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生成并鉴定新型神经嵴标记基因等位基因 Inka1-LacZ,揭示了 Inka1 在小鼠神经管闭合过程中的作用。

Generation and characterization of a novel neural crest marker allele, Inka1-LacZ, reveals a role for Inka1 in mouse neural tube closure.

机构信息

Department of Craniofacial Biology and Cell and Developmental Biology, University of Colorado Denver, Aurora, Colorado 80045, USA.

出版信息

Dev Dyn. 2010 Apr;239(4):1188-96. doi: 10.1002/dvdy.22248.

Abstract

Previous studies identified Inka1 as a gene regulated by AP-2alpha in the neural crest required for craniofacial morphogenesis in fish and frog. Here, we extend the analysis of Inka1 function and regulation to the mouse by generating a LacZ knock-in allele. Inka1-LacZ allele expression occurs in the cephalic mesenchyme, heart, and paraxial mesoderm prior to E8.5. Subsequently, expression is observed in the migratory neural crest cells and their derivatives. Consistent with expression of Inka1 in tissues of the developing head during neurulation, a low percentage of Inka1(-/-) mice show exencephaly while the remainder are viable and fertile. Further studies indicate that AP-2alpha is not required for Inka1 expression in the mouse, and suggest that there is no significant genetic interaction between these two factors during embryogenesis. Together, these data demonstrate that while the expression domain of Inka1 is conserved among vertebrates, its function and regulation are not.

摘要

先前的研究确定 Inka1 是一种受神经嵴中 AP-2alpha 调控的基因,对于鱼类和青蛙的颅面形态发生是必需的。在这里,我们通过生成 LacZ 敲入等位基因,将 Inka1 功能和调控的分析扩展到了小鼠。Inka1-LacZ 等位基因的表达发生在 E8.5 之前的头间质、心脏和轴旁中胚层。随后,在迁移的神经嵴细胞及其衍生物中观察到表达。与 Inka1 在神经胚形成过程中头部发育组织中的表达一致,一小部分 Inka1(-/-) 小鼠表现出无脑畸形,而其余的小鼠则具有活力和生育能力。进一步的研究表明,AP-2alpha 对于小鼠中的 Inka1 表达不是必需的,并且表明在胚胎发生过程中这两个因素之间没有显著的遗传相互作用。总之,这些数据表明,尽管 Inka1 的表达域在脊椎动物中是保守的,但它的功能和调控并不是。

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