Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA326414 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3707996.fastq.gz | Fastqsanger.gz | |||
| SRR3707997.fastq.gz | Fastqsanger.gz | |||
| SRR3707998.fastq.gz | Fastqsanger.gz |
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Project description:From the cell-based investigation, RBPJ is one of the few proteins retained on chromatin during cell division. ChIP-seq experiments were performed to understand the binding pattern of RBPJ between interphase and mitosis and to identify the genes requiring RBPJ binding for the maintenance of transcriptional memory. Our results indicate that ~60% of RBPJ occupancy in interphase is retained on mitotic chromatin, and that accounts for 80% of RBPJ in mitosis. The gene ontology analysis reveals that the genes involved in stem cell maintenance, development and differentiation-related pathways correlated with sites of RBPJ occupancy. GO analysis also suggests that RBPJ plays a role in the metabolism and processing of non-coding RNAs. Motif analysis of RBPJ binding sites reveals that not only RBPJ motif but also CTCF motif are enriched around RBPJ binding sites. From these results, we propose that RBPJ can function as a mitotic bookmark, marking genes for efficient transcriptional activation or repression upon exit from mitosis, and may play a role in higher order chromatin structure by collaborating with CTCF. To compare the genomic RBPJ localization in mitotic and interphase cells, mouse F9 cells were harvested and labeled as cycling cells (containing 95% interphase and 5% mitosis cells); nocodazole treated F9 cells were harvested and labeled as mitotic cells. Cell samples were proceeded to ChIP-seq experiments, and each of the experiment contains a set of ChIP DNA product: input as the background control and IP as the RBPJ binding product. Background noise was substracted and the obtained signal was used for the comparison of interphase and mitosis by statistical analysis. Please note that processed data (*bed) was generated from *rep1 sample (i.e. no processed-data for rep2 sample).
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Project description:We performed ATAC-seq on mouse myoblast cells C2C12 in interphase and mitosis to observe footprinting on CTCF sites
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Project description:From the cell-based investigation, RBPJ is one of the few proteins retained on chromatin during cell division. ChIP-seq experiments were performed to understand the binding pattern of RBPJ between interphase and mitosis and to identify the genes requiring RBPJ binding for the maintenance of transcriptional memory. Our results indicate that ~60% of RBPJ occupancy in interphase is retained on mitotic chromatin, and that accounts for 80% of RBPJ in mitosis. The gene ontology analysis reveals that the genes involved in stem cell maintenance, development and differentiation-related pathways correlated with sites of RBPJ occupancy. GO analysis also suggests that RBPJ plays a role in the metabolism and processing of non-coding RNAs. Motif analysis of RBPJ binding sites reveals that not only RBPJ motif but also CTCF motif are enriched around RBPJ binding sites. From these results, we propose that RBPJ can function as a mitotic bookmark, marking genes for efficient transcriptional activation or repression upon exit from mitosis, and may play a role in higher order chromatin structure by collaborating with CTCF.
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Project description:Myc is an important oncogene. It is considered as a transcription factor, but the function of Myc in normal or cancer cells have not been fully understood. In addition, Myc plays a role in cell proliferation and differentiation. It is also important for cell identity and stay on chromatin throughout the cell cycle. However, the inheritance of Myc is still a mystery. Here we study the function and inheritance of Myc in D. melanogaster by mapping the binding sites of Myc during interphase and mitosis using ChIP-seq. DNA sample of ChIP for Myc are collected from Kc cells in interphase or mitosis. Input sequences from previous study in the same cell type (GSM762848, GSM762849) are used as control.
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Project description:Here we compare the distribution of insulator proteins during interphase and mitosis. We performed ChIP-seq analysis on purified populations of interphase and mitotic Kc cells, using antibodies against CP190, dCTCF, BEAF, and Su(Hw). Examination of 4 different insulator proteins during interphase and mitosis
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Project description:Promoters Active in Interphase are Bookmarked during Mitosis by Ubiquitination
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Project description:Pioneer transcription factors (TFs) such as SOX2 play critical roles in control of stem cell identity and are dysregulated in many human cancers. For example, SOX2 regulates the self-renewal of neural stem cells (NSCs), and is typically highly expressed in glioblastoma stem cells, where it is known to induce an immature NSC-like state. Here, we explored the regulation of SOX2 by phosphorylation during cell division and identify an unexpected role for mitotic SOX2 as an inducer of genomic damage. We find that SOX2 adopts a distinct phosphorylated state in NSCs during mitosis, regulated by the mitotic kinase CDK1. Mapping of SOX2 genome occupancy and chromatin accessibility shows that a subset of SOX2 remains bound to the interphase targets, consistent with mitotic bookmarking, but phosphorylated SOX2 is redistributed to constitutive heterochromatin, including telomeres. Ablation of SOX2 phosphorylation leads to promiscuous chromatin binding across the genome and triggers prolonged mitotic transit times and increased susceptibility to DNA damage. These findings show that excessive levels of SOX2 protein in mitosis trigger inappropriate opening of chromatin and downstream chromosomal damage. Elevated levels of SOX2 in cancers may therefore have dual oncogenic roles: imposing stemness during interphase via their well-known transcriptional roles, but simultaneously inducing genomic damage during mitosis due to their unconstrained pioneer factor activity.
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Project description:Pioneer transcription factors (TFs) such as SOX2 play critical roles in control of stem cell identity and are dysregulated in many human cancers. For example, SOX2 regulates the self-renewal of neural stem cells (NSCs), and is typically highly expressed in glioblastoma stem cells, where it is known to induce an immature NSC-like state. Here, we explored the regulation of SOX2 by phosphorylation during cell division and identify an unexpected role for mitotic SOX2 as an inducer of genomic damage. We find that SOX2 adopts a distinct phosphorylated state in NSCs during mitosis, regulated by the mitotic kinase CDK1. Mapping of SOX2 genome occupancy and chromatin accessibility shows that a subset of SOX2 remains bound to the interphase targets, consistent with mitotic bookmarking, but phosphorylated SOX2 is redistributed to constitutive heterochromatin, including telomeres. Ablation of SOX2 phosphorylation leads to promiscuous chromatin binding across the genome and triggers prolonged mitotic transit times and increased susceptibility to DNA damage. These findings show that excessive levels of SOX2 protein in mitosis trigger inappropriate opening of chromatin and downstream chromosomal damage. Elevated levels of SOX2 in cancers may therefore have dual oncogenic roles: imposing stemness during interphase via their well-known transcriptional roles, but simultaneously inducing genomic damage during mitosis due to their unconstrained pioneer factor activity.
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Project description:Pioneer transcription factors (TFs) such as SOX2 play critical roles in control of stem cell identity and are dysregulated in many human cancers. For example, SOX2 regulates the self-renewal of neural stem cells (NSCs), and is typically highly expressed in glioblastoma stem cells, where it is known to induce an immature NSC-like state. Here, we explored the regulation of SOX2 by phosphorylation during cell division and identify an unexpected role for mitotic SOX2 as an inducer of genomic damage. We find that SOX2 adopts a distinct phosphorylated state in NSCs during mitosis, regulated by the mitotic kinase CDK1. Mapping of SOX2 genome occupancy and chromatin accessibility shows that a subset of SOX2 remains bound to the interphase targets, consistent with mitotic bookmarking, but phosphorylated SOX2 is redistributed to constitutive heterochromatin, including telomeres. Ablation of SOX2 phosphorylation leads to promiscuous chromatin binding across the genome and triggers prolonged mitotic transit times and increased susceptibility to DNA damage. These findings show that excessive levels of SOX2 protein in mitosis trigger inappropriate opening of chromatin and downstream chromosomal damage. Elevated levels of SOX2 in cancers may therefore have dual oncogenic roles: imposing stemness during interphase via their well-known transcriptional roles, but simultaneously inducing genomic damage during mitosis due to their unconstrained pioneer factor activity.
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Project description:Mitosis entails global alterations to chromosome structure and nuclear architecture, concomitant with transient silencing of transcription. How cells transmit transcriptional states through mitosis remains incompletely understood. While many nuclear factors dissociate from mitotic chromosomes, the observation that certain nuclear factors and chromatin features remain associated with individual loci during mitosis originated the hypothesis that they could provide transcriptional memory through mitosis. To obtain the first genome-wide view of the dynamics of chromatin structure during mitosis, we compared the DNase sensitivity of interphase and mitotic chromatin at two stages of cellular maturation in a rapidly dividingmurine erythroblastmodel. Despite global chromosome condensation visible during mitosis at the microscopic level, the chromatin accessibility landscape is largely unaltered. However, mitotic chromatin accessibility is locally dynamic, with individual loci maintaining none, some, or all of their interphase accessibility. Mitotic reduction in accessibility occurs primarily within narrow, highly hypersensitive sites that frequently coincide with transcription factor binding sites, whereas broader domains of moderate accessibility tend to be more stable. In mitosis, proximal promoters generally maintain their accessibility, whereas distal regulatory elements preferentially lose accessibility. Promoters with the highest degree of accessibility preservation in mitosis tend to also be accessible across many murine tissues in interphase. Transcription factor GATA1 exerts site-specific changes in interphase accessibility that are most pronounced at distal regulatory elements, but does not visibly influence mitotic accessibility. We conclude that features of open chromatin are remarkably stable through mitosis and are modulated at the level of individual genes and regulatory elements. Dnase-Seq data is integrated with Chip-seq [GSE36589, GSE30142] and RNA-seq to examine epigentic changes in mitosis. We performed DNase-seq on two cell lines, G1E and G1E-ER4, both on an asynchronus population, and on a sample of cells in mitosis; each of the 4 experiments in triplicate.
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