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The adhesion G protein-coupled receptor GPR56 is a cell-autonomous regulator of oligodendrocyte development

Author

Listed:
  • Stefanie Giera

    (Boston Children’s Hospital and Harvard Medical School)

  • Yiyu Deng

    (Boston Children’s Hospital and Harvard Medical School
    Present address: Department of Emergency & Critical Care Medicine, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, PR China)

  • Rong Luo

    (Boston Children’s Hospital and Harvard Medical School)

  • Sarah D. Ackerman

    (Washington University School of Medicine)

  • Amit Mogha

    (Washington University School of Medicine)

  • Kelly R. Monk

    (Washington University School of Medicine
    Hope Center for Neurological Disorders, Washington University School of Medicine)

  • Yanqin Ying

    (Boston Children’s Hospital and Harvard Medical School)

  • Sung-Jin Jeong

    (Boston Children’s Hospital and Harvard Medical School
    Present address: Convergence Brain Research Department, Korea Brain Research Institute (KBRI), Daegu 701–300, South Korea)

  • Manabu Makinodan

    (F.M. Kirby Neurobiology Center, Children’s Hospital, Harvard Medical School
    Harvard Medical School)

  • Allison R. Bialas

    (F.M. Kirby Neurobiology Center, Children’s Hospital, Harvard Medical School
    Harvard Medical School)

  • Bernard S. Chang

    (Comprehensive Epilepsy Center, Beth Israel Deaconess Medical Center and Harvard Medical School)

  • Beth Stevens

    (F.M. Kirby Neurobiology Center, Children’s Hospital, Harvard Medical School
    Harvard Medical School)

  • Gabriel Corfas

    (F.M. Kirby Neurobiology Center, Children’s Hospital, Harvard Medical School
    Harvard Medical School
    Present address: Kresge Hearing Research Institute, Department of Otolaryngology - Head and Neck Surgery, University of Michigan, Ann Arbor, Michigan 48109, USA))

  • Xianhua Piao

    (Boston Children’s Hospital and Harvard Medical School)

Abstract

Mutations in GPR56, a member of the adhesion G protein-coupled receptor family, cause a human brain malformation called bilateral frontoparietal polymicrogyria (BFPP). Magnetic resonance imaging (MRI) of BFPP brains reveals myelination defects in addition to brain malformation. However, the cellular role of GPR56 in oligodendrocyte development remains unknown. Here, we demonstrate that loss of Gpr56 leads to hypomyelination of the central nervous system in mice. GPR56 levels are abundant throughout early stages of oligodendrocyte development, but are downregulated in myelinating oligodendrocytes. Gpr56-knockout mice manifest with decreased oligodendrocyte precursor cell (OPC) proliferation and diminished levels of active RhoA, leading to fewer mature oligodendrocytes and a reduced number of myelinated axons in the corpus callosum and optic nerves. Conditional ablation of Gpr56 in OPCs leads to a reduced number of mature oligodendrocytes as seen in constitutive knockout of Gpr56. Together, our data define GPR56 as a cell-autonomous regulator of oligodendrocyte development.

Suggested Citation

  • Stefanie Giera & Yiyu Deng & Rong Luo & Sarah D. Ackerman & Amit Mogha & Kelly R. Monk & Yanqin Ying & Sung-Jin Jeong & Manabu Makinodan & Allison R. Bialas & Bernard S. Chang & Beth Stevens & Gabriel, 2015. "The adhesion G protein-coupled receptor GPR56 is a cell-autonomous regulator of oligodendrocyte development," Nature Communications, Nature, vol. 6(1), pages 1-12, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7121
    DOI: 10.1038/ncomms7121
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