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首页> 外文期刊>Biochimica et Biophysica Acta. Gene Regulatory Mechanisms >Dual role of Tlx3 as modulator of Prrxl1 transcription and phosphorylation
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Dual role of Tlx3 as modulator of Prrxl1 transcription and phosphorylation

机译：TLX3的双重作用作为PRRXL1转录和磷酸化的调节剂

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摘要

The proper establishment of the dorsal root ganglion/spinal cord nociceptive circuitry depends on a group of homeodomain transcription factors that includes Prrxl1, Brn3a and Tlx3. By the use of epistatic analysis, it was suggested that Tlx3 and Brn3a, which highly co-localize with Prrxl1 in these tissues, are required to maintain Prrxl1 expression. Here, we report two Tlx3-dependent transcriptional mechanisms acting on Prrxl1 alternative promoters, referred to as P3 and P1/P2 promoters. We demonstrate that (i) Tlx3 induces the transcriptional activity of the TATA-containing promoter P3 by directly binding to a bipartite DNA motif and (ii) it synergistically interacts with Prrxl1 by indirectly activating the Prrxl1 TATA-less promoters P1/P2 via the action of Brn3a. The Tlx3 N-terminal domain 1-38 was shown to have a major role on the overall Tlx3 transcriptional activity and the C-terminus domain (amino acids 256-291) to mediate the Tlx3 effect on promoters P1/P2. On the other hand, the 76-111 domain was shown to decrease Tlx3 activity on the TATA-promoter P3. In addition to its action on Prrxl1 alternative promoters, Tlx3 proved to have the ability to induce Prrxl1 phosphorylation. The Tlx3 domain responsible for Prrxl1 hyperphosphorylation was mapped and encompasses amino acid residues 76 to 111. Altogether, our results suggest that Tlx3 uses distinct mechanisms to tightly modulate Prrxl1 activity, either by controlling its transcriptional levels or by increasing Prrxl1 phosphorylation state.
机译：正根神经节/脊髓伤害电路的适当建立取决于包括PRRXL1，BRN3A和TLX3的一组同源域转录因子。通过使用背景分析，建议需要在这些组织中与PRRXL1高度定位的TLX3和BRN3a以维持PRRXL1表达。这里，我们报告了作用于PRRXL1替代启动子的两种TLX3依赖性转录机制，称为P3和P1 / P2启动子。我们证明（i）TLX3通过直接结合二分DNA基序和（II）通过间接激活PRRXL1较少的启动子P1 / P2通过该作用，通过直接与PRRXL1进行协同相互作用，诱导含塔塔启动子P3的转录活性。 Brn3a。显示TLX3 N-末端结构域1-38在整个TLX3转录活性和C末端结构域（氨基酸256-291）上具有主要作用，以介导TLX3对启动子P1 / P2的影响。另一方面，76-111结构域显示在塔塔启动子P3上降低TLX3活性。除了在PRRXL1替代促进剂上的作用外，TLX3证明有能力诱导PRRXL1磷酸化。映射了负责PRRXL1超磷酸化的TLX3结构域并包括氨基酸残基76-111.通过，我们的结果表明TLX3通过控制其转录水平或通过增加PRRXL1磷酸化状态来紧密调节PRRX11活性的不同机制。

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    RegadasI.; Soares-dos-ReisR.; Falc?oM.; MatosM.R.; MonteiroF.A.; LimaD.; ReguengaC.;

  • 作者单位

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

    Departamento de Biologia Experimental Faculdade de Medicina Universidade do Porto Porto Portugal;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 分子生物学;
  • 关键词

    Alternative promoters; Brn3a; Nociception; Phosphorylation; Prrxl1; Tlx3;

    机译：替代启动子;BRN3A;伤害;磷酸化;PRRXL1;TLX3;

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