Defects in somite formation in lunatic fringe-deficient mice
Defects in somite formation in lunatic fringe-deficient mice
复制标题
疯狂边缘缺陷小鼠的体节形成缺陷
作者：
Niang Zhang;T. Gridley
当未分节的近轴中胚层细分形成称为体节的成对上皮球时，脊椎动物的分节首先出现。 Notch 信号通路对于调节脊椎动物体节的形成和前后模式非常重要。果蝇Notch信号通路的一个组成部分是边缘基因，它编码在翼缘规范期间激活Notch所需的分泌信号分子。在这里，我们发现，疯子边缘（Lfng）基因（小鼠边缘同源物之一）的靶向突变纯合小鼠在体节形成和体节前后图案方面存在缺陷。突变胚胎中的体节大小和形状不规则，并且它们的前后图案被扰乱。标记分析显示，在突变体胚胎的前成体中胚层中，Notch 信号通路的几个组件的清晰划分的表达域被均匀的基因表达梯度所取代。这些结果表明 Lfng 编码小鼠体节发生过程中 Notch 信号通路的重要组成部分。
Segmentation in vertebrates first arises when the unsegmented paraxial mesoderm subdivides to form paired epithelial spheres called somites,. The Notch signalling pathway is important in regulating the formation and anterior–posterior patterning of the vertebrate somite. One component of the Notch signalling pathway in Drosophila is the fringe gene, which encodes a secreted signalling molecule required for activation of Notch during specification of the wing margin. Here we show that mice homozygous for a targeted mutation of the lunatic fringe (Lfng) gene, one of the mouse homologues, of fringe, have defects in somite formation and anterior–posterior patterning of the somites. Somites in the mutant embryos are irregular in size and shape, and their anterior–posterior patterning is disturbed. Marker analysis revealed that in the presomitic mesoderm of the mutant embryos, sharply demarcated domains of expression of several components of the Notch signalling pathway are replaced by even gradients of gene expression. These results indicate that Lfng encodes an essential component of the Notch signalling pathway during somitogenesis in mice.
影响因子：
5
作者：
Chen，Jun-Feng;Zhao，Yu-Yan Sara;Yang，Jing
通讯作者：
Yang，Jing
Mbx，一种新型小鼠同源盒基因。
影响因子：
2.4
作者：
Miyamoto,Toshinobu;Kawahara,Atsuo;Teufel,Andreas;Mukhopadhyay,Mahua;Zhao,Yangu;Dawid,IgorB;Westphal,Heiner
通讯作者：
Westphal,Heiner