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Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

ABSTRACT: Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

PROVIDER: PRJNA541529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR9024850.fastq.gz	Fastqsanger.gz
	SRR9024841.fastq.gz	Fastqsanger.gz
	SRR9024851.fastq.gz	Fastqsanger.gz
	SRR9024842.fastq.gz	Fastqsanger.gz

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Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

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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Dihydroartemisinin suppresses the tumorigenesis and cycle progression of colorectal cancer by targeting CDK1/CCNB1/PLK1 signaling

Project description:Dihydroartemisinin (DHA), a well-known antimalarial drug, has been widely investigated as its anti-tumor effects in multiple malignancies. However, its effects and regulatory mechanisms in colorectal cancer (CRC) are still unproved. In this study, the in vitro experiments including CCK8, EdU, Transwell, flow cytometry analyses and in vivo tumorigenesis model were conducted to assess the effects of DHA on the bio-behaviors of CRC cells. Additionally, RNA-seq combined with gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses was used to obtain the targets of DHA and these were verified by molecular docking, qRT-PCR and Western blot. As a result, we found that DHA significantly suppressed the proliferation, DNA synthesis and invasive capabilities, and induced cell apoptosis and cell cycle arrest in HCT116, DLD1 and RKO cells in vitro and in vivo. Further analyses indicated that the targets of DHA were predominantly enriched in cell cycle-associated pathways, including CDK1, CCNB1 and PLK1, and DHA could bind with CDK1/CCNB1 complex and inhibit the activation of CDK1/CCNB1/PLK1 signaling. Moreover, cucurbitacin E, a specific inhibitor of CDK1/CCNB1 axis enhanced the inhibitory effects of DHA on DNA synthesis and colony formation in HCT116 and DLD1 cells. In short, DHA could suppress the tumorigenesis and cycle progression of CRC cells by targeting CDK1/CCNB1/PLK1 signaling.

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Cdk1 Gates Cell Cycle-Dependent tRNA Synthesis by Regulating RNA Polymerase III Activity

Project description:tRNA genes are transcribed by RNA polymerase III (RNAPIII). During recent years it has become clear that RNAPIII activity is strictly regulated by the cell in response to environmental cues and the homeostatic status of the cell. However, the molecular mechanisms that control RNAPIII activity to regulate the amplitude of tDNA transcription in normally cycling cells are not well understood. Here, we show that tRNA levels fluctuate during the cell cycle and reveal the underlying molecular mechanism. The cyclin Clb5 recruits the cyclin dependent kinase Cdk1 to tRNA genes to boost tDNA transcription during S phase. At tDNA genes, Cdk1 promotes the recruitment of TFIIIC, stimulates the interaction between TFIIIB and TFIIIC, and increases the dynamics of RNA polymerase III in vivo. Furthermore, we identified Bdp1 as an important Cdk1 substrate in this process. Preventing Bdp1 phosphorylation prevented cell cycle-dependent recruitment of TFIIIC and abolished the cell cycle-induced increase in tDNA transcription. Our findings demonstrate that under optimal growth conditions Cdk1 gates tRNA synthesis in S phase by regulating the RNAPIII machinery, revealing a direct link between the cell cycle and RNAPIII activity.

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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.

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