Abstract
Stem cell division is essential for tissue integrity during growth, aging, and pathogenic assaults. Adult gastrointestinal tract encounters numerous stimulations, and impaired tissue regeneration may lead to inflammatory diseases and cancer. Intestinal stem cells in adult Drosophila have recently been identified and shown to replenish the various cell types within the midgut. However, it is not known whether these intestinal stem cells can respond to environmental challenges. By feeding dextran sulfate sodium and bleomycin to flies and by expressing apoptotic proteins, we show that Drosophila intestinal stem cells can increase the rate of division in response to tissue damage. Moreover, if tissue damage results in epithelial cell loss, the newly formed enteroblasts can differentiate into mature epithelial cells. By using this newly established system of intestinal stem cell proliferation and tissue regeneration, we find that the insulin receptor signaling pathway is required for intestinal stem cell division.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Basement Membrane / drug effects
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Basement Membrane / metabolism
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Basement Membrane / pathology
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Bleomycin / pharmacology
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Cell Count
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Cell Differentiation / drug effects
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Cell Division / drug effects
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Cell Lineage / drug effects
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Cell Proliferation / drug effects
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Dextran Sulfate / administration & dosage
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Dextran Sulfate / pharmacology
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Drosophila Proteins / metabolism
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Drosophila melanogaster / cytology*
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Drosophila melanogaster / drug effects
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Drosophila melanogaster / metabolism
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Enterocytes / drug effects
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Enterocytes / metabolism
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Enterocytes / pathology
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Insulin / metabolism
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Intestinal Mucosa / metabolism
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Intestines / cytology*
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Intestines / drug effects
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Intestines / pathology*
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Models, Biological
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Receptor, Insulin / metabolism
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Signal Transduction / drug effects
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Stem Cells / cytology*
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Stem Cells / drug effects
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Stem Cells / metabolism
Substances
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Drosophila Proteins
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Insulin
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Bleomycin
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Dextran Sulfate
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Receptor, Insulin