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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Perinatal abrogation of Cdk5 expression in brain results in neuronal migration defects
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Perinatal abrogation of Cdk5 expression in brain results in neuronal migration defects

机译：围产期脑中Cdk5表达的废除导致神经元迁移缺陷

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摘要

Cyclin-dependent kinase 5 (Cdk5) is essential for the proper development of the CNS, as is evident from the perinatal lethality of conventional Cdk5 knockout (Cdk5-/-) mice. Cdk5 is also implicated in numerous complex functions of the adult CNS such as synaptic transmission, synaptic plasticity, and neuronal signaling. To elucidate the molecular roles of Cdk5 in the adult CNS, we have abrogated neuronal expression of Cdk5 in perinatal mice by using a cre-loxP system. The Cdk5-loxP flanked mice were crossed with the cre-transgenic mice in which the cre expression is driven by the murine neurofilament-heavy chain promoter, resulting in generation of viable Cdk5 conditional knockout mice with the restricted deletion of the Cdk5 gene in specific neurons beginning around embryonic day 16.5. Twenty-five percent of the Cdk5 conditional knockout mice carrying the heterozygous cre allele had neuronal migration defects confined to brain areas where neuronal migration continues through the perinatal period. These results indicate that abrogation of Cdk5 expression in mature neurons results in a viable mouse model that offers further opportunities to investigate the molecular roles of Cdk5 in the adult CNS.
机译：细胞周期蛋白依赖性激酶5（Cdk5）对于中枢神经系统的正常发育至关重要，从常规Cdk5基因敲除（Cdk5-/-）小鼠的围生期致死率可以明显看出。 Cdk5也与成人中枢神经系统的许多复杂功能有关，例如突触传递，突触可塑性和神经元信号传导。为了阐明Cdk5在成年中枢神经系统中的分子作用，我们使用cre-loxP系统消除了围生期小鼠中Cdk5的神经元表达。将Cdk5-loxP侧翼小鼠与cre转基因小鼠杂交，其中cre表达由鼠神经丝重链启动子驱动，从而导致在特定神经元中Cdk5基因的限制性缺失导致可行的Cdk5条件性基因敲除小鼠的产生从胚胎第16.5天开始。携带杂合cre等位基因的Cdk5条件敲除小鼠中有25％的神经元迁移缺陷局限于大脑区域，在整个围产期神经元迁移持续进行。这些结果表明，废除成熟神经元中Cdk5的表达可形成可行的小鼠模型，这为研究Cdk5在成年中枢神经系统中的分子作用提供了进一步的机会。

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