ArticlePloS one2017
How stable is repression of disallowed genes in pancreatic islets in response to metabolic stress?
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- GLP1-E2 therapy delays autoimmune diabetes in late-stage prediabetic NOD mice and potentiates low-dose anti-CD3 therapy for enhanced disease protection.Diabetologia · 2026Article
- TBL1X/TBL1XR1 govern β-cell identity through a PAX6-containing gene regulatory network.Nature communications · 2026Article
- Comprehensive Analysis of Ubiquitously Expressed Genes in Humans from A Data-driven Perspective.Genomics, proteomics & bioinformatics · 2023Article
- MafB MaintainsMolecular and cellular biology · 2022Article
- Polycomb Repressive Complexes: Shaping Pancreatic Beta-Cell Destiny in Development and Metabolic Disease.Frontiers in cell and developmental biology · 2022Review
- LDHA is enriched in human islet alpha cells and upregulated in type 2 diabetes.Biochemical and biophysical research communications · 2021Article
- DNA Methylation Patterning and the Regulation of Beta Cell Homeostasis.Frontiers in endocrinology · 2021Review
- Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation.Communications biology · 2020Article
- Beta cell identity changes with mild hyperglycemia: Implications for function, growth, and vulnerability.Molecular metabolism · 2020Article
- Molecular and genetic regulation of pig pancreatic islet cell development.Development (Cambridge, England) · 2020Article
- Functional peroxisomes are required for β-cell integrity in mice.Molecular metabolism · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The specific phenotype of mature differentiated beta cells not only depends on the specific presence of genes that allow beta cell function but also on the selective absence of housekeeping genes ("disallowed genes") that would interfere with this function. Recent studies have shown that both histone modifications and DNA methylation via the de novo methyltransferase DNMT3A are involved in repression of disallowed genes in neonatal beta cells when these cells acquire their mature phenotype. It is unknown, however, if the environmental influence of advanced age, pregnancy and the metabolic stress of high fat diet or diabetes could alter the repression of disallowed genes in beta cells. In the present study, we show that islet disallowed genes-which are also deeply repressed in FACS-purified beta cells-remain deeply repressed in animals of advanced age and in pregnant females. Moreover, the stability of this repression was correlated with strong and stable histone repression marks that persisted in islets isolated from 2 year old mice and with overall high expression of Dnmt3a in islets. Furthermore, repression of disallowed genes was unaffected by the metabolic stress of high fat diet. However, repression of about half of the disallowed genes was weakened in 16 week-old diabetic db/db mice. In conclusion, we show that the disallowed status of islet genes is stable under physiological challenging conditions (advanced age, pregnancy, high fat diet) but partially lost in islets from diabetic animals.
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