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腹侧无静脉基因,一种POU结构域转录因子,调控果蝇气管分支所需的不同信号转导途径。

ventral veinless, a POU domain transcription factor, regulates different transduction pathways required for tracheal branching in Drosophila.

作者信息

Llimargas M, Casanova J

机构信息

Centre d'Investigació i Desenvolupament (CSIC) C/ Jordi Girona, Barcelona, Spain.

出版信息

Development. 1997 Sep;124(17):3273-81. doi: 10.1242/dev.124.17.3273.

DOI:10.1242/dev.124.17.3273
PMID:9310322
Abstract

Cell migration is an important step in a variety of developmental processes in many multicellular organisms. A particularly appropriate model to address the study of cell migration is the tracheal system of Drosophila, whose formation occurs by migration and fusion from clusters of ectodermal cells specified in each side of ten embryonic segments. Morphogenesis of the tracheal tree requires the activity of many genes, among them breathless (btl) and ventral veinless (vvl) whose mutations abolish tracheal cell migration. Activation of the btl receptor by branchless (bnl), its putative ligand, exerts an instructive role in the process of guiding tracheal cell migration. vvl has been shown to be required for the maintenance of btl expression during tracheal tree formation. Here we show that, in addition, vvl is independently required for the specific expression in the tracheal cells of thick veins (tkv) and rhomboid (rho), two genes whose mutations disrupt only particular branches of the tracheal system. Indeed, we show that expression in the tracheal cells of an activated form of tkv, the putative decapentaplegic (dpp) receptor, is able to induce shifts in their migration, asserting the role of the dpp pathway in establishing the branching pattern of the tracheal tree. In addition, by ubiquitous expression of the btl and tkv genes in vvl mutant embryos we show that both genes contribute to vvl function. These results indicate that through activation of its target genes, vvl makes the tracheal cells competent to further signalling and suggest that the btl transduction pathway could collaborate with other transduction pathways also regulated by vvl to specify the tracheal branching pattern.

摘要

细胞迁移是许多多细胞生物各种发育过程中的重要步骤。研究细胞迁移的一个特别合适的模型是果蝇的气管系统,其形成是通过来自十个胚胎节段每一侧特定的外胚层细胞簇的迁移和融合实现的。气管树的形态发生需要许多基因的活性,其中包括呼吸缺陷(btl)和腹侧无脉(vvl),其突变会消除气管细胞迁移。无分支(bnl)作为btl受体的假定配体,对其激活在引导气管细胞迁移过程中发挥指导作用。已证明vvl在气管树形成过程中对维持btl表达是必需的。在此我们表明,此外,vvl对于厚脉(tkv)和菱形(rho)在气管细胞中的特异性表达也是独立必需的,这两个基因的突变仅破坏气管系统的特定分支。实际上,我们表明,假定的骨形态发生蛋白(dpp)受体tkv的激活形式在气管细胞中的表达能够诱导其迁移发生改变,证实了dpp信号通路在建立气管树分支模式中的作用。此外,通过在vvl突变胚胎中普遍表达btl和tkv基因,我们表明这两个基因都对vvl功能有贡献。这些结果表明,通过激活其靶基因,vvl使气管细胞能够对进一步的信号作出反应,并表明btl转导通路可能与其他也受vvl调节的转导通路协作来确定气管分支模式。

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