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Drosophila intestinal stem and progenitor cells are major sources and regulators of homeostatic niche signals

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Doupe, DP, Marshall, OJ ORCID: 0000-0003-1605-3871, Dayton, H, Brand, AH and Perrimon, N 2018 , 'Drosophila intestinal stem and progenitor cells are major sources and regulators of homeostatic niche signals' , Proceedings of the National Academy of Sciences of The United States of America , pp. 1-6 , doi: 10.1073/pnas.1719169115.

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Abstract

Epithelial homeostasis requires the precise balance of epithelial stem/progenitor proliferation and differentiation. While many signaling pathways that regulate epithelial stem cells have been identified, it is probable that other regulators remain unidentified. Here, we use gene-expression profiling by targeted DamID to identify the stem/progenitor-specific transcription and signaling factors in the Drosophila midgut. Many signaling pathway components, including ligands of most major pathways, exhibit stem/progenitor-specific expression and have regulatory regions bound by both intrinsic and extrinsic transcription factors. In addition to previously identified stem/progenitor-derived ligands, we show that both the insulin-like factor Ilp6 and TNF ligand eiger are specifically expressed in the stem/progenitors and regulate normal tissue homeostasis. We propose that intestinal stem cells not only integrate multiple signals but also contribute to and regulate the homeostatic signaling microenvironmental niche through the expression of autocrine and paracrine factors.

Item Type: Article
Authors/Creators:Doupe, DP and Marshall, OJ and Dayton, H and Brand, AH and Perrimon, N
Keywords: epithelial homeostasis, insulin, microenvironment, niche, stem cells
Journal or Publication Title: Proceedings of the National Academy of Sciences of The United States of America
Publisher: Natl Acad Sciences
ISSN: 0027-8424
DOI / ID Number: 10.1073/pnas.1719169115
Copyright Information:

Copyright 2018 The AuthorsLicensed under Creative Commons Attribution 4.0 International (CC BY 4.0)https://creativecommons.org/licenses/by/4.0/

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