CRMP1 and CRMP4 are required for proper orientation of dendrites of cerebral pyramidal neurons in the developing mouse brain.
Neural circuit formation is a critical process in brain development. Axon guidance molecules, their receptors, and intracellular mediators are important to establish neural circuits. Collapsin response mediator proteins (CRMPs) are known intercellular mediators of a number of repulsive guidance molecules. Studies of mutant mice suggest roles of CRMPs in dendrite development. However, molecular mechanisms of CRMP-mediated dendritic development remain to elucidate. In this study, we show abnormal orientation of basal dendrites (extension to deeper side) of layer V pyramidal neurons in the cerebral cortex of CRMP4-/- mice. Moreover, we observed severe abnormality in orientation of the basal dendrites of these neurons in double knockout of CRMP1 and 4, suggesting redundant functions of these two genes. Redundant gene functions were also observed in proximal bifurcation phenotype in apical dendrites of hippocampal CA1 pyramidal neurons. These results indicate that CRMP1 and CRMP4 regulate proper orientation of the basal dendrites of layer V neurons in the cerebral cortex.
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan.
Ryosuke
R
Takaya
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan; Research Fellow of Japan Society for the Promotion of Science, Japan.
Jun
J
Nagai
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan.
Wenfui
W
Piao
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan.
Emi
E
Niisato
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan.
Takeru
T
Nakabayashi
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan.
Yuki
Y
Yamazaki
Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan.
Fumio
F
Nakamura
Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan.
Naoya
N
Yamashita
Biomolecular Science Center, University of Central Florida, Biomolecular Science, Orlando, FL 32816, USA.
Papachan
P
Kolattukudy
Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan.
Yoshio
Y
Goshima
Department of Life Science and Medical Bio-Science, Waseda University, Shinjuku-ku, Tokyo 162-8480, Japan. Electronic address: ohshima@waseda.jp.
Toshio
T
Ohshima
D000818:Animals; D056547:CA1 Region, Hippocampal / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000254:growth & development* / Q000378:metabolism* / Q000473:pathology; D003712:Dendrites / Q000378:metabolism*; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D017966:Pyramidal Cells / Q000378:metabolism* / Q000473:pathology; D040121:Semaphorin-3A / Q000235:genetics / Q000378:metabolism; D000098855:Collapsin Response Mediator Protein 1
D009419:Nerve Tissue Proteins; D040121:Semaphorin-3A; C526904:Dpysl3 protein, mouse; C502872:Crmp1 protein, mouse; D000098855:Collapsin Response Mediator Protein 1; C488217:Sema3a protein, mouse
CRMP; Dendrite; Development; Guidance