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Nat Commun. 2015 Jan 21;6:6122. doi: 10.1038/ncomms7122.

The adhesion GPCR Gpr56 regulates oligodendrocyte development via interactions with Gα12/13 and RhoA.

Author information

1
Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
2
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
3
Division of Newborn Medicine, Department of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
4
1] Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, USA [2] Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

Abstract

In the vertebrate central nervous system, myelinating oligodendrocytes are postmitotic and derive from proliferative oligodendrocyte precursor cells (OPCs). The molecular mechanisms that govern oligodendrocyte development are incompletely understood, but recent studies implicate the adhesion class of G protein-coupled receptors (aGPCRs) as important regulators of myelination. Here, we use zebrafish and mouse models to dissect the function of the aGPCR Gpr56 in oligodendrocyte development. We show that gpr56 is expressed during early stages of oligodendrocyte development. In addition, we observe a significant reduction of mature oligodendrocyte number and myelinated axons in gpr56 zebrafish mutants. This reduction results from decreased OPC proliferation, rather than increased cell death or altered neural precursor differentiation potential. Finally, we show that these functions are mediated by Gα12/13 proteins and Rho activation. Together, our data establish Gpr56 as a regulator of oligodendrocyte development.

PMID:
25607772
PMCID:
PMC4302765
DOI:
10.1038/ncomms7122
[Indexed for MEDLINE]
Free PMC Article

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