Med1 deficiency alters the somatic hypermutation spectrum in murine B cells

Abstract

The Mediator complex is known to orchestrate transcription. Here we show that B cell conditional deficient mice for the Med1 subunit display robust somatic hypermutation. Nevertheless, the mutation frequency at A residues is decreased and the expected A/T ratio is abolished, implicating Mediator in the second phase of somatic hypermutation.

Keywords: Activation-induced cytidine deaminase; Antibody diversification; B lymphocyte; Mediator; Somatic hypermutation.