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    Cooperative binding of AP-1 and TEAD4 modulates the balance between vascular smooth muscle and hemogenic cell fate.

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    Authors
    Obier, N
    Cauchy, P
    Assi, S
    Gilmour, J
    Lie-A-Ling, Michael
    Lichtinger, M
    Hoogenkamp, M
    Noailles, L
    Cockerill, P
    Lacaud, Georges
    Kouskoff, Valerie
    Bonifer, C
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    Affiliation
    Institute of Biomedical Research, College of Medicine and Dentistry, University of Birmingham, Birmingham, UK
    Issue Date
    2016-10-17
    
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    Abstract
    The transmission of extracellular signals into the nucleus involves inducible transcription factors, but how different signaling pathways act in a cell type-specific fashion is poorly understood. Here, we studied the regulatory role of the AP-1 transcription factor family in blood development using embryonic stem cell differentiation coupled with genome-wide transcription factor binding and gene expression analyses. AP-1 factors respond to MAP kinase signaling and are comprised of dimers of FOS, ATF and JUN proteins. To examine genes regulated by AP-1 and to examine how it interacts with other inducible transcription factors we abrogated its global DNA-binding activity using a dominant negative FOS peptide. We show that FOS and JUN bind to and activate a specific set of vascular genes and that AP-1 inhibition shifts the balance between smooth muscle and hematopoietic differentiation towards blood. Further, AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signaling. Our bottom-up approach demonstrates that AP-1 and TEAD4 associated cis-regulatory elements comprise hubs for multiple signaling responsive transcription factors and defines the cistrome regulating vascular and hematopoietic development by extrinsic signals.
    Citation
    Cooperative binding of AP-1 and TEAD4 modulates the balance between vascular smooth muscle and hemogenic cell fate. 2016 Development
    Journal
    Development
    URI
    http://hdl.handle.net/10541/620022
    DOI
    10.1242/dev.139857
    PubMed ID
    27802171
    Type
    Article
    Language
    en
    ISSN
    1477-9129
    ae974a485f413a2113503eed53cd6c53
    10.1242/dev.139857
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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