MODIFICATION OF BRAIN SPECIFIC CYCLIN DEPENDENT KINASE GENES

蛋白激酶cdc5家族起着重要作用。 在真核生物细胞周期的调节中。为了 确定CDK5在大脑发育中的作用，我们创造了 CDK5基因敲除(-/-)小鼠。这些小鼠的寿命大大延长了 被缩短了。这些小鼠的大脑缺乏皮质片层结构。 和小脑的叶状突起。最近的研究表明，CDK5(-/-) 丘脑轴突通过大脑皮层投射异常 轨迹和皮质板神经元根据 他们的出生日期。预制板的细胞被分离成 亚板和边缘区的神经元形态 正常的锥体神经元。这些细胞的一些轴突 正确地投射到丘脑原基上。结果表明， 在CDK5(-/-)小鼠中，进一步的皮质发育被阻止 预制板分裂后不久的中间阶段。 CDK5(-/-)与卷曲和Scrbler小鼠的比较 表明CDK5缺乏会导致明显的病理改变 改变。结果表明，CDK5参与了一个单独的， 也许是平行的，大脑发育的途径。

The cdc5 family of protein kinases has a major role in the regulation of the cell cycle in eukaryotes. In order to determine the role of the cdk5 in brain development, we created cdk5 knock-out (-/-) mice. The life-span of these mice was greatly shortened. The brains of these mice lack cortical laminar structure and cerebellar foliation. Recent studies revealed that the Cdk5 (-/-) thalamic axons project through the cerebral cortex with abnormal trajectories and cortical plate neurons were inverted according to their birth date. The cells of the preplate were separated into subplate and marginal zone by neurons with the morphology of normal pyramidal neurons. Some of the axons of these cells projected correctly to the thalamic anlage. The results suggest that further cortical development is blocked in the Cdk5 (-/-) mice at an intermediate stage soon after the splitting of the preplate. Comparison with Cdk5 (-/-) with reeler and scrambler mice indicates that the cdk5 deficiency causes distinct pathological changes. The results suggest that Cdk5 participates in a separate, perhaps parallel, pathway of brain development.