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Intestinal Stem Cell Pool Regulation in Drosophila

Intestinal epithelial renewal is mediated by intestinal stem cells (ISCs) that exist in a state of neutral drift, wherein individual ISC lineages are regularly lost and born but ISC numbers remain constant. To test whether an active mechanism maintains stem cell pools in the Drosophila midgut, we pe...

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Autores principales: Jin, Yinhua, Patel, Parthive H., Kohlmaier, Alexander, Pavlovic, Bojana, Zhang, Chenge, Edgar, Bruce A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5469868/
https://www.ncbi.nlm.nih.gov/pubmed/28479306
http://dx.doi.org/10.1016/j.stemcr.2017.04.002
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author Jin, Yinhua
Patel, Parthive H.
Kohlmaier, Alexander
Pavlovic, Bojana
Zhang, Chenge
Edgar, Bruce A.
author_facet Jin, Yinhua
Patel, Parthive H.
Kohlmaier, Alexander
Pavlovic, Bojana
Zhang, Chenge
Edgar, Bruce A.
author_sort Jin, Yinhua
collection PubMed
description Intestinal epithelial renewal is mediated by intestinal stem cells (ISCs) that exist in a state of neutral drift, wherein individual ISC lineages are regularly lost and born but ISC numbers remain constant. To test whether an active mechanism maintains stem cell pools in the Drosophila midgut, we performed partial ISC depletion. In contrast to the mouse intestine, Drosophila ISCs failed to repopulate the gut after partial depletion. Even when the midgut was challenged to regenerate by infection, ISCs retained normal proportions of asymmetric division and ISC pools did not increase. We discovered, however, that the loss of differentiated midgut enterocytes (ECs) slows when ISC division is suppressed and accelerates when ISC division increases. This plasticity in rates of EC turnover appears to facilitate epithelial homeostasis even after stem cell pools are compromised. Our study identifies unique behaviors of Drosophila midgut cells that maintain epithelial homeostasis.
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spelling pubmed-54698682017-06-23 Intestinal Stem Cell Pool Regulation in Drosophila Jin, Yinhua Patel, Parthive H. Kohlmaier, Alexander Pavlovic, Bojana Zhang, Chenge Edgar, Bruce A. Stem Cell Reports Report Intestinal epithelial renewal is mediated by intestinal stem cells (ISCs) that exist in a state of neutral drift, wherein individual ISC lineages are regularly lost and born but ISC numbers remain constant. To test whether an active mechanism maintains stem cell pools in the Drosophila midgut, we performed partial ISC depletion. In contrast to the mouse intestine, Drosophila ISCs failed to repopulate the gut after partial depletion. Even when the midgut was challenged to regenerate by infection, ISCs retained normal proportions of asymmetric division and ISC pools did not increase. We discovered, however, that the loss of differentiated midgut enterocytes (ECs) slows when ISC division is suppressed and accelerates when ISC division increases. This plasticity in rates of EC turnover appears to facilitate epithelial homeostasis even after stem cell pools are compromised. Our study identifies unique behaviors of Drosophila midgut cells that maintain epithelial homeostasis. Elsevier 2017-05-04 /pmc/articles/PMC5469868/ /pubmed/28479306 http://dx.doi.org/10.1016/j.stemcr.2017.04.002 Text en © 2017 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Report
Jin, Yinhua
Patel, Parthive H.
Kohlmaier, Alexander
Pavlovic, Bojana
Zhang, Chenge
Edgar, Bruce A.
Intestinal Stem Cell Pool Regulation in Drosophila
title Intestinal Stem Cell Pool Regulation in Drosophila
title_full Intestinal Stem Cell Pool Regulation in Drosophila
title_fullStr Intestinal Stem Cell Pool Regulation in Drosophila
title_full_unstemmed Intestinal Stem Cell Pool Regulation in Drosophila
title_short Intestinal Stem Cell Pool Regulation in Drosophila
title_sort intestinal stem cell pool regulation in drosophila
topic Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5469868/
https://www.ncbi.nlm.nih.gov/pubmed/28479306
http://dx.doi.org/10.1016/j.stemcr.2017.04.002
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