| First Author | Webb CF | Year | 2011 |
| Journal | Mol Cell Biol | Volume | 31 |
| Issue | 5 | Pages | 1041-53 |
| PubMed ID | 21199920 | Mgi Jnum | J:169178 |
| Mgi Id | MGI:4939979 | Doi | 10.1128/MCB.01448-10 |
| Citation | Webb CF, et al. (2011) The ARID Family Transcription Factor Bright Is Required for both Hematopoietic Stem Cell and B Lineage Development. Mol Cell Biol 31(5):1041-53 |
| abstractText | Bright/Arid3a has been characterized both as an activator of immunoglobulin heavy-chain transcription and as a proto-oncogene. Although Bright expression is highly B lineage stage restricted in adult mice, its expression in the earliest identifiable hematopoietic stem cell (HSC) population suggests that Bright might have additional functions. We showed that >99% of Bright(-/-) embryos die at midgestation from failed hematopoiesis. Bright(-/-) embryonic day 12.5 (E12.5) fetal livers showed an increase in the expression of immature markers. Colony-forming assays indicated that the hematopoietic potential of Bright(-/-) mice is markedly reduced. Rare survivors of lethality, which were not compensated by the closely related paralogue Bright-derived protein (Bdp)/Arid3b, suffered HSC deficits in their bone marrow as well as B lineage-intrinsic developmental and functional deficiencies in their peripheries. These include a reduction in a natural antibody, B-1 responses to phosphocholine, and selective T-dependent impairment of IgG1 class switching. Our results place Bright/Arid3a on a select list of transcriptional regulators required to program both HSC and lineage-specific differentiation. |
