| First Author | Bosè F | Year | 2006 |
| Journal | Mol Cell Biol | Volume | 26 |
| Issue | 10 | Pages | 3942-54 |
| PubMed ID | 16648487 | Mgi Jnum | J:109062 |
| Mgi Id | MGI:3625659 | Doi | 10.1128/MCB.26.10.3942-3954.2006 |
| Citation | Bose F, et al. (2006) Functional interaction of CP2 with GATA-1 in the regulation of erythroid promoters. Mol Cell Biol 26(10):3942-54 |
| abstractText | We observed that binding sites for the ubiquitously expressed transcription factor CP2 were present in regulatory regions of multiple erythroid genes. In these regions, the CP2 binding site was adjacent to a site for the erythroid factor GATA-1. Using three such regulatory regions (from genes encoding the transcription factors GATA-1, EKLF, and p45 NF-E2), we demonstrated the functional importance of the adjacent CP2/GATA-1 sites. In particular, CP2 binds to the GATA-1 HS2 enhancer, generating a ternary complex with GATA-1 and DNA. Mutations in the CP2 consensus greatly impaired HS2 activity in transient transfection assays with K562 cells. Similar results were obtained by transfection of EKLF and p45 NF-E2 mutant constructs. Chromatin immunoprecipitation with K562 cells showed that CP2 binds in vivo to all three regulatory elements and that both GATA-1 and CP2 were present on the same GATA-1 and EKLF regulatory elements. Adjacent CP2/GATA-1 sites may represent a novel module for erythroid expression of a number of genes. Additionally, coimmunoprecipitation and glutathione S-transferase pull-down experiments demonstrated a physical interaction between GATA-1 and CP2. This may contribute to the functional cooperation between these factors and provide an explanation for the important role of ubiquitous CP2 in the regulation of erythroid genes. |
