In vivo conditional deletion of HDAC7 reveals its requirement to establish proper B lymphocyte identity and development

J Exp Med. 2016 Nov 14;213(12):2591-2601. doi: 10.1084/jem.20150821. Epub 2016 Oct 17.


Class IIa histone deacetylase (HDAC) subfamily members are tissue-specific gene repressors with crucial roles in development and differentiation processes. A prominent example is HDAC7, a class IIa HDAC that shows a lymphoid-specific expression pattern within the hematopoietic system. In this study, we explored its potential role in B cell development by generating a conditional knockout mouse model. Our study demonstrates for the first time that HDAC7 deletion dramatically blocks early B cell development and gives rise to a severe lymphopenia in peripheral organs, while also leading to pro-B cell lineage promiscuity. We find that HDAC7 represses myeloid and T lymphocyte genes in B cell progenitors through interaction with myocyte enhancer factor 2C (MEFC2). In B cell progenitors, HDAC7 is recruited to promoters and enhancers of target genes, and its absence leads to increased enrichment of histone active marks. Our results prove that HDAC7 is a bona fide transcriptional repressor essential for B cell development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B-Lymphocytes / metabolism*
  • Cell Lineage
  • Enhancer Elements, Genetic / genetics
  • Gene Deletion*
  • Histone Code
  • Histone Deacetylases / deficiency
  • Histone Deacetylases / metabolism*
  • MEF2 Transcription Factors / metabolism
  • Mice
  • Precursor Cells, B-Lymphoid / metabolism
  • Promoter Regions, Genetic / genetics


  • MEF2 Transcription Factors
  • Mef2c protein, mouse
  • Hdac7 protein, mouse
  • Histone Deacetylases