Lhx1/5 control dendritogenesis and spine morphogenesis of Purkinje cells via regulation of Espin
Nga Chu Lui,
Wing Yip Tam,
Caiji Gao,
Jian-Dong Huang,
Chi Chiu Wang,
Liwen Jiang,
Wing Ho Yung and
Kin Ming Kwan ()
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Nga Chu Lui: School of Life Sciences, The Chinese University of Hong Kong
Wing Yip Tam: School of Life Sciences, The Chinese University of Hong Kong
Caiji Gao: School of Life Sciences, The Chinese University of Hong Kong
Jian-Dong Huang: School of Biomedical Sciences, University of Hong Kong
Chi Chiu Wang: The Chinese University of Hong Kong
Liwen Jiang: School of Life Sciences, The Chinese University of Hong Kong
Wing Ho Yung: School of Biomedical Sciences, The Chinese University of Hong Kong
Kin Ming Kwan: School of Life Sciences, The Chinese University of Hong Kong
Nature Communications, 2017, vol. 8, issue 1, 1-17
Abstract:
Abstract In the cerebellar cortex, Purkinje cells (PCs) receive signals from different inputs through their extensively branched dendrites and serve as an integration centre. Defects in the dendritic development of PCs thus disrupt cerebellar circuitry and cause ataxia. Here we report that specific inactivation of both Lhx1 and Lhx5 in postnatal PCs results in ataxic mutant mice with abnormal dendritic development. The PCs in the mutants have reduced expression of Espin, an F-actin cytoskeleton regulator. We show that Espin expression is transcriptionally activated by Lhx1/5. Downregulation of Espin leads to F-actin mislocalization, thereby impairing dendritogenesis and dendritic spine maturation in the PCs. The mutant PCs therefore fail to form proper synapses and show aberrant electrophysiological properties. By overexpressing Espin, we can successfully rescue the defects in the mutant PCs. Our findings suggest that Lhx1/5, through regulating Espin expression, control dendritogenesis and spine morphogenesis in postnatal PCs.
Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15079
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DOI: 10.1038/ncomms15079
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