CTCF confers local nucleosome resiliency after DNA replication and during mitosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA543327 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9083630.fastq.gz | Fastqsanger.gz | |||
| SRR9083640.fastq.gz | Fastqsanger.gz | |||
| SRR9083650.fastq.gz | Fastqsanger.gz | |||
| SRR9083660_1.fastq.gz | Fastqsanger.gz | |||
| SRR9083660_2.fastq.gz | Fastqsanger.gz |
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Project description:The access of Transcription Factors (TFs) to their cognate DNA binding motifs requires a precise control over nucleosome positioning. This is especially important following DNA replication and during mitosis, both resulting in profound changes in nucleosome organization over TF binding regions. Using mouse Embryonic Stem (ES) cells, we show that the TF CTCF displaces nucleosomes from its binding site and locally organizes large and phased nucleosomal arrays, not only in interphase steady-state but also immediately after replication and during mitosis. While regions bound by other TFs, such as Oct4 and Sox2, display major rearrangement, the post-replication and mitotic nucleosome organization activity of CTCF is not likely to be unique: Esrrb binding regions are also characterized by persistent nucleosome positioning. Therefore, selected TFs such as CTCF and Esrrb act as resilient TFs governing the inheritance of nucleosome positioning at gene regulatory regions throughout the ES cell-cycle.
2019-11-05 | GSE131356 | GEO
Project description:The access of Transcription Factors (TFs) to their cognate DNA binding motifs requires a precise control over nucleosome positioning. This is especially important following DNA replication and during mitosis, both resulting in profound changes in nucleosome organization over TF binding regions. Using mouse Embryonic Stem (ES) cells, we show that the TF CTCF displaces nucleosomes from its binding site and locally organizes large and phased nucleosomal arrays, not only in interphase steady-state but also immediately after replication and during mitosis. Correlative analyses suggest this is associated with fast gene reactivation following replication and mitosis. While regions bound by other TFs (Oct4/Sox2), display major rearrangement, the post-replication and mitotic nucleosome positioning activity of CTCF is not unique: Esrrb binding regions are also characterized by persistent nucleosome positioning. Therefore, selected TFs such as CTCF and Esrrb act as resilient TFs governing the inheritance of nucleosome positioning at regulatory regions throughout the cell-cycle.
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Project description:The experiment was performed to assess the importance of nucleosome eviction for the binding of condensin to chromatin during mitosis. The condensin complex associates with chromatin during mitosis to ensure chromosome condensation and accurate segregation, but how this binding is achieved remains poorly understood. Our study indicates that transcription co-activators Gcn5 and Mst2 assist condensin binding during mitosis by evicting nucleosomes. To reach this conclusion, we mapped nucleosomes, during mitosis, in wild-type and gcn5mst2 mutant strains. This experiment allowed us (1) to identify nucleosome-depleted regions (ndrs) during mitosis and to show that condensin tends to colocalize with ndr at the 3ends of genes, and (2) to confirm the importance of nucleosome eviction from ndrs by gcn5 and mst2, during mitosis, for the binding of condensin to chromatin.this experiment determines the patterns of nucleosomes in wild type and mutant fission yeast cells arrested in early mitosis. We analysed wild-type cells, cells lacking Gcn5 histone acetylatransferase (gcn5D) and cells lacking both Gcn5 and Mst2 histone acetyltransferases (Gcn5Dmst2D). All cells used in this study expressed a GFP-tagged version of condensin (Cnd2-GFP) and were blocked in early mitosis at 19C by the nda3-KM311 mutation. Mitotic indexes were determined by scoring the accumulation of Cnd2-GFP in the nucleus. Mitotic cells were collected and chromatin was digested by increasing amount of MNase to produce mononucleosomes. Mononucleosomal DNA was purified on an agarose gel and sequence on an Illumina Nextseq 500 apparatus. Three replicates of wild type, gcn5D and gcn5Dmst2D were analysed. Nucleosome patterns were determined in wild-type cells, cells lacking Gcn5 and cells lacking both Gcn5 and Mst2.
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Project description:Transcription factor activity and nucleosome organisation in mitosis
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2018-12-04 | GSE122589 | GEO
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
2010-06-24 | E-GEOD-19568 | biostudies-arrayexpress
Project description:Nucleosome eviction in mitosis assists condensin loading and chromosome condensation
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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.
2010-06-24 | GSE19568 | GEO
Project description:Older age is a major risk factor for damage to many tissues, including liver. Aging undermines resiliency (i.e., the ability to recover from injury) and impairs liver regeneration. The mechanisms whereby aging reduces resiliency are poorly understood. Hedgehog is a signaling pathway with critical mitogenic and morphogenic functions during development. Recent studies indicate that Hedgehog regulates metabolic homeostasis in adult liver. The present study evaluates the hypothesis that Hedgehog signaling becomes dysregulated in hepatocytes during aging, resulting in decreased resiliency and therefore, impaired regeneration and enhanced vulnerability to damage. Methods: Partial hepatectomy (PH) was performed on young and old wild type mice and Smoothened (Smo)-floxed mice treated with AAV8-TBG luciferase (control) or AAV8-TBG-Cre vectors to conditionally delete Smo and disrupt Hedgehog signaling specifically in hepatocytes. Changes in signaling were correlated with changes in regenerative responses and compared among groups. Results: Old livers had fewer hepatocytes proliferating after PH. RNA sequencing identified Hedgehog as a top down-regulated pathway in old hepatocytes before and after the regenerative challenge. Deleting Smo in healthy young hepatocytes before PH prevented Hedgehog pathway activation after PH and inhibited regeneration. GO analysis demonstrated that both old and Smo-deleted young hepatocytes had activation of pathways involved in innate immune responses and suppression of several signaling pathways that control liver growth and metabolism including insulin-like growth factor, Wnt and NOTCH. Hedgehog inhibition promoted telomere shortening and mitochondrial dysfunction in hepatocytes, consequences of aging that promote inflammation and impair tissue growth and metabolic homeostasis. Conclusion: Hedgehog signaling is dysregulated in old hepatocytes. This accelerates aging, resulting in decreased resiliency and therefore, impaired liver regeneration and enhanced vulnerability to damage.
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Project description:Javasky E, Shamir I, Gandhi S, Egri S, Sandler O, Rothbart SB, Kaplan N, Jaffe JD, Goren A, and Simon I. Genome Research 2018. Mitosis encompasses key molecular changes including chromatin condensation, nuclear envelope breakdown and reduced transcription levels. Immediately after mitosis, the interphase chromatin structure is reestablished and transcription resumes. The reestablishment of the interphase chromatin requires bookmarking, i.e., the retention of at least partial information during mitosis. Yet, while recent studies demonstrate that chromatin accessibility is generally preserved during mitosis and is only locally modulated, the exact details of the bookmarking process and its components are still unclear. To gain a deeper understanding of the mitotic bookmarking process, we merged proteomics, immunofluorescence, and ChIP-seq approaches to study the mitotic and interphase organization in human cells. We focused on key histone modifications, and employed the HeLa-S3 cells as a model system. Generally, we observed a global concordance between the genomic organization of histone modifications in interphase and mitosis, yet the abundance of the two types of modifications we investigated was different. Whereas histone methylation patterns remain highly similar, histone acetylation patterns show a general reduction while maintaining their genomic organization. In line with a recent study demonstrating that minimal transcription is retained during mitosis, we show that RNA polymerase II does not fully disassociate from the genome, but rather maintains its genomic localization at reduced levels. Next, we followed up on previous studies demonstrating that nucleosome depleted regions (NDRs) become occupied by a nucleosome during mitosis. Surprisingly, we observed that the nucleosome introduced into the NDR during mitosis encompasses a distinctive set of histone modifications, differentiating it from the surrounding nucleosomes. We show that the nucleosomes in the vicinity of the NDR appear to both shift into the NDR during mitosis and undergo deacetylation. HDAC inhibition by the small molecule TSA reverts the deacetylation pattern of the shifted nucleosome. Taken together, our results demonstrate that the epigenomic landscape can serve as a major component of the mitotic bookmarking process, and provide evidence for a mitotic deposition and deacetylation of the nucleosomes surrounding the NDR.
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