1. Med1 deficiency alters the somatic hypermutation spectrum in murine B cells
- Author
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Vincent Heyer, Bernardo Reina-San-Martin, Ebe Schiavo, Léa Gaudot, Anne-Sophie Thomas-Claudepierre, Isabelle Robert, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and univOAK, Archive ouverte
- Subjects
0301 basic medicine ,[SDV.IMM] Life Sciences [q-bio]/Immunology ,Protein subunit ,Immunology ,Somatic hypermutation ,Mice, Transgenic ,Biology ,MED1 ,Mediator Complex Subunit 1 ,Mice ,03 medical and health sciences ,Mediator ,Transcription (biology) ,Activation-induced (cytidine) deaminase ,medicine ,Animals ,Immunology and Allergy ,Mutation frequency ,B cell ,B-Lymphocytes ,Germinal Center ,Cell biology ,030104 developmental biology ,medicine.anatomical_structure ,biology.protein ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Somatic Hypermutation, Immunoglobulin - 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.
- Published
- 2018
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