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

Simona Infantino (), Amanda Light, Kristy O’Donnell, Vanessa Bryant, Danielle T. Avery, Michael Elliott, Stuart G. Tangye, Gabrielle Belz, Fabienne Mackay, Stephane Richard and David Tarlinton ()
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Simona Infantino: Walter and Eliza Hall Institute of Medical Research
Amanda Light: Walter and Eliza Hall Institute of Medical Research
Kristy O’Donnell: Walter and Eliza Hall Institute of Medical Research
Vanessa Bryant: Walter and Eliza Hall Institute of Medical Research
Danielle T. Avery: Garvan Institute of Medical Research
Michael Elliott: University of Sydney
Stuart G. Tangye: Garvan Institute of Medical Research
Gabrielle Belz: Walter and Eliza Hall Institute of Medical Research
Fabienne Mackay: University of Melbourne
Stephane Richard: McGill University
David Tarlinton: Walter and Eliza Hall Institute of Medical Research

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: 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.

Date: 2017
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DOI: 10.1038/s41467-017-01009-1

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