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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >VIP1 response elements mediate mitogen-activated protein kinase 3-induced stress gene expression
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VIP1 response elements mediate mitogen-activated protein kinase 3-induced stress gene expression

机译：VIP1反应元件介导有丝分裂原激活的蛋白激酶3诱导的应激基因表达

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摘要

The plant pathogen Agrobacterium tumefaciens transforms plant cells by delivering its T-DNA into the plant cell nucleus where it integrates into the plant genome and causes tumor formation. A key role of VirE2-interacting protein 1 (VIP1) in the nuclear import of T-DNA during Agrobacterium-mediated plant transformation has been unravelled and VIP1 was shown to undergo nuclear localization upon phosphorylation by the mitogen-activated protein kinase MPK3. Here, we provide evidence that VIP1 encodes a functional bZIP transcription factor that stimulates stress-dependent gene expression by binding to VIP1 response elements (VREs), a DNA hexamer motif. VREs are overrepresented in promoters responding to activation of the MPK3 pathway such as Trxh8 and MYB44. Accordingly, plants overexpressing VIP1 accumulate high levels of Trxh8 and MYB44 transcripts, whereas stress-induced expression of these genes is impaired in mpk3 mutants. Trxh8 and MYB44 promoters are activated by VIP1 in a VRE-dependent manner. VIP1 strongly enhances expression from a synthetic promoter harboring multiple VRE copies and directly interacts with VREs in vitro and in vivo. Chromatin immuno-precipitation assays of the MYB44 promoter confirm that VIP1 binding to VREs is enhanced under conditions of MPK3 pathway stimulation. These results provide molecular insight into the cellular mechanism of target gene regulation by the MPK3 pathway.
机译：植物病原土壤杆菌通过将其T-DNA传递到植物细胞核中来转化植物细胞，并整合到植物基因组中并导致肿瘤形成。在农杆菌介导的植物转化过程中，VirE2相互作用蛋白1（VIP1）在T-DNA的核输入中的关键作用已被阐明，并且有丝分裂原激活的蛋白激酶MPK3磷酸化显示VIP1经历核定位。在这里，我们提供的证据表明VIP1编码功能性bZIP转录因子，该因子通过结合到DNA六聚体基序VIP1响应元件（VRE）来刺激应激依赖性基因表达。 VRE在响应MPK3途径激活的启动子（如Trxh8和MYB44）中过分表达。因此，过表达VIP1的植物积累高水平的Trxh8和MYB44转录本，而在mpk3突变体中这些基因的胁迫诱导表达受到损害。 Trxh8和MYB44启动子被VIP1依赖于VRE激活。 VIP1强烈增强了具有多个VRE拷贝的合成启动子的表达，并在体内外与VRE直接相互作用。 MYB44启动子的染色质免疫沉淀分析证实，在MPK3途径刺激条件下，VIP1与VRE的结合增强。这些结果为通过MPK3途径调控靶基因调控细胞机制提供了分子认识。

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    Andrea Pitzschke; Armin Djamei; Markus Teige; Heribert Hirt;

  • 作者单位

    Department of Plant Molecular Biology, Max F. Perutz Laboratories, University of Vienna, Dr.-Bohr-Gasse 9, 1030 Vienna, Austria;

    Department of Plant Molecular Biology, Max F. Perutz Laboratories, University of Vienna, Dr.-Bohr-Gasse 9, 1030 Vienna, Austria Department of Organismic Interactions, Max-Planck-lnstitut fur terres-trische Mikrobiologie, Karl-von-Frisch-Strasse, 35043 Marburg, Germany;

    Department of Plant Molecular Biology, Max F. Perutz Laboratories, University of Vienna, Dr.-Bohr-Gasse 9, 1030 Vienna, Austria;

    Department of Plant Molecular Biology, Max F. Perutz Laboratories, University of Vienna, Dr.-Bohr-Gasse 9, 1030 Vienna, Austria URGV Plant Genomics Laboratory, 2 Rue Gaston Cremieux, 91057 Evry, France;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    signal propagation; transcription factor; promoter motif; bZIP; Arabidopsis;

    机译：信号传播转录因子启动子基序bZIP;拟南芥;

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