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Transcriptional down-regulation of metabolic genes by Gdown1 ablation induces quiescent cell re-entry into the cell cycle

ABSTRACT: Transcriptional down-regulation of metabolic genes by Gdown1 ablation induces quiescent cell re-entry into the cell cycle

PROVIDER: PRJNA603063 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10961169.fastq.gz	Fastqsanger.gz
	SRR10961170.fastq.gz	Fastqsanger.gz
	SRR10961171.fastq.gz	Fastqsanger.gz
	SRR10961172.fastq.gz	Fastqsanger.gz
	SRR10961173.fastq.gz	Fastqsanger.gz

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Transcriptional down-regulation of metabolic genes by Gdown1 ablation induces quiescent cell re-entry into the cell cycle.

Project description:Liver regeneration and metabolism are highly interconnected. Here, we show that hepatocyte-specific ablation of RNA polymerase II (Pol II)-associated Gdown1 leads to down-regulation of highly expressed genes involved in plasma protein synthesis and metabolism, a concomitant cell cycle re-entry associated with induction of cell cycle-related genes (including cyclin D1), and up-regulation of p21 through activation of p53 signaling. In the absence of p53, Gdown1-deficient hepatocytes show a severe dysregulation of cell cycle progression, with incomplete mitoses, and a premalignant-like transformation. Mechanistically, Gdown1 is associated with elongating Pol II on the highly expressed genes and its ablation leads to reduced Pol II recruitment to these genes, suggesting that Pol II redistribution may facilitate hepatocyte re-entry into the cell cycle. These results establish an important physiological function for a Pol II regulatory factor (Gdown1) in the maintenance of normal liver cell transcription through constraints on cell cycle re-entry of quiescent hepatocytes.

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RSC primes the quiescent genome for hypertranscription upon cell cycle re-entry

Project description:RSC primes the quiescent genome for hypertranscription upon cell cycle re-entry

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Transcriptional down-regulation of metabolic genes by Gdown1 ablation induces quiescent cell re-entry into the cell cycle

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-06 | GSE144212 | GEO

Paxbp1 is indispensable for cell cycle re-entry of adult muscle stem cells

Project description:Adult muscle stem cells (MuSCs) transit from a quiescent state to a highly proliferative state to support muscle repair. Paxbp1 deletion in MuSCs blocked their cell cycle re-entry and caused subsequent muscle regeneration failures. To understand the underlying molecular mechanisms, we compared the transcriptomes of control and Paxbp1 mutant MuSCs by RNA-seq. Our data confirmed a marked repression of cell cycle machineries in Paxbp1 mutant MuSCs. We also uncovered down-regulation of mutliple metabolic pathways in mutant MuSCs. In summary, our study highlights an essential role of Paxbp1 in MuSCs growth and cell cycle re-entry.

2021-03-23 | GSE141881 | GEO

Chromatin structure restricts origin utilization when quiescent cells re-enter the cell cycle

Project description:Quiescent cells reside in G0 phase, which is characterized by the absence of cell growth and proliferation. These cells remain viable and re-enter the cell cycle when prompted by appropriate signals. Using a budding yeast model of cellular quiescence, we investigated the program that initiated DNA replication when these G0 cells resumed growth. We performed BrdU IP-Seq to examine the DNA replication profile genome-wide. These data revealed that the initiation of replication was delayed and fewer origins were active when G0 cells entered the cell cycle compared to the entry of G1 cells into S phase. We found that both the transcript and protein levels of these replication factors were significantly diminished during the development of proliferating cells into quiescence. The levels of these factors, including MCM2-7 helicase, increased as G0 cells re-entered the cell cycle, suggesting that the replication program is re-established de novo. Consistent with these results, Mcm4 ChIP-seq analysis showed fewer and reduced binding at a number of origins during the re-entry of G0 cells into the cell cycle. In support of this evidence, the chromatin context surrounding inactive origins of G0 cells exhibits greater increased nucleosome occupancy and reduced periodicity of nucleosome positioning. Altogether, these observations provide insights into the important role of chromatin context that determines the ability of replication origin to accrue limiting replication factors during the the re-entry of quiescent cells into the cell cycle.

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RSC primes the quiescent genome for hypertranscription upon cell-cycle re-entry.

Project description:Quiescence is a reversible G0 state essential for differentiation, regeneration, stem-cell renewal, and immune cell activation. Necessary for long-term survival, quiescent chromatin is compact, hypoacetylated, and transcriptionally inactive. How transcription activates upon cell-cycle re-entry is undefined. Here we report robust, widespread transcription within the first minutes of quiescence exit. During quiescence, the chromatin-remodeling enzyme RSC was already bound to the genes induced upon quiescence exit. RSC depletion caused severe quiescence exit defects: a global decrease in RNA polymerase II (Pol II) loading, Pol II accumulation at transcription start sites, initiation from ectopic upstream loci, and aberrant antisense transcription. These phenomena were due to a combination of highly robust Pol II transcription and severe chromatin defects in the promoter regions and gene bodies. Together, these results uncovered multiple mechanisms by which RSC facilitates initiation and maintenance of large-scale, rapid gene expression despite a globally repressive chromatin state.

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Targeting of cytosolic phospholipase A2? impedes cell cycle re-entry of quiescent prostate cancer cells.

Project description:Cell cycle re-entry of quiescent cancer cells has been proposed to be involved in cancer progression and recurrence. Cytosolic phospholipase A2? (cPLA2?) is an enzyme that hydrolyzes membrane glycerophospholipids to release arachidonic acid and lysophospholipids that are implicated in cancer cell proliferation. The aim of this study was to determine the role of cPLA2? in cell cycle re-entry of quiescent prostate cancer cells. When PC-3 and LNCaP cells were rendered to a quiescent state, the active form of cPLA2? with a phosphorylation at Ser505 was lower compared to their proliferating state. Conversely, the phospho-cPLA2? levels were resurgent during the induction of cell cycle re-entry. Pharmacological inhibition of cPLA2? with Efipladib upon induction of cell cycle re-entry inhibited the re-entry process, as manifested by refrained DNA synthesis, persistent high proportion of cells in G0/G1 and low percentage of cells in S and G2/M phases, together with a stagnant recovery of Ki-67 expression. Simultaneously, Efipladib prohibited the emergence of Skp2 while maintained p27 at a high level in the nuclear compartment during cell cycle re-entry. Inhibition of cPLA2? also prevented an accumulation of cyclin D1/CDK4, cyclin E/CDK2, phospho-pRb, pre-replicative complex proteins CDC6, MCM7, ORC6 and DNA synthesis-related protein PCNA during induction of cell cycle re-entry. Moreover, a pre-treatment of the prostate cancer cells with Efipladib during induction of cell cycle re-entry subsequently compromised their tumorigenic capacity in vivo. Hence, cPLA2? plays an important role in cell cycle re-entry by quiescent prostate cancer cells.

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Effect of Exportin-5 expression on Mouse fibroblasts in cell cycle re-entry phase

Project description:To analyze the effect of Exportin-5 expression on the MEF cells in cell cycle re-entry phase, we have employed whole genome microarray expression profiling on the MEF cells in cell cycle re-entry phase with and without down regulation of Exportin-5 gene. Mouse MEF cells were transfected with 60nM of siRNA targeting either Exportin-5 or negative control, and incubated for 12 hours. After incubation, cells were starved with DMEM containing 0.2% FCS for 48 hours and re-fed with DMEM containing 20%FCS for 24 hours, along with second siRNA transfection. Two independant expreiments were preformed.

2013-01-01 | E-GEOD-25498 | biostudies-arrayexpress

Scalloped and Yorkie are required for cell cycle re-entry of quiescent cells after tissue damage.

Project description:Regeneration of damaged tissues typically requires a population of active stem cells. How damaged tissue is regenerated in quiescent tissues lacking a stem cell population is less well understood. We used a genetic screen in the developing Drosophila melanogaster eye to investigate the mechanisms that trigger quiescent cells to re-enter the cell cycle and proliferate in response to tissue damage. We discovered that Hippo signaling regulates compensatory proliferation after extensive cell death in the developing eye. Scalloped and Yorkie, transcriptional effectors of the Hippo pathway, drive Cyclin E expression to induce cell cycle re-entry in cells that normally remain quiescent in the absence of damage. Ajuba, an upstream regulator of Hippo signaling that functions as a sensor of epithelial integrity, is also required for cell cycle re-entry. Thus, in addition to its well-established role in modulating proliferation during periods of tissue growth, Hippo signaling maintains homeostasis by regulating quiescent cell populations affected by tissue damage.

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Effect of Exportin-5 expression on Mouse fibroblasts in cell cycle re-entry phase

2013-01-01 | GSE25498 | GEO