Cdk1 controls global epigenetic landscape in embryonic stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA556259 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9736890.fastq.gz | Fastqsanger.gz | |||
| SRR9736900.fastq.gz | Fastqsanger.gz | |||
| SRR9736891.fastq.gz | Fastqsanger.gz | |||
| SRR9736901.fastq.gz | Fastqsanger.gz | |||
| SRR9736892.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we found that in ES cells the majority of Cdk1 substrates are localized on chromatin. Cdk1 phosphorylates a large number of proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. High levels of Cdk1 in ES cells phosphorylate and partially inactivate Dot1l, the histone H3 lysine 79 methyltransferase responsible for placing activating H3K79 marks on gene bodies. Decrease of Cdk1 activity during ES cell differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ES cells.
2020-04-04 | GSE134645 | GEO
Project description:The cyclin-dependent kinase 1 (Cdk1) represents an ancient cell cycle kinase that has been conserved from yeast to humans. Cdk1 is the only essential mammalian Cdk, which drives cytokinesis by phosphorylating a large number of cellular proteins. To uncover additional functions of Cdk1, we generated a knock-in strain of mice expressing an analog-sensitive version of Cdk1 in place of wild-type Cdk1. These mice and cells derived from them allow us to investigate Cdk1 function in essentially any compartment and at any stage of development. In our study, we focused on embryonic stem (ES) cells, as this cell type expresses particularly high levels of Cdk1. Very unexpectedly, we found that in ES cells the majority of Cdk1 substrates are localized on chromatin. Cdk1 phosphorylates a large number of proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. Consistent with this finding, inhibition of Cdk1 altered histone modification status of ES cells. High levels of Cdk1 in ES cells (and in induced pluripotent stem cells) phosphorylate and partially inactivate Dot1l, the histone H3 lysine 79 methyltransferase responsible for placing activating H3K79 marks on gene bodies. Decrease of Cdk1 activity during ES cell differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ES cells.
2020-10-05 | PXD015173 | Pride
Project description:The cyclin-dependent kinase 1 (Cdk1) drives cell division. To uncover additional functions of Cdk1, we generated knockin mice expressing an analog-sensitive version of Cdk1 in place of wild-type Cdk1. In our study, we focused on embryonic stem cells (ESCs), because this cell type displays particularly high Cdk1 activity. We found that in ESCs, a large fraction of Cdk1 substrates is localized on chromatin. Cdk1 phosphorylates many proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. Consistent with these findings, inhibition of Cdk1 altered histone-modification status of ESCs. High levels of Cdk1 in ESCs phosphorylate and partially inactivate Dot1l, the H3K79 methyltransferase responsible for placing activating marks on gene bodies. Decrease of Cdk1 activity during ESC differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ESCs.
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Project description:Purpose: Determine whether Cdk1 only regulates a specific subset of tDNAs, or whether Cdk1 has a more global impact on tDNA expression; Method: We study the expression of tRNA genes in WT cells and cdk1-as1 mutants during S phase by small-RNAseq; Result: We found that expression of at least 77% of all tDNAs is significantly downregulated in S-phase in the cdk1-as1 mutant compared with the WT strain; Conclussions: Cdk1 promotes transcription of the majority of tRNA genes during the cell cycle.
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Project description:We addressed the role of cell cycle regulator CDK1 during differentiation by either inhibiting its activity with the specific inhibitor RO3306 (10µM) or by knocking its expression down using specific shRNAs, during mesendoderm differentiation. Human pluripotent stem cells (H9 cells) were synchronized in their cell cycle and then induced to differentiate into mesendoderm for 24h. shRNAs against CDK1 were induced 4 days before starting the differentiation. The CDK1 inhibitor was added to the medium 8h after the induction of differentiation. At the end of the experiment, the cells were harvested and processed for total RNA extraction. RNA-IP was carried out using RiboCluster Profiler RIP-Assay Kit (MBL) following the manufacture’s recommendations.
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Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte (CM) proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.
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Project description:Analysis of gene expression across the cell cycle from wild type cells, and cells expressing alleles of Yox1, Yhp1, Hcm1, and Tos4 that cannot be phosphorylated by Cdk1. Expression of S-phase and M/G1 transcripts are downregulated when phosphorylation of these factors is blocked, demonstrating that Cdk1 promotes expression of late cell cycle genes.
2014-04-10 | GSE55121 | GEO
Project description:Analysis of gene expression across the cell cycle from wild type cells, and cells expressing alleles of Yox1, Yhp1, Hcm1, and Tos4 that cannot be phosphorylated by Cdk1. Expression of S-phase and M/G1 transcripts are downregulated when phosphorylation of these factors is blocked, demonstrating that Cdk1 promotes expression of late cell cycle genes. These experiments are two-color hybridizations of RNA isolated from synchronized wild type (WT) or phosphomutant (4P) cells, compared to RNA from asyncrhonous wild type cells in mid-log phase. Wild type and mutant cells were synchronized in G1 phase, released into the cell cycle and samples collected at 15 minute intervals. Each time course was carried out in duplicate, the replicate experiment was performed as a dye swap.
2014-04-10 | E-GEOD-55121 | biostudies-arrayexpress
Project description:Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)
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