Kruppel-like factor KLF10 is a link between ...
Type de document :
Compte-rendu et recension critique d'ouvrage
DOI :
PMID :
Titre :
Kruppel-like factor KLF10 is a link between the circadian clock and metabolism in liver.
Auteur(s) :
Guillaumond, Fabienne [Auteur]
Gréchez-Cassiau, Aline [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Subramaniam, Malayannan [Auteur]
Brangolo, Sophie [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Peteri-Brünback, Brigitta [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Staels, Bart [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Fiévet, Catherine [Auteur]
Spelsberg, Thomas C [Auteur]
Delaunay, Franck [Auteur]
Laboratoire de physiologie des membranes cellulaires [LPMC]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Teboul, Michèle [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Gréchez-Cassiau, Aline [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Subramaniam, Malayannan [Auteur]
Brangolo, Sophie [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Peteri-Brünback, Brigitta [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Staels, Bart [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Fiévet, Catherine [Auteur]
Spelsberg, Thomas C [Auteur]
Delaunay, Franck [Auteur]
Laboratoire de physiologie des membranes cellulaires [LPMC]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Teboul, Michèle [Auteur]
Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer [IBDC]
Titre de la revue :
Molecular and Cellular Biology
Pagination :
3059-70
Éditeur :
American Society for Microbiology
Date de publication :
2010-06
ISSN :
0270-7306
Discipline(s) HAL :
Sciences du Vivant [q-bio]/Biologie du développement
Résumé en anglais : [en]
The circadian timing system coordinates many aspects of mammalian physiology and behavior in synchrony with the external light/dark cycle. These rhythms are driven by endogenous molecular clocks present in most body cells. ...
Lire la suite >The circadian timing system coordinates many aspects of mammalian physiology and behavior in synchrony with the external light/dark cycle. These rhythms are driven by endogenous molecular clocks present in most body cells. Many clock outputs are transcriptional regulators, suggesting that clock genes primarily control physiology through indirect pathways. Here, we show that Krüppel-like factor 10 (KLF10) displays a robust circadian expression pattern in wild-type mouse liver but not in clock-deficient Bmal1 knockout mice. Consistently, the Klf10 promoter recruited the BMAL1 core clock protein and was transactivated by the CLOCK-BMAL1 heterodimer through a conserved E-box response element. Profiling the liver transcriptome from Klf10(-/-) mice identified 158 regulated genes with significant enrichment for transcripts involved in lipid and carbohydrate metabolism. Importantly, approximately 56% of these metabolic genes are clock controlled. Male Klf10(-/-) mice displayed postprandial and fasting hyperglycemia, a phenotype accompanied by a significant time-of-day-dependent upregulation of the gluconeogenic gene Pepck and increased hepatic glucose production. Consistently, functional data showed that the proximal Pepck promoter is repressed directly by KLF10. Klf10(-/-) females were normoglycemic but displayed higher plasma triglycerides. Correspondingly, rhythmic gene expression of components of the lipogenic pathway, including Srebp1c, Fas, and Elovl6, was altered in females. Collectively, these data establish KLF10 as a required circadian transcriptional regulator that links the molecular clock to energy metabolism in the liver.Lire moins >
Lire la suite >The circadian timing system coordinates many aspects of mammalian physiology and behavior in synchrony with the external light/dark cycle. These rhythms are driven by endogenous molecular clocks present in most body cells. Many clock outputs are transcriptional regulators, suggesting that clock genes primarily control physiology through indirect pathways. Here, we show that Krüppel-like factor 10 (KLF10) displays a robust circadian expression pattern in wild-type mouse liver but not in clock-deficient Bmal1 knockout mice. Consistently, the Klf10 promoter recruited the BMAL1 core clock protein and was transactivated by the CLOCK-BMAL1 heterodimer through a conserved E-box response element. Profiling the liver transcriptome from Klf10(-/-) mice identified 158 regulated genes with significant enrichment for transcripts involved in lipid and carbohydrate metabolism. Importantly, approximately 56% of these metabolic genes are clock controlled. Male Klf10(-/-) mice displayed postprandial and fasting hyperglycemia, a phenotype accompanied by a significant time-of-day-dependent upregulation of the gluconeogenic gene Pepck and increased hepatic glucose production. Consistently, functional data showed that the proximal Pepck promoter is repressed directly by KLF10. Klf10(-/-) females were normoglycemic but displayed higher plasma triglycerides. Correspondingly, rhythmic gene expression of components of the lipogenic pathway, including Srebp1c, Fas, and Elovl6, was altered in females. Collectively, these data establish KLF10 as a required circadian transcriptional regulator that links the molecular clock to energy metabolism in the liver.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Source :
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- https://mcb.asm.org/content/30/12/3059.full.pdf
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- https://mcb.asm.org/content/30/12/3059.full.pdf
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- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876690/pdf
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