https://hdl.handle.net/21.11116/0000-0007-C916-E
Zusammenfassung
In the phytopathogenic fungus Ustilago maydis, fusion of haploid cells is a prerequisite for infection. This process is controlled by a pheromone-receptor system. The receptors belong to the seven-transmembrane class that are coupled to heterotrimeric G proteins. Of four Galpha subunits in U. maydis, only gpa3 has a function during mating and cyclic AMP (cAMP) signaling. Activation of the cAMP cascade induces pheromone gene expression; however, it does not lead to the induction of conjugation tubes seen after pheromone stimulation. To investigate the possibility that a Gbeta subunit participates in pheromone signaling, we isolated the single beta subunit gene, bpp1, from U. maydis. bpp1 deletion mutants grew filamentously and showed attenuated pheromone gene expression, phenotypes associated with deltagpa3 strains. In addition, a constitutively active allele of gpa3 suppressed the phenotype of the bpp1 deletion strains. We suggest that Bpp1 and Gpa3 are components of the same heterotrimeric G protein acting on adenylyl cyclase. Interestingly, while deltagpa3 strains are impaired in pathogenicity, deltabpp1 mutants are able to induce plant tumors. This could indicate that Gpa3 operates independently of Bpp1 during pathogenic development.