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首页> 美国卫生研究院文献>other >Transient Early Embryonic Expression of Nkx2-5 Mutations Linked to Congenital Heart Defects in Human Causes Heart Defects in Xenopus laevis
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Transient Early Embryonic Expression of Nkx2-5 Mutations Linked to Congenital Heart Defects in Human Causes Heart Defects in Xenopus laevis

机译：Nkx2-5突变与人的先天性心脏缺陷相关的瞬时早期胚胎表达导致非洲爪蟾的心脏缺陷。

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Nkx2-5 is a homeobox containing transcription factor that is conserved and expressed in organisms that form hearts. Fruit flies lacking the gene (tinman) fail to form a dorsal vessel, mice that are homozygous null for Nkx2-5 form small, deformed hearts, and several human cardiac defects have been linked to dominant mutations in the Nkx2-5 gene. The Xenopus homologs (XNkx2-5) of two truncated forms of Nkx2-5 that have been identified in humans with congenital heart defects were used in the studies reported here. mRNAs encoding these mutations were injected into single cell Xenopus embryos, and heart development was monitored. Our results indicate that the introduction of truncated XNkx2-5 variants leads to three principle developmental defects. The atrial septum and the valve of the atrioventricular canal were both abnormal. In addition, video microscopic timing of heart contraction indicated that embryos injected with either mutant form of XNkx2-5 have conduction defects.
机译：Nkx2-5是一个含有转录因子的同源盒，在形成心脏的生物体中保守并表达。缺少该基因的果蝇（tinman）无法形成背脉，对Nkx2-5纯合的小鼠形成小的畸形心脏，并且一些人类心脏缺陷与Nkx2-5基因的显性突变有关。本文报道的研究中使用了在人类先天性心脏缺陷患者中鉴定出的两种截短形式的Nkx2-5的非洲爪蟾同源物（XNkx2-5）。将编码这些突变的mRNA注射到单细胞非洲爪蟾胚胎中，并监测心脏发育。我们的结果表明，引入截短的XNkx2-5变体会导致三个主要的开发缺陷。房间隔和房室瓣膜均异常。另外，心脏收缩的视频显微定时表明注射有XNkx2-5突变形式的胚胎具有传导缺陷。

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