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  Hap2 regulates the pheromone response transcription factor prf1 in Ustilago maydis

Mendoza-Mendoza, A., Eskova, A., Weise, C., Czajkowski, R., & Kahmann, R. (2009). Hap2 regulates the pheromone response transcription factor prf1 in Ustilago maydis. Molecular Microbiology, 72(3), 683-698. doi:10.1111/j.1365-2958.2009.06676.x.

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アイテムのパーマリンク: https://hdl.handle.net/21.11116/0000-0007-C4B3-1 版のパーマリンク: https://hdl.handle.net/21.11116/0000-000D-6D1B-C
資料種別: 学術論文

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 作成者:
Mendoza-Mendoza, Artemio1, 著者           
Eskova, Anastasia, 著者
Weise, Carolin1, 著者           
Czajkowski, Robert1, 著者           
Kahmann, Regine2, 著者           
所属:
1Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society, ou_3266313              
2Emeriti Molecular Phytopathology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society, ou_3266291              

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 要旨: In Ustilago maydis the pheromone signal is transmitted via a mitogen-activated protein kinase (MAP kinase) module to the transcription factor Prf1. Prf1 activates transcription of a and b mating type genes by binding to pheromone response elements (PREs) located in regulatory regions of these genes. Here we show that the CCAAT-box binding protein Hap2 from U. maydis regulates prf1 expression. Hap2 was initially identified as a potential interaction partner of the MAP kinase Kpp6 in yeast two-hybrid screens and was subsequently also shown to interact with the MAPK Kpp2. Deletion of hap2 in haploid cells abolished mating, resulting from a defect in pheromone-induced gene expression. Crosses of haploid hap2 deletion strains were completely impaired in pathogenicity. Constitutive expression of prf1 complemented the pheromone response defect in Δhap2 strains. Chromatin immunoprecipitation assays indicated that Hap2 binds directly to CCAAT motifs in the prf1 promoter. Point mutations in two putative MAPK phosphorylation sites in Hap2 attenuated the pheromone response. In a solopathogenic strain hap2 deletion affected filamentation and the mutants showed reduced pathogenicity symptoms. These data suggest that Hap2 is a novel regulator of prf1 with additional functions after cell fusion.

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言語: eng - English
 日付: 2009
 出版の状態: 出版
 ページ: -
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 目次: -
 査読: 査読あり
 識別子(DOI, ISBNなど): eDoc: 442090
DOI: 10.1111/j.1365-2958.2009.06676.x
 学位: -

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出版物名: Molecular Microbiology
種別: 学術雑誌
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出版社, 出版地: -
ページ: - 巻号: 72 (3) 通巻号: - 開始・終了ページ: 683 - 698 識別子(ISBN, ISSN, DOIなど): -