Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size

The gut is the primary interface between an animal and food, but how it adapts to qualitative dietary variation is poorly defined. We find that the Drosophila midgut plastically resizes following changes in dietary composition. A panel of nutrients collectively promote gut growth, which sugar oppose...

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Autores principales:	Alessandro Bonfini, Adam J Dobson, David Duneau, Jonathan Revah, Xi Liu, Philip Houtz, Nicolas Buchon
Formato:	article
Lenguaje:	EN
Publicado:	eLife Sciences Publications Ltd 2021
Materias:	organ plasticity gut growth shrinkage diet cell size intestinal stem cell Medicine R Science Q Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/e3a13cacf234480291f8284122088071
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spelling	oai:doaj.org-article:e3a13cacf234480291f82841220880712021-11-25T14:34:19ZMultiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size10.7554/eLife.641252050-084Xe64125https://doaj.org/article/e3a13cacf234480291f82841220880712021-09-01T00:00:00Zhttps://elifesciences.org/articles/64125https://doaj.org/toc/2050-084XThe gut is the primary interface between an animal and food, but how it adapts to qualitative dietary variation is poorly defined. We find that the Drosophila midgut plastically resizes following changes in dietary composition. A panel of nutrients collectively promote gut growth, which sugar opposes. Diet influences absolute and relative levels of enterocyte loss and stem cell proliferation, which together determine cell numbers. Diet also influences enterocyte size. A high sugar diet inhibits translation and uncouples intestinal stem cell proliferation from expression of niche-derived signals, but, surprisingly, rescuing these effects genetically was not sufficient to modify diet’s impact on midgut size. However, when stem cell proliferation was deficient, diet’s impact on enterocyte size was enhanced, and reducing enterocyte-autonomous TOR signaling was sufficient to attenuate diet-dependent midgut resizing. These data clarify the complex relationships between nutrition, epithelial dynamics, and cell size, and reveal a new mode of plastic, diet-dependent organ resizing.Alessandro BonfiniAdam J DobsonDavid DuneauJonathan RevahXi LiuPhilip HoutzNicolas BuchoneLife Sciences Publications Ltdarticleorgan plasticitygut growthshrinkagedietcell sizeintestinal stem cellMedicineRScienceQBiology (General)QH301-705.5ENeLife, Vol 10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	organ plasticity gut growth shrinkage diet cell size intestinal stem cell Medicine R Science Q Biology (General) QH301-705.5
spellingShingle	organ plasticity gut growth shrinkage diet cell size intestinal stem cell Medicine R Science Q Biology (General) QH301-705.5 Alessandro Bonfini Adam J Dobson David Duneau Jonathan Revah Xi Liu Philip Houtz Nicolas Buchon Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
description	The gut is the primary interface between an animal and food, but how it adapts to qualitative dietary variation is poorly defined. We find that the Drosophila midgut plastically resizes following changes in dietary composition. A panel of nutrients collectively promote gut growth, which sugar opposes. Diet influences absolute and relative levels of enterocyte loss and stem cell proliferation, which together determine cell numbers. Diet also influences enterocyte size. A high sugar diet inhibits translation and uncouples intestinal stem cell proliferation from expression of niche-derived signals, but, surprisingly, rescuing these effects genetically was not sufficient to modify diet’s impact on midgut size. However, when stem cell proliferation was deficient, diet’s impact on enterocyte size was enhanced, and reducing enterocyte-autonomous TOR signaling was sufficient to attenuate diet-dependent midgut resizing. These data clarify the complex relationships between nutrition, epithelial dynamics, and cell size, and reveal a new mode of plastic, diet-dependent organ resizing.
format	article
author	Alessandro Bonfini Adam J Dobson David Duneau Jonathan Revah Xi Liu Philip Houtz Nicolas Buchon
author_facet	Alessandro Bonfini Adam J Dobson David Duneau Jonathan Revah Xi Liu Philip Houtz Nicolas Buchon
author_sort	Alessandro Bonfini
title	Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
title_short	Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
title_full	Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
title_fullStr	Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
title_full_unstemmed	Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
title_sort	multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size
publisher	eLife Sciences Publications Ltd
publishDate	2021
url	https://doaj.org/article/e3a13cacf234480291f8284122088071
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Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size

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