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Arginine methylation catalyzed by PRMT1 is required for B cell activation and differentiation

Author

Listed:
  • Simona Infantino

    (Walter and Eliza Hall Institute of Medical Research
    University of Melbourne
    Monash University)

  • Amanda Light

    (Walter and Eliza Hall Institute of Medical Research
    University of Melbourne)

  • Kristy O’Donnell

    (Walter and Eliza Hall Institute of Medical Research
    University of Melbourne
    Monash University)

  • Vanessa Bryant

    (Walter and Eliza Hall Institute of Medical Research
    University of Melbourne)

  • Danielle T. Avery

    (Garvan Institute of Medical Research)

  • Michael Elliott

    (University of Sydney
    Royal Prince Alfred Hospital)

  • Stuart G. Tangye

    (Garvan Institute of Medical Research
    University of NSW)

  • Gabrielle Belz

    (Walter and Eliza Hall Institute of Medical Research
    University of Melbourne)

  • Fabienne Mackay

    (University of Melbourne)

  • Stephane Richard

    (McGill University)

  • David Tarlinton

    (Walter and Eliza Hall Institute of Medical Research
    University of Melbourne
    Monash University)

Abstract

Arginine methylation catalyzed by protein arginine methyltransferases (PRMT) is a common post-translational modification in mammalian cells, regulating many important functions including cell signalling, proliferation and differentiation. Here we show the role of PRMT1 in B-cell activation and differentiation. PRMT1 expression and activity in human and mouse peripheral B cells increases in response to in vitro or in vivo activation. Deletion of the Prmt1 gene in mature B cells establishes that although the frequency and phenotype of peripheral B cell subsets seem unaffected, immune responses to T-cell-dependent and -independent antigens are substantially reduced. In vitro activation of Prmt1-deficient B cells with a variety of mitogens results in diminished proliferation, differentiation and survival, effects that are correlated with altered signal transduction from the B cell receptor. Thus PRMT1 activity in B cells is required for correct execution of multiple processes that in turn are necessary for humoral immunity.

Suggested Citation

  • Simona Infantino & Amanda Light & Kristy O’Donnell & Vanessa Bryant & Danielle T. Avery & Michael Elliott & Stuart G. Tangye & Gabrielle Belz & Fabienne Mackay & Stephane Richard & David Tarlinton, 2017. "Arginine methylation catalyzed by PRMT1 is required for B cell activation and differentiation," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01009-1
    DOI: 10.1038/s41467-017-01009-1
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    Cited by:

    1. Jing Liu & Xia Bu & Chen Chu & Xiaoming Dai & John M. Asara & Piotr Sicinski & Gordon J. Freeman & Wenyi Wei, 2023. "PRMT1 mediated methylation of cGAS suppresses anti-tumor immunity," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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