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Identification and characterization of a novel receptor-like kinase involved in the initiation and regulation of Arabidopsis innate immunity.

机译:拟南芥先天免疫的启动和调节中涉及的新型受体样激酶的鉴定和表征。

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摘要

Receptor-like kinases (RLKs) are known to be involved in the recognition of pathogen-associated molecular patterns (PAMPs) and subsequently activate resistance pathways against broad classes of pathogens. While initiation and maintenance of defense pathways is critical for survival, mechanisms to damp down these responses are just as necessary though currently not as well understood. We have identified CRLK1, an Arabidopsis RLK that is highly induced by chitin at early time points and localizes to the plasma membrane. Knock-out mutants in crlk1 are more susceptible to both biotrophic and necrotrophic fungal pathogens though the response of the mutants to bacterial pathogens is unaffected. Interestingly expression of MAPK3, an important positive regulator of innate immunity, is increased in crlk1 mutants. Our data show that CRLK1 is essential for the establishment of defense against biotrophic and necrotrophic fungi and that the mutation in CRLK1 does not fully block chitin-enhanced Arabidopsis resistance. We show that CRLK1 is a functional kinase in vitro and its kinase activity required the presence of manganese. Overexpression of a 35S:CRLK1: GUS fusion protein in Arabidopsis confers enhanced resistance to the powdery mildew pathogen Golovinomycetes cichoracearum. In addition, CRLK1 induction by chitin is increased in mapk3 and several wrky mutants indicating that CRLK1 may be repressed by MAPK3 and WRKY transcription factors in planta. The results presented provide important information about the function and regulation of CRLK1 in Arabidopsis.
机译:已知受体样激酶(RLK)参与病原体相关分子模式(PAMPs)的识别,并随后激活针对多种病原体的抗性途径。虽然防御途径的启动和维持对于生存至关重要,但尽管目前尚不十分了解,抑制这些反应的机制还是必要的。我们已经鉴定出CRLK1,一种由甲壳素在早期时间点高度诱导并定位于质膜的拟南芥RLK。尽管突变体对细菌病原体的反应不受影响,但crlk1中的敲除突变体更容易受到生物营养性和坏死性真菌病原体的影响。有趣的是,MAPK3(一种先天免疫的重要正调节剂)的表达在crlk1突变体中增加。我们的数据表明CRLK1对于建立针对生物营养性和坏死性真菌的防御至关重要,并且CRLK1中​​的突变并不能完全阻断几丁质增强的拟南芥抗性。我们显示CRLK1是体外功能性激酶,其激酶活性需要锰的存在。在拟南芥中过表达35S:CRLK1:GUS融合蛋白可增强对白粉病病原菌Golovinomycetes cichoracearum的抗性。此外,几丁质对mapk3的诱导对CRLK1的诱导作用增强,一些突变的突变体表明CRLK1可能被植物中的MAPK3和WRKY转录因子抑制。提出的结果提供了有关拟南芥中CRLK1的功能和调控的重要信息。

著录项

  • 作者

    Yang, Xin.;

  • 作者单位

    The University of Alabama.;

  • 授予单位 The University of Alabama.;
  • 学科 Biology Molecular.;Chemistry Biochemistry.;Agriculture Plant Culture.
  • 学位 Ph.D.
  • 年度 2011
  • 页码 119 p.
  • 总页数 119
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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