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A cell-specific enhancer that specifies lin-3 expression in the C. elegans anchor cell for vulval development.

机译:一种细胞特异性增强子,可在秀丽隐杆线虫锚定细胞中指定lin-3表达以促进外阴发育。

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摘要

During C. elegans vulval development, the anchor cell (AC) in the somatic gonad expresses lin-3, activating the EGF receptor signaling pathway in vulval precursor cells (VPCs) and thereby inducing and patterning VPCs. Previous studies with lin-3 mutants and transgene expression have revealed that the level of LIN-3 in the AC must be precisely regulated for proper vulval development. To understand how lin-3 expression is achieved in the AC, we identified a 59 bp lin-3 enhancer sufficient to activate lin-3 transcription solely in the AC. The enhancer contains two E-box elements, and one FTZ-F1 nuclear hormone receptor (NHR) binding site that is mutated in a vulvaless mutant, lin-3(e1417). Mutagenesis studies show that both E-boxes and the NHR binding site are necessary to express lin-3 in the AC. In vitro DNA-binding studies and in vivo functional assays indicate that distinct trans-acting factors, including the E-protein/Daughterless homolog HLH-2 and unidentified nuclear hormone receptor(s), are necessary for lin-3 transcription in the AC and thus are involved in vulval development.
机译:在秀丽隐杆线虫的外阴发育过程中,体细胞性腺中的锚定细胞(AC)表达lin-3,激活外阴前体细胞(VPC)中的EGF受体信号传导途径,从而诱导并构图VPC。先前对lin-3突变体和转基因表达的研究表明,AC中LIN-3的水平必须精确调节才能正常外阴发育。为了了解如何在AC中实现lin-3的表达,我们确定了一个59 bp的lin-3增强子,足以单独激活AC中的lin-3转录。增强子包含两个E-box元件和一个FTZ-F1核激素受体(NHR)结合位点,该结合位点在无性状突变体lin-3(e1417)中发生了突变。诱变研究表明,E盒和NHR结合位点都是在AC中表达lin-3所必需的。体外DNA结合研究和体内功能分析表明,不同的反式作用因子,包括E蛋白/无女儿同源物HLH-2和未知的核激素受体,对于AC和LIN-3转录是必需的。因此参与外阴发育。

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