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    The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl-/- phenotype.

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    Authors
    Chan, Wan Y I
    Follows, George A
    Lacaud, Georges
    Pimanda, John E
    Landry, Josette-Renee
    Kinston, Sarah
    Knezevic, Kathy
    Piltz, Sandie
    Donaldson, Ian J
    Gambardella, Laure
    Sablitzky, Fred
    Green, Anthony R
    Kouskoff, Valerie
    Göttgens, Berthold
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    Affiliation
    Department of Haematology, Cambridge Institute for Medical Research, University of Cambridge, United Kingdom.
    Issue Date
    2007-03-01
    
    Metadata
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    Abstract
    Transcription factors are key regulators of hematopoietic stem cells (HSCs), yet the molecular mechanisms that control their expression are largely unknown. Previously, we demonstrated that expression of Scl/Tal1, a transcription factor required for the specification of HSCs, is controlled by Ets and GATA factors. Here we characterize the molecular mechanisms controlling expression of Lyl1, a paralog of Scl also required for HSC function. Two closely spaced promoters directed expression to hematopoietic progenitor, megakaryocytic, and endothelial cells in transgenic mice. Conserved binding sites required for promoter activity were bound in vivo by GATA-2 and the Ets factors Fli1, Elf1, Erg, and PU.1. However, despite coregulation of Scl and Lyl1 by the same Ets and GATA factors, Scl expression was initiated prior to Lyl1 in embryonic stem (ES) cell differentiation assays. Moreover, ectopic expression of Scl but not Lyl1 rescued hematopoietic differentiation in Scl-/- ES cells, thus providing a molecular explanation for the vastly different phenotypes of Scl-/- and Lyl1-/- mouse embryos. Furthermore, coregulation of Scl and Lyl1 later during development may explain the mild phenotype of Scl-/- adult HSCs.
    Citation
    The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl-/- phenotype. 2007, 109 (5):1908-16 Blood
    Journal
    Blood
    URI
    http://hdl.handle.net/10541/70325
    DOI
    10.1182/blood-2006-05-023226
    PubMed ID
    17053063
    Type
    Article
    Language
    en
    ISSN
    0006-4971
    ae974a485f413a2113503eed53cd6c53
    10.1182/blood-2006-05-023226
    Scopus Count
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    All Paterson Institute for Cancer Research

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