Hedgehog signalling is required for cloacal development in the zebrafish embryo.

C. Parkin, C. Allen, P. Ingham
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引用次数: 34

Abstract

The Hedgehog (Hh) family of signalling molecules is essential for a wide range of developmental processes. Mammalian studies have implicated the Hedgehog pathway in the aetiology of anorectal malformations (ARMs), relatively common congenital anomalies caused by failures in the development of the cloaca. In this study we demonstrate that Hh signalling is absolutely required for the formation of the zebrafish cloaca and that the severity of the posterior gut abnormalities induced by a reduction in Hh activity is dependent on the levels of Hh signal transduction. The complete loss of all Hh activity results in the most severe defects and the critical period for Hh activity is between 34 and 74 hours post fertilisation. Using a range of mutant genotypes that cause notochord and floorplate abnormalities, we show that the source of the Hh signals required for posterior gut formation is the endoderm and not the notochord, as previously postulated in mammalian models of ARMs. We show that Adriamycin, a drug known to cause ARMs in rat, but not chick embryos, has no effect on the development of the zebrafish gastrointestinal tract. These studies establish the zebrafish as a model for ARMs, and for the elucidation of other pathways involved in hindgut developmental processes.
斑马鱼胚胎的泄殖腔发育需要Hedgehog信号。
Hedgehog (Hh)信号分子家族对广泛的发育过程至关重要。哺乳动物研究表明,Hedgehog通路与肛肠畸形(ARMs)的病因学有关,这是由泄殖腔发育失败引起的相对常见的先天性异常。在这项研究中,我们证明了Hh信号对于斑马鱼泄殖腔的形成是绝对必需的,并且由Hh活性降低引起的后肠异常的严重程度取决于Hh信号转导的水平。Hh活性的完全丧失会导致最严重的缺陷,而Hh活性的关键时期是受精后34至74小时。利用一系列引起脊索和底板异常的突变基因型,我们发现后肠形成所需的Hh信号的来源是内胚层,而不是脊索,正如之前在哺乳动物ARMs模型中假设的那样。我们发现阿霉素,一种在大鼠体内引起ARMs的药物,对斑马鱼胃肠道的发育没有影响。这些研究建立了斑马鱼作为ARMs的模型,并阐明了参与后肠发育过程的其他途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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