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Article ; Online: A window in time for β-cell regeneration.

Weidemann, Benjamin J / Bass, Joseph

2020 Volume 34, Issue 23-24, Page(s) 1559–1561

Abstract: In vivo regeneration of β cells provides hope for self-renewal of functional insulin-secreting cells following β-cell failure, a historically fatal condition now sustainable only by administration of exogenous insulin. Despite advances in the treatment ... ...

Abstract	In vivo regeneration of β cells provides hope for self-renewal of functional insulin-secreting cells following β-cell failure, a historically fatal condition now sustainable only by administration of exogenous insulin. Despite advances in the treatment of diabetes mellitus, the path toward endogenous renewal of β-cell populations has remained elusive. Intensive efforts have focused on elucidating pancreatic transcriptional programs that can drive the division and (
MeSH term(s)	Circadian Clocks ; Diabetes Mellitus ; Humans ; Insulin ; Insulin-Secreting Cells ; Pancreas
Chemical Substances	Insulin
Language	English
Publishing date	2020-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review ; Comment
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.345769.120
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Article ; Online: Repression of latent NF-κB enhancers by PDX1 regulates β cell functional heterogeneity.

Weidemann, Benjamin J / Marcheva, Biliana / Kobayashi, Mikoto / Omura, Chiaki / Newman, Marsha V / Kobayashi, Yumiko / Waldeck, Nathan J / Perelis, Mark / Lantier, Louise / McGuinness, Owen P / Ramsey, Kathryn Moynihan / Stein, Roland W / Bass, Joseph

Cell metabolism

2024 Volume 36, Issue 1, Page(s) 90–102.e7

Abstract: Interactions between lineage-determining and activity-dependent transcription factors determine single-cell identity and function within multicellular tissues through incompletely known mechanisms. By assembling a single-cell atlas of chromatin state ... ...

Abstract	Interactions between lineage-determining and activity-dependent transcription factors determine single-cell identity and function within multicellular tissues through incompletely known mechanisms. By assembling a single-cell atlas of chromatin state within human islets, we identified β cell subtypes governed by either high or low activity of the lineage-determining factor pancreatic duodenal homeobox-1 (PDX1). β cells with reduced PDX1 activity displayed increased chromatin accessibility at latent nuclear factor κB (NF-κB) enhancers. Pdx1 hypomorphic mice exhibited de-repression of NF-κB and impaired glucose tolerance at night. Three-dimensional analyses in tandem with chromatin immunoprecipitation (ChIP) sequencing revealed that PDX1 silences NF-κB at circadian and inflammatory enhancers through long-range chromatin contacts involving SIN3A. Conversely, Bmal1 ablation in β cells disrupted genome-wide PDX1 and NF-κB DNA binding. Finally, antagonizing the interleukin (IL)-1β receptor, an NF-κB target, improved insulin secretion in Pdx1 hypomorphic islets. Our studies reveal functional subtypes of single β cells defined by a gradient in PDX1 activity and identify NF-κB as a target for insulinotropic therapy.
MeSH term(s)	Animals ; Humans ; Mice ; Chromatin/metabolism ; Genes, Homeobox ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Insulin-Secreting Cells/metabolism ; NF-kappa B/metabolism
Chemical Substances	Chromatin ; Homeodomain Proteins ; NF-kappa B ; pancreatic and duodenal homeobox 1 protein
Language	English
Publishing date	2024-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.11.018
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Article ; Online: A day in the life of chromatin: how enhancer-promoter loops shape daily behavior.

Weidemann, Benjamin J / Ramsey, Kathryn Moynihan / Bass, Joseph

Genes & development

2018 Volume 32, Issue 5-6, Page(s) 321–323

Abstract: Each spring, we get out of bed 1 h ahead of our biological wake-up time due to the misalignment of internal clocks with the light-dark cycle. Genetic discoveries revealed that clock genes encode transcription factors that are expressed throughout many ... ...

Abstract	Each spring, we get out of bed 1 h ahead of our biological wake-up time due to the misalignment of internal clocks with the light-dark cycle. Genetic discoveries revealed that clock genes encode transcription factors that are expressed throughout many tissues, yet a gap has remained in understanding the temporal dynamics of transcription. Two groups now apply circular chromosome conformation capture and high-throughput sequencing to dissect how "time of day"-dependent changes in chromatin drive core clock oscillations. A surprise is the finding that disruption of enhancer-promoter contacts within chromatin leads to an advance in the "wake-up" time of mice. Furthermore, the assembly of transcriptionally active domains of chromatin requires the ordered recruitment of core clock transcription factors each day. These studies show that waking up involves highly dynamic changes in the three-dimensional positioning of genes within the cell.
MeSH term(s)	Animals ; Chromatin/genetics ; Circadian Rhythm/genetics ; Enhancer Elements, Genetic/genetics ; Enhancer Elements, Genetic/physiology ; Humans ; Photoperiod ; Promoter Regions, Genetic/genetics ; Promoter Regions, Genetic/physiology
Chemical Substances	Chromatin
Language	English
Publishing date	2018-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.314187.118
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Article ; Online: Time-restricted feeding mitigates obesity through adipocyte thermogenesis.

Hepler, Chelsea / Weidemann, Benjamin J / Waldeck, Nathan J / Marcheva, Biliana / Cedernaes, Jonathan / Thorne, Anneke K / Kobayashi, Yumiko / Nozawa, Rino / Newman, Marsha V / Gao, Peng / Shao, Mengle / Ramsey, Kathryn M / Gupta, Rana K / Bass, Joseph

Science (New York, N.Y.)

2022 Volume 378, Issue 6617, Page(s) 276–284

Abstract: Misalignment of feeding rhythms with the light-dark cycle leads to disrupted peripheral circadian clocks and obesity. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. We found that ... ...

Abstract	Misalignment of feeding rhythms with the light-dark cycle leads to disrupted peripheral circadian clocks and obesity. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. We found that genetic enhancement of adipocyte thermogenesis through ablation of the zinc finger protein 423 (ZFP423) attenuated obesity caused by consumption of a high-fat diet during the inactive (light) period by increasing futile creatine cycling in mice. Circadian control of adipocyte creatine metabolism underlies the timing of diet-induced thermogenesis, and enhancement of adipocyte circadian rhythms through overexpression of the clock activator brain and muscle Arnt-like protein-1 (BMAL1) ameliorated metabolic complications during diet-induced obesity. These findings uncover rhythmic creatine-mediated thermogenesis as an essential mechanism that drives metabolic benefits during time-restricted feeding.
MeSH term(s)	Animals ; Mice ; Adipocytes/metabolism ; ARNTL Transcription Factors/genetics ; Creatine/metabolism ; Obesity/etiology ; Obesity/prevention & control ; Thermogenesis/genetics ; Time Factors ; Circadian Clocks ; Circadian Rhythm ; Diet, High-Fat/adverse effects ; DNA-Binding Proteins/genetics ; Transcription Factors/genetics ; Mice, Knockout
Chemical Substances	ARNTL Transcription Factors ; Creatine (MU72812GK0) ; Bmal1 protein, mouse ; Ebfaz protein, mouse ; DNA-Binding Proteins ; Transcription Factors
Language	English
Publishing date	2022-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.abl8007
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Article ; Online: P2Y1 purinergic receptor identified as a diabetes target in a small-molecule screen to reverse circadian β-cell failure.

Marcheva, Biliana / Weidemann, Benjamin J / Taguchi, Akihiko / Perelis, Mark / Ramsey, Kathryn Moynihan / Newman, Marsha V / Kobayashi, Yumiko / Omura, Chiaki / Manning Fox, Jocelyn E / Lin, Haopeng / Macdonald, Patrick E / Bass, Joseph

eLife

2022 Volume 11

Abstract: The mammalian circadian clock drives daily oscillations in physiology and behavior through an autoregulatory transcription feedback loop present in central and peripheral cells. Ablation of the core clock within the endocrine pancreas of adult animals ... ...

Abstract	The mammalian circadian clock drives daily oscillations in physiology and behavior through an autoregulatory transcription feedback loop present in central and peripheral cells. Ablation of the core clock within the endocrine pancreas of adult animals impairs the transcription and splicing of genes involved in hormone exocytosis and causes hypoinsulinemic diabetes. Here, we developed a genetically sensitized small-molecule screen to identify druggable proteins and mechanistic pathways involved in circadian β-cell failure. Our approach was to generate β-cells expressing a nanoluciferase reporter within the proinsulin polypeptide to screen 2640 pharmacologically active compounds and identify insulinotropic molecules that bypass the secretory defect in CRISPR-Cas9-targeted clock mutant β-cells. We validated hit compounds in primary mouse islets and identified known modulators of ligand-gated ion channels and G-protein-coupled receptors, including the antihelmintic ivermectin. Single-cell electrophysiology in circadian mutant mouse and human cadaveric islets revealed ivermectin as a glucose-dependent secretagogue. Genetic, genomic, and pharmacological analyses established the P2Y1 receptor as a clock-controlled mediator of the insulinotropic activity of ivermectin. These findings identify the P2Y1 purinergic receptor as a diabetes target based upon a genetically sensitized phenotypic screen.
MeSH term(s)	ARNTL Transcription Factors ; Animals ; Cell Line ; Circadian Clocks ; Circadian Rhythm ; Cryptochromes/genetics ; Cryptochromes/metabolism ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/metabolism ; Gene Expression Regulation/drug effects ; Glucose/metabolism ; High-Throughput Screening Assays ; Homeostasis ; Humans ; Hypoglycemic Agents/pharmacology ; Insulin/metabolism ; Insulin-Secreting Cells ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Purinergic P2Y1/metabolism
Chemical Substances	ARNTL Transcription Factors ; BMAL1 protein, human ; Bmal1 protein, mouse ; Cry1 protein, mouse ; Cry2 protein, mouse ; Cryptochromes ; Hypoglycemic Agents ; Insulin ; Receptors, Purinergic P2Y1 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-02-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.75132
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Article ; Online: P2Y1 purinergic receptor identified as a diabetes target in a small-molecule screen to reverse circadian β-cell failure

Biliana Marcheva / Benjamin J Weidemann / Akihiko Taguchi / Mark Perelis / Kathryn Moynihan Ramsey / Marsha V Newman / Yumiko Kobayashi / Chiaki Omura / Jocelyn E Manning Fox / Haopeng Lin / Patrick E Macdonald / Joseph Bass

eLife, Vol

2022 Volume 11

Abstract	The mammalian circadian clock drives daily oscillations in physiology and behavior through an autoregulatory transcription feedback loop present in central and peripheral cells. Ablation of the core clock within the endocrine pancreas of adult animals impairs the transcription and splicing of genes involved in hormone exocytosis and causes hypoinsulinemic diabetes. Here, we developed a genetically sensitized small-molecule screen to identify druggable proteins and mechanistic pathways involved in circadian β-cell failure. Our approach was to generate β-cells expressing a nanoluciferase reporter within the proinsulin polypeptide to screen 2640 pharmacologically active compounds and identify insulinotropic molecules that bypass the secretory defect in CRISPR-Cas9-targeted clock mutant β-cells. We validated hit compounds in primary mouse islets and identified known modulators of ligand-gated ion channels and G-protein-coupled receptors, including the antihelmintic ivermectin. Single-cell electrophysiology in circadian mutant mouse and human cadaveric islets revealed ivermectin as a glucose-dependent secretagogue. Genetic, genomic, and pharmacological analyses established the P2Y1 receptor as a clock-controlled mediator of the insulinotropic activity of ivermectin. These findings identify the P2Y1 purinergic receptor as a diabetes target based upon a genetically sensitized phenotypic screen.
Keywords	circadian clock ; high-throughput screen ; diabetes ; ivermectin ; purinergic receptor ; insulin ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Erratum: A role for alternative splicing in circadian control of exocytosis and glucose homeostasis.

Marcheva, Biliana / Perelis, Mark / Weidemann, Benjamin J / Taguchi, Akihiko / Lin, Haopeng / Omura, Chiaki / Kobayashi, Yumiko / Newman, Marsha V / Wyatt, Eugene J / McNally, Elizabeth M / Manning Fox, Jocelyn E / Hong, Heekyung / Shankar, Archana / Wheeler, Emily C / Ramsey, Kathryn Moynihan / MacDonald, Patrick E / Yeo, Gene W / Bass, Joseph

Genes & development

2021 Volume 35, Issue 5-6, Page(s) 425

Language	English
Publishing date	2021-03-01
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.348303.121
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Article ; Online: NAD

Levine, Daniel C / Hong, Heekyung / Weidemann, Benjamin J / Ramsey, Kathryn M / Affinati, Alison H / Schmidt, Mark S / Cedernaes, Jonathan / Omura, Chiaki / Braun, Rosemary / Lee, Choogon / Brenner, Charles / Peek, Clara Bien / Bass, Joseph

Molecular cell

2020 Volume 78, Issue 5, Page(s) 835–849.e7

Abstract: Disrupted sleep-wake and molecular circadian rhythms are a feature of aging associated with metabolic disease and reduced levels of ... ...

Abstract	Disrupted sleep-wake and molecular circadian rhythms are a feature of aging associated with metabolic disease and reduced levels of NAD
MeSH term(s)	ARNTL Transcription Factors/genetics ; Age Factors ; Aging/genetics ; Animals ; CLOCK Proteins/genetics ; Circadian Clocks/physiology ; Circadian Rhythm/genetics ; Circadian Rhythm/physiology ; Cytokines/metabolism ; Female ; HEK293 Cells ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; NAD/metabolism ; Period Circadian Proteins/genetics ; Period Circadian Proteins/metabolism ; Sirtuin 1/metabolism ; Sirtuins/metabolism
Chemical Substances	ARNTL Transcription Factors ; Cytokines ; PER2 protein, human ; Per2 protein, mouse ; Period Circadian Proteins ; NAD (0U46U6E8UK) ; CLOCK Proteins (EC 2.3.1.48) ; Sirtuin 1 (EC 3.5.1.-) ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2020-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.04.010
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Article ; Online: A role for alternative splicing in circadian control of exocytosis and glucose homeostasis.

Marcheva, Biliana / Perelis, Mark / Weidemann, Benjamin J / Taguchi, Akihiko / Lin, Haopeng / Omura, Chiaki / Kobayashi, Yumiko / Newman, Marsha V / Wyatt, Eugene J / McNally, Elizabeth M / Fox, Jocelyn E Manning / Hong, Heekyung / Shankar, Archana / Wheeler, Emily C / Ramsey, Kathryn Moynihan / MacDonald, Patrick E / Yeo, Gene W / Bass, Joseph

Genes & development

2020 Volume 34, Issue 15-16, Page(s) 1089–1105

Abstract: The circadian clock is encoded by a negative transcriptional feedback loop that coordinates physiology and behavior through molecular programs that remain incompletely understood. Here, we reveal rhythmic genome-wide alternative splicing (AS) of pre- ... ...

Abstract	The circadian clock is encoded by a negative transcriptional feedback loop that coordinates physiology and behavior through molecular programs that remain incompletely understood. Here, we reveal rhythmic genome-wide alternative splicing (AS) of pre-mRNAs encoding regulators of peptidergic secretion within pancreatic β cells that are perturbed in
MeSH term(s)	ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/physiology ; Alternative Splicing ; Animals ; CLOCK Proteins/genetics ; CLOCK Proteins/physiology ; Cells, Cultured ; Circadian Clocks/genetics ; Death Domain Receptor Signaling Adaptor Proteins/genetics ; Death Domain Receptor Signaling Adaptor Proteins/metabolism ; Exocytosis ; Glucose/metabolism ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Guanylate Kinases/genetics ; Guanylate Kinases/metabolism ; Homeostasis ; Insulin Secretion/genetics ; Insulin-Secreting Cells/metabolism ; Islets of Langerhans/metabolism ; Male ; Mice, Inbred C57BL ; Nuclear Proteins/physiology ; Obesity/genetics ; Obesity/metabolism ; Synaptosomal-Associated Protein 25/genetics ; Synaptosomal-Associated Protein 25/metabolism ; Transcription Factors/physiology
Chemical Substances	ARNTL Transcription Factors ; Bmal1 protein, mouse ; Death Domain Receptor Signaling Adaptor Proteins ; Guanine Nucleotide Exchange Factors ; Madd protein, mouse ; Nuclear Proteins ; Snap25 protein, mouse ; Synaptosomal-Associated Protein 25 ; Thrap3 protein, mouse ; Transcription Factors ; CLOCK Proteins (EC 2.3.1.48) ; Clock protein, mouse (EC 2.3.1.48) ; CASK kinases (EC 2.7.11.1) ; Guanylate Kinases (EC 2.7.4.8) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-07-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.338178.120
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Article ; Online: Selective Deletion of Renin-b in the Brain Alters Drinking and Metabolism.

Shinohara, Keisuke / Nakagawa, Pablo / Gomez, Javier / Morgan, Donald A / Littlejohn, Nicole K / Folchert, Matthew D / Weidemann, Benjamin J / Liu, Xuebo / Walsh, Susan A / Ponto, Laura L / Rahmouni, Kamal / Grobe, Justin L / Sigmund, Curt D

Hypertension (Dallas, Tex. : 1979)

2017 Volume 70, Issue 5, Page(s) 990–997

Abstract: The brain-specific isoform of renin (Ren-b) has been proposed as a negative regulator of the brain renin-angiotensin system (RAS). We analyzed mice with a selective deletion of Ren-b which preserved expression of the classical renin (Ren-a) isoform. We ... ...

Abstract	The brain-specific isoform of renin (Ren-b) has been proposed as a negative regulator of the brain renin-angiotensin system (RAS). We analyzed mice with a selective deletion of Ren-b which preserved expression of the classical renin (Ren-a) isoform. We reported that Ren-b
MeSH term(s)	Animals ; Basal Metabolism/physiology ; Brain/metabolism ; Drinking/physiology ; Energy Metabolism/physiology ; Hypertension/metabolism ; Mice ; Protein Isoforms ; Renin/metabolism ; Renin-Angiotensin System/physiology ; Sympathetic Nervous System/metabolism
Chemical Substances	Protein Isoforms ; Renin (EC 3.4.23.15)
Language	English
Publishing date	2017-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.117.09923
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