Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

A C/EBP beta isoform recruits the SWI/SNF complex to activate myeloid genes

Official URL:https://doi.org/10.1016/S1097-2765(00)80384-6
PubMed:View item in PubMed
Creators Name:Kowenz-Leutz, E. and Leutz, A.
Journal Title:Molecular Cell
Journal Abbreviation:Mol Cell
Volume:4
Number:5
Page Range:735-743
Date:November 1999
Keywords:Acetyltransferases, Adenosine Triphosphatases, Binding Sites, CCAAT-Enhancer-Binding Proteins, Cell Cycle Proteins, Cell Line, Chromatin, DNA Helicases, DNA-Binding Proteins, Drosophila Proteins, Erythroblasts, Fibroblasts, Genetic Promoter Regions, Multienzyme Complexes, Nuclear Proteins, Protein Binding, Protein Isoforms, Proteins, Proto-Oncogene Proteins c-myb, Recombinant Fusion Proteins, Saccharomyces Cerevisiae Proteins, Sequence Deletion, Trans-Activators, Transcription Factors, Transcriptional Activation, Animals
Abstract:The activation of many genes requires the concerted effort of two or more transcription factors. Although C/EBP beta is known to cooperate with Myb to induce transcription of the granulocyte-specific mim-1 gene, the molecular mechanism of this cooperativity is undefined. We show that the N terminus of the full-length C/EBP beta isoform, which is essential for induction of the mim-1 gene in chromatin, interacts specifically with the SWI/SNF complex. Grafting this domain onto Myb generates a chimeric activator that recruits SWI/SNF and induces mim-1 transcription in the absence of C/EBP beta. Interaction between C/EBP beta and SWI/SNF is essential for activating a subgroup of resident target genes in chromatin and may represent a major determinant of combinatorial gene regulation in eukaryotes.
ISSN:1097-2765
Publisher:Cell Press (U.S.A.)
Item Type:Article

Repository Staff Only: item control page

Open Access
MDC Library