{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bonfini A"],"funding":["Agence Nationale de la Recherche","NIA NIH HHS","NIAID NIH HHS","Medical Research Council","National Institutes of Health","UK Research and Innovation","National Science Foundation"],"pagination":["e64125"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8528489"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10"],"pubmed_abstract":["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 <i>Drosophila</i> 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 enteroc"],"journal":["eLife"],"pubmed_title":["Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size."],"pmcid":["PMC8528489"],"funding_grant_id":["ANR-10-LABX-41 ANR-11-IDEX-0002-02","R21 AG065733","IOS-1656118 IOS-1653021","1R21AG065733-01 1R01AI148541-01A1","MR/S033939/1","R01 AI148541"],"pubmed_authors":["Dobson AJ","Revah J","Liu X","Buchon N","Houtz P","Duneau D","Bonfini A"],"additional_accession":[]},"is_claimable":false,"name":"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 <i>Drosophila</i> 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 enteroc","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-05-28T05:18:02.239Z","creation":"2022-02-11T14:52:23.905Z"},"accession":"S-EPMC8528489","cross_references":{"pubmed":["34553686"],"doi":["10.7554/eLife.64125"]}}