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    Drosophila Myc integrates multiple signaling pathways to regulate intestinal stem cell proliferation during midgut regeneration

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    Authors
    Ren, Fangfang
    Shi, Qing
    Chen, Yongbin
    Jiang, Alice
    Ip, Y. Tony
    Jiang, Huaqi
    Jiang, Jin
    UMass Chan Affiliations
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2013-09-01
    Keywords
    Animals
    Bleomycin
    Cell Differentiation
    Cell Proliferation
    DNA-Binding Proteins
    Dextran Sulfate
    Drosophila
    Drosophila Proteins
    Female
    Green Fluorescent Proteins
    Intestines
    Intracellular Signaling Peptides and Proteins
    Janus Kinases
    Nuclear Proteins
    Protein-Serine-Threonine Kinases
    RNA Interference
    RNA, Small Interfering
    Receptor, Epidermal Growth Factor
    Receptors, Invertebrate Peptide
    STAT Transcription Factors
    Signal Transduction
    Stem Cells
    Trans-Activators
    Transcription Factors
    Transcription, Genetic
    Cell Biology
    Cells
    Cellular and Molecular Physiology
    Digestive System
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    Link to Full Text
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760623/
    Abstract
    Intestinal stem cells (ISCs) in the Drosophila adult midgut are essential for maintaining tissue homeostasis, and their proliferation and differentiation speed up in order to meet the demand for replenishing the lost cells in response to injury. Several signaling pathways including JAK-STAT, EGFR and Hippo (Hpo) pathways have been implicated in damage-induced ISC proliferation, but the mechanisms that integrate these pathways have remained elusive. Here, we demonstrate that the Drosophila homolog of the oncoprotein Myc (dMyc) functions downstream of these signaling pathways to mediate their effects on ISC proliferation. dMyc expression in precursor cells is stimulated in response to tissue damage, and dMyc is essential for accelerated ISC proliferation and midgut regeneration. We show that tissue damage caused by dextran sulfate sodium feeding stimulates dMyc expression via the Hpo pathway, whereas bleomycin feeding activates dMyc through the JAK-STAT and EGFR pathways. We provide evidence that dMyc expression is transcriptionally upregulated by multiple signaling pathways, which is required for optimal ISC proliferation in response to tissue damage. We have also obtained evidence that tissue damage can upregulate dMyc expression post-transcriptionally. Finally, we show that a basal level of dMyc expression is required for ISC maintenance, proliferation and lineage differentiation during normal tissue homeostasis.
    Source
    Cell Res. 2013 Sep;23(9):1133-46. doi: 10.1038/cr.2013.101. Epub 2013 Jul 30. Link to article on publisher's site
    DOI
    10.1038/cr.2013.101
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/30331
    PubMed ID
    23896988
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1038/cr.2013.101
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