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    Transcription factor-mediated lineage switching reveals plasticity in primary committed progenitor cells.

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    Authors
    Heyworth, Clare M
    Pearson, Stella
    May, Gillian
    Enver, Tariq
    Affiliation
    Section of Gene Function and Regulation, Institute of Cancer Research, Chester Beatty Laboratories, London SW3 6JB, UK.
    Issue Date
    2002-07-15
    
    Metadata
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    Abstract
    The developmental plasticity of transplanted adult stem cells challenges the notion that tissue-restricted stem cells have stringently limited lineage potential and prompts a re-evaluation of the stability of lineage commitment. Transformed cell systems are inappropriate for such studies, since transformation potentially dysregulates the processes governing lineage commitment. We have therefore assessed the stability of normal lineage commitment in primary adult haematopoietic cells. For these studies we have used prospectively isolated primary bipotent progenitors, which normally display only neutrophil and monocyte differentiation in vitro. In response to ectopic transcription factor expression, these neutrophil/monocyte progenitors were reprogrammed to take on erythroid, eosinophil and basophil-like cell fates, with the resultant colonies resembling the mixed lineage colonies normally generated by multipotential progenitors. Clone-marking and daughter cell experiments identified lineage switching rather than differential cell selection as the mechanism of altered lineage output. These results demonstrate that the cell type-specific programming of apparently committed primary progenitors is not irrevocably fixed, but may be radically re-specified in response to a single transcriptional regulator.
    Citation
    Transcription factor-mediated lineage switching reveals plasticity in primary committed progenitor cells. 2002, 21 (14):3770-81 EMBO J.
    Journal
    The EMBO Journal
    URI
    http://hdl.handle.net/10541/82438
    DOI
    10.1093/emboj/cdf368
    PubMed ID
    12110589
    Type
    Article
    Language
    en
    ISSN
    0261-4189
    ae974a485f413a2113503eed53cd6c53
    10.1093/emboj/cdf368
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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