Abstract:
:The Mediator complex forms the bridge between transcriptional activators and RNA polymerase II. Mediator subunit Med1/TRAP220 is a key component of Mediator originally found to associate with nuclear hormone receptors. Med1 deficiency causes lethality at embryonic day 11.5 because of defects in heart and placenta development. Here we show that Med1-deficient 10.5 days postcoitum embryos are anemic but have normal numbers of hematopoietic progenitor cells. Med1-deficient progenitor cells have a defect in forming erythroid burst-forming units (BFU-E) and colony-forming units (CFU-E), but not in forming myeloid colonies. At the molecular level, we demonstrate that Med1 interacts physically with the erythroid master regulator GATA-1. In transcription assays, Med1 deficiency leads to a defect in GATA-1-mediated transactivation. In chromatin immunoprecipitation experiments, we find Mediator components at GATA-1-occupied enhancer sites. Thus, we conclude that Mediator subunit Med1 acts as a pivotal coactivator for GATA-1 in erythroid development.
journal_name
Proc Natl Acad Sci U S Aauthors
Stumpf M,Waskow C,Krötschel M,van Essen D,Rodriguez P,Zhang X,Guyot B,Roeder RG,Borggrefe Tdoi
10.1073/pnas.0604494103subject
Has Abstractpub_date
2006-12-05 00:00:00pages
18504-9issue
49eissn
0027-8424issn
1091-6490pii
0604494103journal_volume
103pub_type
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