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ABSTRACT:
PROVIDER: PRJNA1005412 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Molecular analysis of circadian rhythm in mice. Liver tissue of wildtype, Clock mutant and Cry deficient C57BL/6 8- to 10-week-old male mice examined. Keywords = circadian rhythm Keywords: other
2003-11-08 | GSE454 | GEO
Project description:Sleep disorder caused by abnormal circadian rhythm is one of the main symptoms and risk factors of depression. N-acetylserotonin methyltransferase (ASMT), the last rate-limiting enzyme of melatonin (MT, a known hormone regulating circadian rhythms), has been reportedly associated with depression. Exercise can regulate circadian rhythm and play an important role in depression treatment. Recently, gene chip has been widely used in depression research. In the present study, we showed that ASMT knockout induced depression-like behaviors, which were ameliorated by swimming exercise. Moreover, swimming exercise increased serum levels of MT and 5-HT in ASMT knockout mice. In addition, transcriptome analysis identified 10 differentially expressed genes (DEGs) in KO mice compared with WT mice, and 29 DEGs in KO mice after swimming exercise. Among the DEGs, the direction and magnitude of change in Eps8l1 and Plcb2 were confirmed by qRT-PCR partly. Subsequent bioinformatic analysis showed that p53 signaling pathway, long-term depression and estrogen signaling pathway were enriched significantly. In the protein-protein interaction (PPI) networks, Mpp1 and Pidd1 were hub genes. These findings may provide new targets for the treatment of circadian rhythm-associated depression.
2022-03-06 | GSE197888 | GEO
Project description:Mammalian circadian rhythm is established by the negative feedback loops consisting of a set of clock genes, which lead to the circadian expression of thousands of downstream genes. As genome-wide transcription is organized under the high-order chromosome structure, it is unclear how circadian gene expression is influenced by chromosome structure. In this study, we focus on the function of chromatin structure proteins cohesin as well as CTCF (CCCTC-binding factor) in circadian rhythm. We analyzed the interactome of a Bmal1-bound enhancer upstream of a clock gene, Nr1d1, by 4C-seq and observed that cohesin binding sites are enriched in the interactome. Integrating circadian transcriptome data and cistrome data, we found that cohesin-CTCF co-binding sites tend to insulate the phases of circadian oscillating genes while cohesin-non-CTCF sites facilitate the interaction between circadian enhancer and promoter. A coarse-grained model integrating the long-range effect of cohesin and CTCF markedly improved our mechanistic understanding of circadian gene expression. This model is subsequently supported by our RNA-seq data from cohesin knockout cells. Cohesin is required at least in part for driving the circadian gene expression by facilitating the enhancer-promoter looping. Taken together, our study provided a novel insight into the relationship between circadian transcriptome and the high-order chromosome structure. Bmal1 ChIP-Seq in WT mouse embryonic fibroblast cells
2016-04-04 | E-GEOD-77162 | biostudies-arrayexpress
Project description:Increased susceptibility of circadian clock mutant mice to metabolic diseases has led to the understanding that a molecular circadian clock is necessary for metabolic homeostasis. Circadian clock produces a daily rhythm in activity-rest and an associated rhythm in feeding-fasting. Feeding-fasting driven programs and cell autonomous circadian oscillator act synergistically in the liver to orchestrate daily rhythm in metabolism. However, an imposed feeding-fasting rhythm, as in time-restricted feeding, can drive some rhythm in liver gene expression in clock mutant mice. We tested if TRF alone, in the absence of a circadian clock in the liver or in the whole animal can prevent obesity and metabolic syndrome. Mice lacking the clock component Bmal1 in the liver, Rev-erb alpha/beta in the liver or cry1-/-;cry2-/- (CDKO) mice rapidly gain weight and show genotype specific increased susceptibility to dyslipidemia, hypercholesterolemia and glucose intolerance under ad lib fed condition. However, when the mice were fed the same diet under time-restricted feeding regimen that imposed 10 h feeding during the night, they were protected from weight gain and other metabolic diseases. Transcriptome and metabolome analyses of the liver from there mutant mice showed TRF reduces de novo lipogenesis, increased beta-oxidation independent of a circadian clock. TRF also enhanced cellular defense to metabolic stress. These results suggest a major function of the circadian clock in metabolic homeostasis is to sustain a daily rhythm in feeding and fasting. The feeding-fasting cycle orchestrates a balance between nutrient stress and cellular response to maintain homeostasis.
2018-08-30 | GSE102072 | GEO
Project description:Exploring the effect of circadian rhythm disturbance on the expression of adipose tissue proteins in mice
2022-03-09 | PXD032129 |
Project description:To identify microRNAs which differentially expressed in hematopoietic stem cells from wt mice and db/db mice We used microRNA microarrays to identify miroRNAs which can directly regulate dnmt1 expression in hematopoietic stem cells
2017-11-20 | GSE89842 | GEO
Project description:Zhou2015 - Circadian clock with immune
regulator NPR1
Arabidopsis clock model modified from
P2012 (Pokhilko et al., 2013 -
BIOMD0000000445)
model to include the master immune regulator NPR1 coupling to LHY,
TOC1 and PRR7.
Triggers: The Global Quantities contain triggers that allow
one to change coupling settings, Salicyclic acid (SA) treatment and
npr1 mutants.
LHY_on: true->NPR1 couples to LHY
PRR7_on: true->NPR1 couples to PRR7
WT: true->WT plants, false->npr1 mutant plants
SA: true->SA treated plants, false->no treatment
This model has L=1, i.e. operates only under constant light
conditions and is not aiming to make preditions under diurnal
conditions. Due to period overshoot only time points after 28h are
relevant.
This model is described in the article:
Redox rhythm reinforces the
circadian clock to gate immune response.
Zhou M, Wang W, Karapetyan S, Mwimba
M, Marqués J, Buchler NE, Dong X.
Nature 2015 Jun;
Abstract:
Recent studies have shown that in addition to the
transcriptional circadian clock, many organisms, including
Arabidopsis, have a circadian redox rhythm driven by the
organism's metabolic activities. It has been hypothesized that
the redox rhythm is linked to the circadian clock, but the
mechanism and the biological significance of this link have
only begun to be investigated. Here we report that the master
immune regulator NPR1 (non-expressor of pathogenesis-related
gene 1) of Arabidopsis is a sensor of the plant's redox state
and regulates transcription of core circadian clock genes even
in the absence of pathogen challenge. Surprisingly, acute
perturbation in the redox status triggered by the immune signal
salicylic acid does not compromise the circadian clock but
rather leads to its reinforcement. Mathematical modelling and
subsequent experiments show that NPR1 reinforces the circadian
clock without changing the period by regulating both the
morning and the evening clock genes. This balanced network
architecture helps plants gate their immune responses towards
the morning and minimize costs on growth at night. Our study
demonstrates how a sensitive redox rhythm interacts with a
robust circadian clock to ensure proper responsiveness to
environmental stimuli without compromising fitness of the
organism.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000577.
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To the extent possible under law, all copyright and related or
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2024-09-02 | BIOMD0000000577 | BioModels
Project description:Dibenzo[a,h]anthracene DB[a,h]A is a polycyclic aromatic hydrocarbon potent carcinogen. Few studies have investigated the role of DB[a,h]A on mRNA and miRNA expression. In this study a 10-week old male MutaTM Mouse were exposed to 6.25, 12.5, and 25 mg/kg/day DB[a,h]A by oral gavage for 28 consecutive days. DNA adducts were detected in the livers at each DB[a,h]A dose tested, and a dose-dependent increase in lacZ mutants was observed in the same samples. MAANOVA analysis revealed minor changes in the mRNA expression for the two lowest doses. Differential expression of 19 up-regulated and 22 down-regulated transcripts with fold-change > 1.5 (FDR-adjusted P < 0.05) were identified in the 6.25 mg/kg/day DB[a,h]A treatment group. For the 12.5 mg/kg/day treatment group 13 transcripts were up-regulated and 32 down-regulated (FDR-adjusted P < 0.05 and fold-change > 1.5). Major effect on mRNA expression resulted from exposure to the highest dose (25 mg/kg/day) of DB[a,h]A with 135 up-regulated and 104 down-regulated genes with fold-change > 1.5 (FDR-adjusted P < 0.05). The significantly regulated genes are involved in circadian rhythm, drug metabolism, glucose metabolism, cholestrol and lipid metabolism, immune response, cell cycle, and apoptosis. We also investigated miRNA response to the three doses of DB[a,h]A. MiRNA expression was relatively unaffected. Only miR-34a showed significant (FDR-adjusted P < 0.05) up-regulation with a fold change above 1.3-fold. RNA samples from 5 control and 4-5 mice per treatment group (6.25mg/kg, 12.50mg/kg, and 25mg/kg) containing 100 ng were labelled using AgilentM-bM-^@M-^Ys miRNA complete labelling and Hyb Kit (Agilent Tech, Mississauga, ON, Canada).
2013-07-02 | E-GEOD-35195 | biostudies-arrayexpress