Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Non-syndromic mild mental retardation candidate gene CDKL3 regulates neuronal morphogenesis.

Authors: Liu, Z  Xu, D  Zhao, Y  Zheng, J 
Citation: Liu Z, etal., Neurobiol Dis. 2010 Sep;39(3):242-51. doi: 10.1016/j.nbd.2010.03.015. Epub 2010 Mar 27.
Pubmed: (View Article at PubMed) PMID:20347982
DOI: Full-text: DOI:10.1016/j.nbd.2010.03.015

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.


Gene Ontology Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 8693354
Created: 2014-07-11
Species: All species
Last Modified: 2014-07-11
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.