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as soon as is submitted to ZB.
Sox9 regulates alternative splicing and pancreatic beta cell function.
Nat. Commun. 15:588 (2024)
Despite significant research, mechanisms underlying the failure of islet beta cells that result in type 2 diabetes (T2D) are still under investigation. Here, we report that Sox9, a transcriptional regulator of pancreas development, also functions in mature beta cells. Our results show that Sox9-depleted rodent beta cells have defective insulin secretion, and aging animals develop glucose intolerance, mimicking the progressive degeneration observed in T2D. Using genome editing in human stem cells, we show that beta cells lacking SOX9 have stunted first-phase insulin secretion. In human and rodent cells, loss of Sox9 disrupts alternative splicing and triggers accumulation of non-functional isoforms of genes with key roles in beta cell function. Sox9 depletion reduces expression of protein-coding splice variants of the serine-rich splicing factor arginine SRSF5, a major splicing enhancer that regulates alternative splicing. Our data highlight the role of SOX9 as a regulator of alternative splicing in mature beta cell function.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Transcriptional Network; Progenitor Cells; Stem-cells; Endocrine; Expression; Insulin; Dedifferentiation; Inactivation; Pdx1; Differentiation
Language
english
Publication Year
2024
HGF-reported in Year
2024
ISSN (print) / ISBN
2041-1723
e-ISSN
2041-1723
Journal
Nature Communications
Quellenangaben
Volume: 15,
Issue: 1,
Article Number: 588
Publisher
Nature Publishing Group
Publishing Place
London
Reviewing status
Peer reviewed
Institute(s)
Institute for Diabetes und Organoid Technology (IDOT)
POF-Topic(s)
30201 - Metabolic Health
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-509600-001
Grants
JDRF postdoctoral fellowship
Kraft Family Fellowship
UCSF Flow Cytometry Core
JDRF
Kraft Family Fellowship
UCSF Flow Cytometry Core
JDRF
WOS ID
001145563900008
Scopus ID
85182651286
PubMed ID
38238288
Erfassungsdatum
2024-01-22