| First Author | Azagra A | Year | 2016 |
| Journal | J Exp Med | Volume | 213 |
| Issue | 12 | Pages | 2591-2601 |
| PubMed ID | 27810920 | Mgi Jnum | J:237521 |
| Mgi Id | MGI:5812848 | Doi | 10.1084/jem.20150821 |
| Citation | Azagra A, et al. (2016) In vivo conditional deletion of HDAC7 reveals its requirement to establish proper B lymphocyte identity and development. J Exp Med 213(12):2591-2601 |
| abstractText | 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. |
