Role of TBP in reactivation of transcription following mitosis [RNA-Seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE109963 | GEO | 2018/07/04
REPOSITORIES: GEO
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Project description:Role of TBP in reactivation of transcription following mitosis [RNA-Seq]
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Project description:During mitosis, transcription is globally attenuated and chromatin architecture is dramatically reconfigured. Here we exploited the M-phase to G1-phase progression to interrogate the contributions of the architectural factor CTCF and the process of transcription to re-sculpting the genome in newborn nuclei. While CTCF appears to be dispensable for large scale post-mitotic compartmentalization, depletion of CTCF specifically during the M-phase to G1-phase transition alters the re-establishment of local short-range compartmentalization after mitosis. Without CTCF, structural loops fail to reform, leading to illegitimate contacts between cis-regulatory elements (CREs) and altered gene expression in G1-phase. Transient CRE contacts that are normally resolved after telophase persist deeply into G1-phase in CTCF depleted cells. Boundary reformation is largely disrupted upon CTCF loss. Yet, a subset (~27%) of boundaries emerges normally in the absence of CTCF and is characterized by transitions in chromatin states. Reformation of gene domains can occur prior to the full onset of transcription and can be linked to tri-methylation at lysine 36 of histone 3 (H3K36me3), a mark stable throughout mitosis. The focus on the de novo formation of nuclear architecture during G1 entry yielded novel insights into how CTCF and the process of transcription contribute to the dynamic re-configuration of chromatin architecture during the mitosis to G1 phase progression.
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Project description:During mitosis, transcription is globally attenuated and chromatin architecture is dramatically reconfigured. Here we exploited the M-phase to G1-phase progression to interrogate the contributions of the architectural factor CTCF and the process of transcription to re-sculpting the genome in newborn nuclei. While CTCF appears to be dispensable for large scale post-mitotic compartmentalization, depletion of CTCF specifically during the M-phase to G1-phase transition alters the re-establishment of local short-range compartmentalization after mitosis. Without CTCF, structural loops fail to reform, leading to illegitimate contacts between cis-regulatory elements (CREs) and altered gene expression in G1-phase. Transient CRE contacts that are normally resolved after telophase persist deeply into G1-phase in CTCF depleted cells. Boundary reformation is largely disrupted upon CTCF loss. Yet, a subset (~27%) of boundaries emerges normally in the absence of CTCF and is characterized by transitions in chromatin states. Reformation of gene domains can occur prior to the full onset of transcription and can be linked to tri-methylation at lysine 36 of histone 3 (H3K36me3), a mark stable throughout mitosis. The focus on the de novo formation of nuclear architecture during G1 entry yielded novel insights into how CTCF and the process of transcription contribute to the dynamic re-configuration of chromatin architecture during the mitosis to G1 phase progression.
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Project description:We report genome wide mapping of the histone variant H2A.Z during G0/G1 and mitosis in T24 bladder cancer cells. The results show that the broad enrichment pattern of H2A.Z near transcription start sites of active genes is maintained during mitosis. Furthermore, using H2A.Z localization to visualize nucleosome positioning near the start site, we see that the +1 nucleosome of active genes shifts upstream to occupy the transcription start sites during mitosis and the nucleosome depleted region is shortened. H2A.Z is also maintained on the -2 nucleosome which also shifts towrds the transcription start site during mitosis, further contributing to the shorteneing of the nucleosome depleted region. Examination of H2A.Z duing G0/G1 and mitosis in bladder cancer cells
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Project description:Chromatin is highly condensed and transcriptionally repressed during mitosis. Although it is established that some general transcription factors are inactivated by phosphorylation at mitosis, many details of mitotic transcriptional repression and its underlying mechanisms are largely unknown. Here, we provide evidence that as cells enter mitosis, genes with transcriptionally engaged RNA Polymerase II (Pol II) can continue transcription until the end of the gene to clear Pol II from mitotic chromatin. Using ChIP-Seq, we find that the transcriptional reinitiation process is globally impaired in early mitosis (prophase/prometaphase), with loss of TFIIB occupancy and nucleosome-free regions at promoters. Pretreatment of nocodazole-arrested mitotic cells with the P-TEFb inhibitor flavopiridol prevents the release of promoter-proximal engaged Pol II. Global nascent RNA sequencing and RNA fluorescence in situ hybridization (FISH) of individual genes demonstrate the existence of transcriptionally engaged Pol II in early mitosis. Chemical and mutational inhibition of P-TEFb in mitosis leads to delays in the progression of cell division. Together, our study reveals a novel mechanism for mitotic transcriptional repression whereby transcriptionally engaged Pol II can progress into productive elongation and finish transcription to allow proper cellular division. ChIP-Seq of Pol II of different forms, TFIIB, H3K4me3 in human HeLa cells at different cell cycle stages. ChIP-Seq of Pol II in HeLa mitotic cells with or without CDK9 inhibitor flavopiridol pretreatment. Nascent RNA-seq in asynchronous and arrested mitotic cells.
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Project description:To test of TBP binds in the same genomic regions in mitosis compared to interphase cells, we performed Chromatin ImmunoPrecipitation coupled with sequencing (ChIP-seq).
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Project description:We report genome wide mapping of the histone variant H2A.Z during G0/G1 and mitosis in T24 bladder cancer cells. The results show that the broad enrichment pattern of H2A.Z near transcription start sites of active genes is maintained during mitosis. Furthermore, using H2A.Z localization to visualize nucleosome positioning near the start site, we see that the +1 nucleosome of active genes shifts upstream to occupy the transcription start sites during mitosis and the nucleosome depleted region is shortened. H2A.Z is also maintained on the -2 nucleosome which also shifts towrds the transcription start site during mitosis, further contributing to the shorteneing of the nucleosome depleted region.
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