Long-range chromosome interactions mediated by cohesin shape circadian gene expression
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Yichi Xu
PROVIDER: E-GEOD-68832 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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: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. RNA-Seq in WT and Smc3-/- mouse embryonic fibroblast cells
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Project description:[Gro-seq] Precursor B acute leukemia cells measured using global nuclear run-on sequencing [ChIP-Seq] The genome-wide occupancy of ser2 and ser5 phosphorylated RNA pol2 and H3K4me3 was measured in precursor B acute leukemia cells measured using chip-seq. [Gro-seq] Nascent RNA expression profiles were generated at cells in various basal culture conditions. [ChIP-Seq] Performed from REH and Nalm6 cells cultured under basal culture conditions. Mnase digestion was used for DNA fragmentation. Antibodies against Ser2 and Ser5 phosphorylated RNA polymerase and H3K4me3 compared to input. ****************************** This study includes reanalysis of Samples in Series GSE39878 (GSM980645, GSM980644), GSE60454 (GSM1480326), and GSE41009 (GSM1006728, GSM100672). The processed data files for the reanalyses are linked to GSE67540 as supplementary files (see the GSE67540_README.txt file for additional information).
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2015-12-10 | E-GEOD-70081 | biostudies-arrayexpress
Project description:In the ciliated protozoan Tetrahymena, de novo heterochromatin body formation is accompanied by programmed DNA elimination. We previously reported that dephosphorylation of the HP1-like protein Pdd1p is required for the formation of heterochromatin bodies during the process of programmed DNA elimination in the ciliated protozoan Tetrahymena. Here, we show that the heterochromatin body component Jub4p is required for Pdd1p phosphorylation, heterochromatin body formation and DNA elimination. Moreover, our analyses of unphosphorylatable Pdd1p mutants demonstrate that Pdd1p phosphorylation is required for heterochromatin body formation and DNA elimination, while it is dispensable for local heterochromatin assembly. Therefore, both phosphorylation and the following dephosphorylation of Pdd1p are necessary to facilitate the formation of heterochromatin bodies. We suggest that Jub4p-mediated phosphorylation of Pdd1p creates a chromatin environment that is a prerequisite for subsequent heterochromatin body assembly and DNA elimination. New macronuclei (MACs) of exconjugants were isolated from wild-type and various mutant cells at 12 hpm (hours post-mixing), sheared chromatin was immunoprecipitated andprecipitated DNA was analyzed by high-throughput sequencing
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Project description:A comparative ChIP-chip analysis of TFIIB and NC2 in human B cells reveals that basal core promoter architectures control the equilibrium between NC2 and preinitiation complexes. We conducted a comparative ChIP-chip and gene expression analysis of TFIIB in human B cells and analyze associated core promoter architectures. TFIIB occupancy relates well to gene expression, with the vast majority of promoters being GC-rich and lacking defined core promoter elements. TATA consensus and TATA-like motifs but not the previously in vitro defined TFIIB recognition elements (BREs) are enriched in approximately 5% of the genes. Further insight was obtained by performing a parallel ChIP-chip analysis of the TFIIB antagonist NC2. The latter identifies a highly related target gene set. Nonetheless, subpopulations show strong variations in TFIIB/NC2 ratios, with high NC2/TFIIB ratios correlating to promoters that show dispersed transcription start site patterns and lacking defined core elements. Conversely, high TFIIB/NC2 ratios select for conserved core promoter elements that include TATA and INR (initiator), the upstream TFIIB recognition element (BREu) and the downstream promoter element (DPE). Two biological samples from LCL 721 lymphoblastoid human B cells were subjected to ChIP-chip analysis of TFIIB and NC2 using a Nimblegen human promoter array (based on the HG17 genome build) covering 1.5 kb DNA around transcription start sites.
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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