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  • 1
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    Nuclear receptor corepressor and histone deacetylase 3 govern circadian metabolic physiology (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-11-28
    Description: Rhythmic changes in histone acetylation at circadian clock genes suggest that temporal modulation of gene expression is regulated by chromatin modifications. Furthermore, recent studies demonstrate a critical relationship between circadian and metabolic physiology. The nuclear receptor corepressor 1 (Ncor1) functions as an activating subunit for the chromatin modifying enzyme histone deacetylase 3 (Hdac3). Lack of Ncor1 is incompatible with life, and hence it is unknown whether Ncor1, and particularly its regulation of Hdac3, is critical for adult mammalian physiology. Here we show that specific, genetic disruption of the Ncor1-Hdac3 interaction in mice causes aberrant regulation of clock genes and results in abnormal circadian behaviour. These mice are also leaner and more insulin-sensitive owing to increased energy expenditure. Unexpectedly, loss of a functional Ncor1-Hdac3 complex in vivo does not lead to sustained increases in known catabolic genes, but instead significantly alters the oscillatory patterns of several metabolic genes, demonstrating that circadian regulation of metabolism is critical for normal energy balance. These findings indicate that activation of Hdac3 by Ncor1 is a nodal point in the epigenetic regulation of circadian and metabolic physiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2742159/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2742159/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alenghat, Theresa -- Meyers, Katherine -- Mullican, Shannon E -- Leitner, Kirstin -- Adeniji-Adele, Adetoun -- Avila, Jacqueline -- Bucan, Maja -- Ahima, Rexford S -- Kaestner, Klaus H -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- DK50306/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-15/DK/NIDDK NIH HHS/ -- R37 DK043806-16/DK/NIDDK NIH HHS/ -- R37 DK043806-17/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Dec 18;456(7224):997-1000. doi: 10.1038/nature07541. Epub 2008 Nov 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19037247" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Biological Clocks/genetics/physiology ; Cells, Cultured ; Circadian Rhythm/genetics/*physiology ; Diet ; Energy Metabolism/genetics/physiology ; Female ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Liver/enzymology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/chemistry/genetics/*metabolism ; Nuclear Receptor Co-Repressor 1 ; Obesity/enzymology/genetics/metabolism ; Repressor Proteins/chemistry/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Ligand-induced transformation by a noninternalizing epidermal growth factor receptor (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-23
    Description: Identification of a mutant epidermal growth factor (EGF) receptor that does not undergo downregulation has provided a genetic probe to investigate the role of internalization in ligand-induced mitogenesis. Contact-inhibited cells expressing this internalization-defective receptor exhibited a normal mitogenic response at significantly lower ligand concentrations than did cells expressing wild-type receptors. A transformed phenotype and anchorage-independent growth were observed at ligand concentrations that failed to elicit these responses in cells expressing wild-type receptors. These findings imply that activation of the protein tyrosine kinase activity at the cell membrane is sufficient for the growth-enhancing effects of EGF. Thus, downregulation can serve as an attenuation mechanism, without which transformation ensues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wells, A -- Welsh, J B -- Lazar, C S -- Wiley, H S -- Gill, G N -- Rosenfeld, M G -- DDK 13149/DK/NIDDK NIH HHS/ -- DDK 18477/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):962-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California-San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305263" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cell Line ; Down-Regulation ; *Endocytosis ; Enzyme Activation ; Epidermal Growth Factor/pharmacology ; Genetic Vectors ; Moloney murine leukemia virus/genetics ; Mutation ; Phenotype ; Protein-Tyrosine Kinases/metabolism ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-05
    Description: The development and severity of inflammatory bowel diseases and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that mice with an intestinal epithelial cell (IEC)-specific deletion of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3(DeltaIEC) mice) exhibited extensive dysregulation of IEC-intrinsic gene expression, including decreased basal expression of genes associated with antimicrobial defence. Critically, conventionally housed HDAC3(DeltaIEC) mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3(DeltaIEC) mice showed significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 has a central role in maintaining intestinal homeostasis. Re-derivation of HDAC3(DeltaIEC) mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis and intestinal barrier function were largely restored in the absence of commensal bacteria. Although the specific mechanisms through which IEC-intrinsic HDAC3 expression regulates these complex phenotypes remain to be determined, these data indicate that HDAC3 is a critical factor that integrates commensal-bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949438/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949438/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alenghat, Theresa -- Osborne, Lisa C -- Saenz, Steven A -- Kobuley, Dmytro -- Ziegler, Carly G K -- Mullican, Shannon E -- Choi, Inchan -- Grunberg, Stephanie -- Sinha, Rohini -- Wynosky-Dolfi, Meghan -- Snyder, Annelise -- Giacomin, Paul R -- Joyce, Karen L -- Hoang, Tram B -- Bewtra, Meenakshi -- Brodsky, Igor E -- Sonnenberg, Gregory F -- Bushman, Frederic D -- Won, Kyoung-Jae -- Lazar, Mitchell A -- Artis, David -- 2-P30 CA016520/CA/NCI NIH HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- DK043806/DK/NIDDK NIH HHS/ -- DP5 OD012116/OD/NIH HHS/ -- DP5OD012116/OD/NIH HHS/ -- F31-GM082187/GM/NIGMS NIH HHS/ -- K08 DK084347/DK/NIDDK NIH HHS/ -- K08 DK093784/DK/NIDDK NIH HHS/ -- K08-DK084347/DK/NIDDK NIH HHS/ -- K08-DK093784/DK/NIDDK NIH HHS/ -- P01 AI106697/AI/NIAID NIH HHS/ -- P30 CA016520/CA/NCI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- P30-DK19525/DK/NIDDK NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- R21 AI105346/AI/NIAID NIH HHS/ -- R21-AI105346/AI/NIAID NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- T32-RR007063/RR/NCRR NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Dec 5;504(7478):153-7. doi: 10.1038/nature12687. Epub 2013 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [2] Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [3] Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24185009" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Bacteria/genetics ; Colitis, Ulcerative/enzymology/genetics/microbiology ; Crohn Disease/enzymology/genetics/microbiology ; Female ; Gene Deletion ; Gene Expression Profiling ; *Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; *Homeostasis ; Humans ; Intestinal Mucosa/*enzymology/pathology ; Intestines/*microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Paneth Cells/cytology/metabolism ; RNA, Ribosomal, 16S/genetics ; Signal Transduction ; *Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    The nuclear receptor Rev-erbalpha controls circadian thermogenic plasticity (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-10-29
    Description: Circadian oscillation of body temperature is a basic, evolutionarily conserved feature of mammalian biology. In addition, homeostatic pathways allow organisms to protect their core temperatures in response to cold exposure. However, the mechanism responsible for coordinating daily body temperature rhythm and adaptability to environmental challenges is unknown. Here we show that the nuclear receptor Rev-erbalpha (also known as Nr1d1), a powerful transcriptional repressor, links circadian and thermogenic networks through the regulation of brown adipose tissue (BAT) function. Mice exposed to cold fare considerably better at 05:00 (Zeitgeber time 22) when Rev-erbalpha is barely expressed than at 17:00 (Zeitgeber time 10) when Rev-erbalpha is abundant. Deletion of Rev-erbalpha markedly improves cold tolerance at 17:00, indicating that overcoming Rev-erbalpha-dependent repression is a fundamental feature of the thermogenic response to cold. Physiological induction of uncoupling protein 1 (Ucp1) by cold temperatures is preceded by rapid downregulation of Rev-erbalpha in BAT. Rev-erbalpha represses Ucp1 in a brown-adipose-cell-autonomous manner and BAT Ucp1 levels are high in Rev-erbalpha-null mice, even at thermoneutrality. Genetic loss of Rev-erbalpha also abolishes normal rhythms of body temperature and BAT activity. Thus, Rev-erbalpha acts as a thermogenic focal point required for establishing and maintaining body temperature rhythm in a manner that is adaptable to environmental demands.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839416/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839416/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerhart-Hines, Zachary -- Feng, Dan -- Emmett, Matthew J -- Everett, Logan J -- Loro, Emanuele -- Briggs, Erika R -- Bugge, Anne -- Hou, Catherine -- Ferrara, Christine -- Seale, Patrick -- Pryma, Daniel A -- Khurana, Tejvir S -- Lazar, Mitchell A -- F-32 DK095563/DK/NIDDK NIH HHS/ -- F32 DK095526/DK/NIDDK NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30 DK19525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R01 DK45586/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- England -- Nature. 2013 Nov 21;503(7476):410-3. doi: 10.1038/nature12642. Epub 2013 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [2] The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24162845" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization/genetics/physiology ; Adipose Tissue, Brown/metabolism ; Animals ; Body Temperature Regulation/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; Cold Temperature ; Down-Regulation ; Ion Channels/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondrial Proteins/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/deficiency/genetics/*metabolism ; Thermogenesis/genetics/physiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Nuclear receptor Rev-erbalpha is a critical lithium-sensitive component of the circadian clock (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Lithium is commonly used to treat bipolar disorder, which is associated with altered circadian rhythm. Lithium is a potent inhibitor of glycogen synthase kinase 3 (GSK3), which regulates circadian rhythm in several organisms. In experiments with cultured cells, we show here that GSK3beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erbalpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erbalpha and activation of clock gene Bmal1. A form of Rev-erbalpha that is insensitive to lithium interferes with the expression of circadian genes. Control of Rev-erbalpha protein stability is thus a critical component of the peripheral clock and a biological target of lithium therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wang, Jing -- Klein, Peter S -- Lazar, Mitchell A -- DK 19525/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- MH058324/MH/NIMH NIH HHS/ -- R01 MH058324/MH/NIMH NIH HHS/ -- R01 MH058324-07/MH/NIMH NIH HHS/ -- R01 MH058324-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1002-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, and University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484495" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biological Clocks/*physiology ; Cell Line ; Cell Line, Tumor ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Glycogen Synthase Kinase 3/antagonists & inhibitors/metabolism ; Humans ; Lithium Chloride/*pharmacology ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Phosphorylation ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Physiology. The health risk of obesity--better metrics imperative (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahima, Rexford S -- Lazar, Mitchell A -- P01-DK-049210/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 23;341(6148):856-8. doi: 10.1126/science.1241244.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, and the Institute for Diabetes, Obesity and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. ahima@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23970691" target="_blank"〉PubMed〈/a〉
    Keywords: *Body Mass Index ; Body Weight/*physiology ; Cardiovascular Diseases/epidemiology/mortality ; *Cause of Death ; Diabetes Mellitus/epidemiology/mortality ; Female ; Humans ; Male ; Obesity/*mortality/*physiopathology ; Risk
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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