文献类型：期刊文献

英文题名：Non-syndromic mild mental retardation candidate gene CDKL3 regulates neuronal morphogenesis

作者：Liu, Zanhua[1];Xu, Dafeng[2];Zhao, Yongbo[1];Zheng, Jing[2]

机构：[1]Shanghai Jiao Tong Univ, Dept Neurol, Sch Med, Shanghai Peoples Hosp 1, Shanghai, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Shanghai 200237, Peoples R China

年份：2010

卷号：39

期号：3

起止页码：242

外文期刊名：NEUROBIOLOGY OF DISEASE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000280544100002)】；

基金：We would like to thank Professor Zhiqi Xiong for providing some laboratory apparatus and guidance, and also we thank Guohe Tan, Sheng Miao and Tingjia Lu for their help with the experiments. This study was supported by the Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

语种：英文

外文关键词：CDKL3; Neuronal morphogenesis; Development; Mental retardation

摘要：Mental retardation is a common neurological disorder characterized by various clinical manifestations, primarily impaired cognitive function. To date, only a few genes linked to mental retardation have been well characterized, and the genetics of mental retardation remains poorly understood. Here, we investigated the role of the Cdkl3, a mental retardation candidate gene, in neuronal morphogenesis. We show that Cdkl3 mRNA expression is developmentally regulated in the central nervous system, peaking during neonatal stages, and CDKL3 protein is enriched in neuronal nuclei. Downregulating CDKL3 by RNAi decreased dendrite branching, total dendritic length and complexity in cultured cortical neurons, whereas it promoted axon growth without affecting axon/dendrite specification. Furthermore, depleting CDKL3 in developing cortical neurons also inhibited dendritic growth and maturation, and reduced spine density on basal dendrites in vivo. In contrast, overexpressing CDKL3 enhanced dendritic elaboration both in vitro and in vivo and suppressed axonal outgrowth in vitro. Taken together, these findings demonstrate that CDKL3 is involved in neuronal morphogenesis during development. (C) 2010 Elsevier Inc. All rights reserved.