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Non-circadian expression masking clock-driven weak transcription rhythms in U2OS cells

ABSTRACT: U2OS cells harbor a circadian clock but express only a few rhythmic genes in constant conditions. We identified 3040 binding sites of the circadian regulators BMAL1, CLOCK and CRY1 in the U2OS genome. Most binding sites even in promoters do not correlate with detectable rhythmic transcript levels. Luciferase fusions reveal that the circadian clock supports robust but low amplitude transcription rhythms of representative promoters. However, rhythmic transcription of these potentially clock-controlled genes is masked by non-circadian transcription that overwrites the weaker contribution of the clock in constant conditions. Our data suggest that U2OS cells harbor an intrinsically rather weak circadian oscillator. The oscillator has the potential to regulate a large number of genes. The contribution of circadian versus non-circadian transcription is dependent on the metabolic state of the cell and may determine the apparent complexity of the circadian transcriptome. Analysis of temporal expression profiles of 5708 expressed genes in synchronized U2OS cells. A 60k customized microarray was designed for 6356 genes, which corresponds to roughly one fourth of the human genome. 1373 genes were assigned to circadian regulator binding sites (CRBSs), 1503 genes were specifically selected in addition to a set of 3480 random genes. For each gene 10 independent probes in two microarray replicates were performed to increase reliability of the data.

ORGANISM(S): Homo sapiens

SUBMITTER: Anton Shostak

PROVIDER: E-GEOD-57891 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Non-circadian expression masking clock-driven weak transcription rhythms in U2OS cells

Project description:U2OS cells harbor a circadian clock but express only a few rhythmic genes in constant conditions. We identified 3040 binding sites of the circadian regulators BMAL1, CLOCK and CRY1 in the U2OS genome. Most binding sites even in promoters do not correlate with detectable rhythmic transcript levels. Luciferase fusions reveal that the circadian clock supports robust but low amplitude transcription rhythms of representative promoters. However, rhythmic transcription of these potentially clock-controlled genes is masked by non-circadian transcription that overwrites the weaker contribution of the clock in constant conditions. Our data suggest that U2OS cells harbor an intrinsically rather weak circadian oscillator. The oscillator has the potential to regulate a large number of genes. The contribution of circadian versus non-circadian transcription is dependent on the metabolic state of the cell and may determine the apparent complexity of the circadian transcriptome. Analysis of temporal expression profiles of 5708 expressed genes in synchronized U2OS cells.

2014-05-23 | GSE57891 | GEO

ChIP-seq of three core components of the circadian clock (BMAL1, CLOCK and CRY1) in unsynchronized human U2OS cells

2016-02-11 | GSE44236 | GEO

Transcription profiling of mouse adrenal gland from Wildtype and Per2Cry1 double mutant mice - time series

Project description:This SuperSeries is composed of the following subset Series:; GSE4238: rhythmic transcriptome in the murine wt adrenal; GSE4239: Transcriptome regulation in the adrenal gland of circadian clock deficient Per2Cry1 double mutant mice Experiment Overall Design: Refer to individual Series

2008-06-20 | E-GEOD-4253 | biostudies-arrayexpress

Global Mapping at the Core of the Arabidopsis Circadian Clock Defines the Network Structure of the Oscillator

Project description:In many organisms, the circadian clock is composed of functionally coupled morning and evening oscillators that regulate the bouts of dawn and dusk activity. In Arabidopsis, oscillator coupling relies on a core loop in which the evening oscillator component TOC1 was proposed to activate a subset of morning-expressed oscillator genes. Our systems-biological approach overturns the current view of the Arabidopsis circadian clock showing that TOC1 does not function as an activator but as a timely-controlled general repressor of morning and evening oscillator components. Repression occurs through rhythmic binding to the promoters of all oscillator genes, suggesting a previously unexpected direct connection between the morning and evening loops.

2012-03-08 | GSE35952 | GEO

Circadian Clock Activity in Mouse and Human CD4+ T Cells

Project description:Though it is well established that immunological functions of CD4+ T cells are time of day-dependent, the underlying molecular mechanisms remain largely obscure. To address the question whether T cells themselves harbor a functional clock driving circadian rhythms of immune function, we analyzed clock gene expression and immune responses of CD4+ T cells purified from blood of healthy subjects at different time points throughout the day. Circadian clock function as well as immune function was further analyzed in cultivated T cells and circadian clock reporter systems. We found robust rhythms of clock gene expression as well as, after stimulation, of IFN-g production and CD40L expression in both freshly isolated and in cultured CD4+ T cells. Moreover, circadian luciferase reporter activities in CD4+ T cells and in thymic sections from PER2::LUCIFERASE reporter mice suggest that endogenous T cell clock rhythms are self-sustained under constant culture conditions. Microarray analysis of stimulated CD4+ T cell cultures revealed a rhythmic regulation of the NF-kB pathway as a candidate mechanism regulating circadian immune responses. Collectively, these data demonstrate for the first time that CD4+ T cell responses are regulated by an intrinsic cellular circadian oscillator capable of driving rhythmic adaptive immune responses in vitro and in vivo. The study is designed with 3 biological replicates from three different time points.

2012-04-30 | E-GEOD-29583 | biostudies-arrayexpress

ChIP-seq of three core components of the circadian clock (BMAL1, CLOCK and CRY1) in unsynchronized human U2OS cells

Project description:The human osteosarcoma cell line U2OS contains a functional circadian clock but expresses only a few rhythmic genes. We identified by ChIP-seq analysis 3040 binding sites of the circadian transcription factors BMAL1, CLOCK, and CRY1 in the genome of U2OS cells, comparable to the number found in highly rhythmic tissues like liver. ChIP was performed as described previously (Rey et al, 2011; doi:10.1371/journal.pbio.1000595) using confluent desynchronized U2OS cells and BMAL1, CLOCK, and CRY1-antibodies. Immunoprecipitated chromatin (10 ng DNA of 8 independent BMAL1 ChIPs with enrichment levels > 80-fold, 9 ng DNA of a CRY1 ChIP with 10-fold enrichment, and 8 ng DNA of a CLOCK ChIP with 40-fold enrichment) was used for library preparation. Three lanes of the BMAL1 library, and one lane each of the CRY1 and CLOCK library were sequenced on the Illumina Genome Analyzer IIx using Single-Read Cluster Generation Kit and 36 Cycle Sequencing Kit v2 (Lausanne Genomics Technologies Facility).

2016-02-11 | E-GEOD-44236 | biostudies-arrayexpress

Global Mapping at the Core of the Arabidopsis Circadian Clock Defines the Network Structure of the Oscillator

2012-03-08 | E-GEOD-35952 | biostudies-arrayexpress

Circadian Clock Activity in Mouse and Human CD4+ T Cells

2012-05-01 | GSE29583 | GEO

Intercellular coupling between peripheral circadian oscillators by TGF-beta signaling [RNA-seq]

Project description:Intercellular coupling is crucial to prevent desynchronization of cell-autonomous oscillator networks and thus, the disruption of circadian tissue functions. While, neuronal oscillators within the mammalian central clock, the suprachiasmatic nucleus (SCN), couple intercellularly via the exchange of secreted neurotransmitters, intercellular coupling among peripheral oscillators is highly debated and molecular mechanisms are unknown. In our study, we show that peripheral circadian oscillators couple intercellularly via the exchange of secreted signaling molecules and identify TGF-beta as peripheral coupling factor. TGF-beta signaling induces the cAMP response element dependent, immediate-early expression of the clock gene PER2, thereby phase-adjusting the molecular circadian oscillator. Genetic or pharmacologic disruption of TGF-beta signaling causes desynchronization of cellular oscillators resulting in amplitude reduction and increased sensitivity towards Zeitgeber cues. Our findings reveal a previously unknown mechanism of peripheral coupling and open a new perspective on the importance of peripheral clock synchrony for rhythmic organ functions and circadian health.

2021-07-23 | GSE158577 | GEO

CIRP, a cold-inducible RNA-binding protein, modulates circadian gene expression posttranscriptionally

Project description:In mammalian tissues circadian gene expression can be driven by local oscillators or systemic signals controlled by the master pacemaker in the suprachiasmatic nucleus. Here we show that simulated body temperature cycles, but not peripheral oscillators, can control the rhythmic expression of Cold-Inducible RNA binding Protein (CIRP) in cultured fibroblasts. In turn, loss-of-function experiments indicate that CIRP is required for high amplitude circadian gene expression. The transcriptome-wide identification of CIRP-bound RNAs by a biotin-streptavidin based CLIP-seq procedure revealed several CIRP-bound transcripts encoding circadian oscillator proteins. One of these, CLOCK, accumulated to particularly low levels in CIRP-depleted fibroblasts. Since ectopic expression of CLOCK improved circadian gene expression in these cells, we surmise that CIRP confers robustness to circadian oscillators via the regulation of CLOCK expression. Identification of CIRP-interacting RNA molecules in NIH3T3 cells and RNA expression in NIH3T3 cells treated with Control or CIRP siRNA after incubation of the cells at 33M-BM-0C for 8 hours

2012-08-24 | E-GEOD-37685 | biostudies-arrayexpress

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