| First Author | Tripic T | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 10 | Pages | 2191-201 |
| PubMed ID | 19011221 | Mgi Jnum | J:146089 |
| Mgi Id | MGI:3836678 | Doi | 10.1182/blood-2008-07-169417 |
| Citation | Tripic T, et al. (2009) SCL and associated proteins distinguish active from repressive GATA transcription factor complexes. Blood 113(10):2191-201 |
| abstractText | GATA-1 controls hematopoietic development by activating and repressing gene transcription, yet the in vivo mechanisms that specify these opposite activities are unknown. By examining the composition of GATA-1-associated protein complexes in a conditional erythroid rescue system as well as through the use of tiling arrays we detected the SCL/TAL1, LMO2, Ldb1, E2A complex at all positively acting GATA-1-bound elements examined. Similarly, the SCL complex is present at all activating GATA elements in megakaryocytes and mast cells. In striking contrast, at sites where GATA-1 functions as a repressor, the SCL complex is depleted. A DNA-binding defective form of SCL maintains association with a subset of active GATA elements indicating that GATA-1 is a key determinant for SCL recruitment. Knockdown of LMO2 selectively impairs activation but not repression by GATA-1. ETO-2, an SCL-associated protein with the potential for transcription repression, is also absent from GATA-1-repressed genes but, unlike SCL, fails to accumulate at GATA-1-activated genes. Together, these studies identify the SCL complex as a critical and consistent determinant of positive GATA-1 activity in multiple GATA-1-regulated hematopoietic cell lineages. |
