Brain-specific Crmp2 deletion leads to neuronal development deficits and behavioural impairments in mice

Hongsheng Zhang, Eunchai Kang, Yaqing Wang, Chaojuan Yang, Hui Yu, Qin Wang, Zheyu Chen, Chen Zhang, Kimberly M. Christian, Hongjun Song, Guo-li Ming () and Zhiheng Xu ()
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Hongsheng Zhang: State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Eunchai Kang: Institute for Cell Engineering, Johns Hopkins University School of Medicine
Yaqing Wang: State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Chaojuan Yang: State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University
Hui Yu: Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University
Qin Wang: State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Zheyu Chen: Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University
Chen Zhang: State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University
Kimberly M. Christian: Institute for Cell Engineering, Johns Hopkins University School of Medicine
Hongjun Song: Institute for Cell Engineering, Johns Hopkins University School of Medicine
Guo-li Ming: Institute for Cell Engineering, Johns Hopkins University School of Medicine
Zhiheng Xu: State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: Abstract Several genome- and proteome-wide studies have associated transcription and translation changes of CRMP2 (collapsing response mediator protein 2) with psychiatric disorders, yet little is known about its function in the developing or adult mammalian brain in vivo. Here we show that brain-specific Crmp2 knockout (cKO) mice display molecular, cellular, structural and behavioural deficits, many of which are reminiscent of neural features and symptoms associated with schizophrenia. cKO mice exhibit enlarged ventricles and impaired social behaviour, locomotor activity, and learning and memory. Loss of Crmp2 in the hippocampus leads to reduced long-term potentiation, abnormal NMDA receptor composition, aberrant dendrite development and defective synapse formation in CA1 neurons. Furthermore, knockdown of crmp2 specifically in newborn neurons results in stage-dependent defects in their development during adult hippocampal neurogenesis. Our findings reveal a critical role for CRMP2 in neuronal plasticity, neural function and behavioural modulation in mice.

Date: 2016
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DOI: 10.1038/ncomms11773

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