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首页> 外文学位 >Characterization of MST7, a MAPK kinase gene essential for appressorium formation in Magnaporthe grisea.
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Characterization of MST7, a MAPK kinase gene essential for appressorium formation in Magnaporthe grisea.

机译：MST7的特征，MST7激酶是稻瘟病菌形成食欲所必需的。

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摘要

Many fungal pathogens invade plants by forming specialized infection structures called appressoria. In the rice blast fungus Magnaporthe grisea, the PMK1 MAP kinase is essential for appressorium formation and invasive growth. I have identified the MEK (MST7) and MEK kinase (MST11) genes that are responsible for the activation of PMK1. The mst7 and mst11 mutants are nonpathogenic and fail to form appressoria. Although expressing a dominant active MST7 allele results in the activation of Pmk1 in the absence of Mst11 and improper regulation of appressorium formation, the direct interaction between Mst7 and Pmk1 is not observed in yeast two-hybrid assays. Thus, it is not clear how Mst7 transmits the upstream signals to Pmk1. Mst7 contains a well-conserved putative MAPK-docking site at its N-terminus. Deletion of this docking site has no obvious effect on the expression of MST7 but blocks appressorium formation and plant infection. The kinase activity of Mst7 is not affected by the deletion of this docking site, but Mst7Delta12-20 fails to activate Pmk1 in M. grisea. In both co-immunoprecipitation and bimolecular fluorescence complementation (BiFC) assays, the direct interaction between Mst7 and Pmk1 is detected only during appressorium formation. These observations indicate that the MAPK-docking site of Mst7 is essential for its association and activation of downstream Pmk1 and the Mst7-Pmk1 interaction is enhanced during appressorium formation.
机译：许多真菌病原体通过形成称为Appressoria的专门感染结构侵入植物。在稻瘟病菌Magnaporthe grisea中，PMK1 MAP激酶对于包皮的形成和侵袭性生长至关重要。我已经确定了负责激活PMK1的MEK（MST7）和MEK激酶（MST11）基因。 mst7和mst11突变体是非致病性的，不能形成Appressoria。尽管在没有Mst11的情况下表达主导性活跃的MST7等位基因会导致Pmk1的活化和对食堂形成的不适当调节，但在酵母双杂交试验中未观察到Mst7和Pmk1之间的直接相互作用。因此，不清楚Mst7如何将上游信号传输到Pmk1。 Mst7在其N端包含一个保守的MAPK对接位点。删除该停靠位点对MST7的表达没有明显影响，但阻止了app的形成和植物感染。 Mst7的激酶活性不受此停靠位点的删除的影响，但Mst7Delta12-20未能激活稻瘟病菌中的Pmk1。在共免疫沉淀和双分子荧光互补（BiFC）分析中，Mst7和Pmk1之间的直接相互作用仅在前肢形成期间被检测到。这些观察结果表明，Mst7的MAPK停靠位点对于其缔合和下游Pmk1的激活必不可少，并且Mst7-Pmk1的相互作用在包皮形成过程中得到增强。

著录项

  • 作者

    Zhao, Xinhua.;

  • 作者单位

    Purdue University.;

  • 授予单位 Purdue University.;
  • 学科 Agriculture Plant Pathology.
  • 学位 Ph.D.
  • 年度 2006
  • 页码 122 p.
  • 总页数 122
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 植物病理学;
  • 关键词

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