RGD Reference Report - Bcl11A/CTIP1 regulates expression of DCC and MAP1b in control of axon branching and dendrite outgrowth. - Rat Genome Database

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Bcl11A/CTIP1 regulates expression of DCC and MAP1b in control of axon branching and dendrite outgrowth.

Authors: Kuo, TY  Hong, CJ  Hsueh, YP 
Citation: Kuo TY, etal., Mol Cell Neurosci. 2009 Nov;42(3):195-207. doi: 10.1016/j.mcn.2009.07.006. Epub 2009 Jul 17.
RGD ID: 11100018
Pubmed: (View Article at PubMed) PMID:19616629
DOI: Full-text: DOI:10.1016/j.mcn.2009.07.006

The extension of axon branches is important for target innervation but how axon branching is regulated is currently not well understood. Here, we report that Bcl11A/CTIP1/Evi9, a zinc finger transcription factor, downregulates axon branching. Knockdown of Bcl11A induced axon branching and multi-axon formation, as well as dendrite outgrowth. Due to alternative splicing, a single Bcl11A gene encodes two protein products, Bcl11A-L and -S. Bcl11A-L was found to be the main Bcl11A player in regulation of neurite arborization; Bcl11A-S is an antagonist of Bcl11A-L. Time-lapse study further suggests that Bcl11A-L knockdown enhances axon dynamics and increases the duration of axon outgrowth. Finally, the expression of DCC and MAP1b, two molecules involved in direction and branching of axon outgrowth, is controlled by Bcl11A-L. DCC overexpression rescues the phenotype induced by Bcl11A-L knockdown. In conclusion, this report provides the first evidence that Bcl11A is important for neurite arborization.

Annotation

Objects Annotated

Genes (Rattus norvegicus)
Bcl11a  (BAF chromatin remodeling complex subunit BCL11A)


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