dc.contributor.author | Petrenko, Volodymyr | |
dc.contributor.author | Stolovich-Rain, Miri | |
dc.contributor.author | Vandereycken, Bart | |
dc.contributor.author | Giovannoni, Laurianne | |
dc.contributor.author | Storch, Kai-Florian | |
dc.contributor.author | Dor, Yuval | |
dc.contributor.author | Chera, Simona | |
dc.contributor.author | Dibner, Charna | |
dc.date.accessioned | 2021-05-11T12:43:21Z | |
dc.date.available | 2021-05-11T12:43:21Z | |
dc.date.created | 2020-12-13T22:22:59Z | |
dc.date.issued | 2020 | |
dc.Published | Genes & Development. 2020, 34 (23-24), 1650-1665. | |
dc.identifier.issn | 0890-9369 | |
dc.identifier.uri | https://hdl.handle.net/11250/2754946 | |
dc.description.abstract | Circadian clocks in pancreatic islets participate in the regulation of glucose homeostasis. Here we examined the role of these timekeepers in β-cell regeneration after the massive ablation of β cells by doxycycline-induced expression of diphtheria toxin A (DTA) in Insulin-rtTA/TET-DTA mice. Since we crossed reporter genes expressing α- and β-cell-specific fluorescent proteins into these mice, we could follow the fate of α- and β cells separately. As expected, DTA induction resulted in an acute hyperglycemia, which was accompanied by dramatic changes in gene expression in residual β cells. In contrast, only temporal alterations of gene expression were observed in α cells. Interestingly, β cells entered S phase preferentially during the nocturnal activity phase, indicating that the diurnal rhythm also plays a role in the orchestration of β-cell regeneration. Indeed, in arrhythmic Bmal1-deficient mice, which lack circadian clocks, no compensatory β-cell proliferation was observed, and the β-cell ablation led to aggravated hyperglycemia, hyperglucagonemia, and fatal diabetes. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | CSH Press | en_US |
dc.rights | Navngivelse-Ikkekommersiell 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc/4.0/deed.no | * |
dc.title | The core clock transcription factor BMAL1 drives circadian β-cell proliferation during compensatory regeneration of the endocrine pancreas | en_US |
dc.type | Journal article | en_US |
dc.type | Peer reviewed | en_US |
dc.description.version | publishedVersion | en_US |
dc.rights.holder | Copyright 2020 The Authors | en_US |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 2 | |
dc.identifier.doi | 10.1101/gad.343137.120 | |
dc.identifier.cristin | 1859258 | |
dc.source.journal | Genes & Development | en_US |
dc.source.40 | 34 | |
dc.source.14 | 23-24 | |
dc.source.pagenumber | 1650-1665 | en_US |
dc.identifier.citation | Genes & Development. 2020, 34: 1650-1665 | en_US |
dc.source.volume | 34 | en_US |