Title: TAF10 interacts with GATA1 transcription factor and controls mouse erythropoiesis
Authors: Papadopoulos, Petros ×
Gutiérrez, Laura
Demmers, Jeroen
Scheer, Elisabeth
Pourfarzad, Farzin
Papageorgiou, Dimitris N
Karkoulia, Elena
Strouboulis, John
van de Werken, Harmen J G
van der Linden, Reinier
Vandenberghe, Peter
Dekkers, Dick H W
Philipsen, Sjaak
Grosveld, Frank
Tora, Làszlò #
Issue Date: Jun-2015
Publisher: American Society for Microbiology (ASM)
Series Title: Molecular and Cellular Biology vol:35 issue:12 pages:2103-18
Article number: MCB.01370-14
Abstract: The ordered assembly of a functional pre-initiation complex (PIC), composed of general transcription factors (GTFs), is a prerequisite for the transcription of protein-coding genes by RNA polymerase II. TFIID, comprised of the TATA binding protein (TBP) and 13 TBP-associated factors (TAFs), is the GTF that is thought to recognize the promoter sequences allowing site-specific PIC assembly. Transcriptional cofactors, such as SAGA, are also necessary for tightly regulated transcription initiation. The contribution of the two TAF10-containing complexes (TFIID, SAGA) to erythropoiesis remains elusive. By ablating TAF10 specifically in erythroid cells in vivo we observed a differentiation block accompanied by deregulated GATA1 target genes, including Gata1 itself, suggesting functional crosstalk between GATA1 and TAF10. Additionally, we analyzed the composition of TFIID and SAGA complexes by mass spectrometry in mouse and human cells and found that their global integrity is maintained, with minor changes, during erythroid differentiation and development. In agreement with our functional data, we show that TAF10 interacts directly with GATA1 and that TAF10 is enriched on the GATA1 locus in human fetal erythroid cells. Thus, our findings demonstrate a crosstalk between canonical TFIID and SAGA complexes and cell-specific transcription activators during development and differentiation.
ISSN: 0270-7306
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Department of Human Genetics - miscellaneous
Laboratory for Genetics of Malignant Disorders
× corresponding author
# (joint) last author

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