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Reshaping Circadian Metabolism in the Suprachiasmatic Nucleus and Prefrontal Cortex by Nutritional Challenge

ABSTRACT: We compared the transcriptome of Suprachiasmatic Nucleus in C57BL/6J mice fed a high-fat diet or normal chow through an entire circadian cycle: 6 time points (TP) every four hours.

ORGANISM(S): Mus musculus

PROVIDER: GSE157077 | GEO | 2020/11/07

REPOSITORIES: GEO

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Reshaping Circadian Metabolism in the Suprachiasmatic Nucleus and Prefrontal Cortex by Nutritional Challenge

Project description:Reshaping Circadian Metabolism in the Suprachiasmatic Nucleus and Prefrontal Cortex by Nutritional Challenge

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Reprogramming of the circadian clock by nutritional challenge.

Project description:Circadian rhythms and cellular metabolism are intimately linked. Here, we reveal that a high-fat diet (HFD) generates a profound reorganization of specific metabolic pathways, leading to widespread remodeling of the liver clock. Strikingly, in addition to disrupting the normal circadian cycle, HFD causes an unexpectedly large-scale genesis of de novo oscillating transcripts, resulting in reorganization of the coordinated oscillations between coherent transcripts and metabolites. The mechanisms underlying this reprogramming involve both the impairment of CLOCK:BMAL1 chromatin recruitment and a pronounced cyclic activation of surrogate pathways through the transcriptional regulator PPAR?. Finally, we demonstrate that it is specifically the nutritional challenge, and not the development of obesity, that causes the reprogramming of the clock and that the effects of the diet on the clock are reversible.

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Transcriptome profiling of circadian day and night gene expression in the suprachiasmatic nucleus of wild-type and Gpr176-deficient mice

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2024-09-17 | GSE184440 | GEO

TDP-43 deficiency in suprachiasmatic nucleus perturbs rhythmicity of neuroactivity in prefrontal cortex.

Project description:Individuals within the amyotrophic lateral sclerosis and frontotemporal dementia disease spectrum (ALS/FTD) often experience disruptive mental behaviors and sleep-wake disturbances. The hallmark of ALS/FTD is the pathological involvement of TAR DNA-binding protein 43 (TDP-43). Understanding the role of TDP-43 in the circadian clock holds promise for addressing these behavioral abnormalities. In this study, we unveil TDP-43 as a pivotal regulator of the circadian clock. TDP-43 knockdown induces intracellular arrhythmicity, disrupts transcriptional activation regulation, and diminishes clock genes expression. Moreover, our experiments in adult mouse reveal that TDP-43 knockdown, specifically within the suprachiasmatic nucleus (SCN), induces locomotor arrhythmia, arrhythmic c-Fos expression, and depression-like behavior. This observation offers valuable insights into the substantial impact of TDP-43 on the behavioral aberrations associated with ALS/FTD. In summary, our study illuminates the significance of TDP-43 in circadian regulation, shedding light on the circadian regulatory mechanisms that may elucidate the pathological underpinnings of ALS/FTD.

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Circadian VIPergic neurons of the suprachiasmatic nuclei sculpt the sleep-wake cycle

Project description:Although the mammalian rest-activity cycle is controlled by a "master clock" in the suprachiasmatic nuclei (SCN) of the hypothalamus, it is unclear how firing of individual SCN neurons gates individual features of daily activity. Here, we demonstrate that a specific transcriptomically identified population of mouse VIP+ SCN neurons is active at the "wrong" time of the day -nighttime- when most SCN neurons are silent. Using chemogenetic and optogenetic strategies, we show that these neurons and their cellular clocks are necessary and sufficient to gate and time nighttime sleep, but have no effect upon daytime sleep. We propose mouse nighttime sleep, analogous to the human siesta, is a "hard-wired" property gated by specific neurons of the master clock to favor subsequent alertness prior to dawn (a circadian "wake maintenance zone"). Thus, the SCN is not simply a 24h metronome: specific populations sculpt critical features of the sleep-wake cycle.

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Project description:The aim of our study was to investigate the circadian regulation of cellular processes in mouse choroid plexus (ChP) and to determine their dependence on signals from the clock in the suprachiasmatic nuclei (SCN). We performed time-resolved transcriptomics of ChP samples from C57Bl6J mice with intact (Ctrl) or surgically removed SCN (SCNx) collected every 4 h over 2 days in constant darkness and from FoxJ1-ERT2-Cre+/-; Bmal1fl/fl mice with ChP-specific clock disruption (Bmal1-KO) collected at 2 time points. We found widespread circadian gene expression in Ctrl mice that was not present in SCNx mice, and the SCNx day/night ratios were reduced similarly to Bmal1-KO.

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High-Fat Nutritional Challenge Reshapes Circadian Signatures in Murine Extraorbital Lacrimal Glands.

Project description:PurposeA high-fat diet (HFD) increases the risk of developing many systemic diseases; however, the effects of high fat intake on lacrimal gland functions and the molecular mechanisms underlying these effects are unknown. We explored the effects of an HFD on the circadian rhythms of the extraorbital lacrimal glands (ELGs).MethodsMale C57BL/6J mice maintained on a 12/12-hour light/dark cycle were fed an ad libitum HFD or normal chow (NC) for 2 weeks. The ELGs were collected from euthanized animals every 3 hours throughout the circadian cycle (24 hours). Using high-throughput RNA-sequencing (RNA-Seq), we studied the circadian transcriptomic profile of the ELGs. Circadian oscillations in cell size, secretion response, lipid deposition, and immune cell trafficking of the ELGs were also analyzed.ResultsAn HFD modulated the circadian transcriptomic profile of the ELGs, including the composition, phase, and amplitude of cyclical transcript oscillations, and affected the associated signaling pathways at spatiotemporal levels. HFD feeding significantly altered the normal rhythmic oscillations of ELG cell size, immune cell trafficking, secretion response, and lipid deposition. After dietary reversal in HFD-fed animals, the activity, core temperature, and lipid accumulation in lacrimal glands recovered partially to the level of NC-fed animals. However, the average cell size of the ELGs, the recruitment of immune cells, and the rhythm of lacrimal secretion did not return to the levels of the NC-fed group.ConclusionsHFD perturbation interferes with the cyclical transcriptomic profile, cell size, immune cell trafficking, and secretion function of the ELGs with a strikingly high sensitivity.

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2023-02-12 | GSE224877 | GEO

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