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

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

PROVIDER: PRJNA595082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10676423_1.fastq.gz	Fastqsanger.gz
	SRR10676423_2.fastq.gz	Fastqsanger.gz
	SRR10676424_1.fastq.gz	Fastqsanger.gz
	SRR10676424_2.fastq.gz	Fastqsanger.gz
	SRR10676425_1.fastq.gz	Fastqsanger.gz

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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.

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

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

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MicroRNA-host gene lncRNA regulates the cell cycle re-entry post cellular quiescence

Project description:Cellular quiescence is coupled with cellular development, tissue homeostasis, and cancer progression. Both quiescence and cell cycle re-entry are controlled by active and precise regulation of gene expression. However, the roles of long noncoding RNAs (lncRNAs) during these processes remain to be elucidated. By performing a genome-wide transcriptome analyses, we identify thousands of differentially expressed lncRNAs, including ~30 of the less-characterized class of microRNA-host-gene lncRNAs (lnc-MIRHGs), during cellular quiescence and during serum-stimulation in human diploid cells. We observe that the mature MIR222HG display serum-stimulated induction due to enhanced pre-RNA splicing. Serum-stimulated binding of the pre-mRNA splicing factor SRSF1 to a micro-exon, which partially overlaps with the primary miR-222 precursor, facilitates enhanced MIR222HG splicing. In serum-stimulated cells, SRSF1 negatively regulates the Drosha/DGCR8-catalyzed cleavage of pri-miR-222, thereby increasing the cellular pool of the mature MIR222HG. Further, loss-of-function studies indicate that the mature MIR222HG facilitates the serum-stimulated cell cycle re-entry in a microRNA-independent manner. Mechanistically, MIR222HG, along with ILF3/2 complex, forms RNA:RNA duplex with DNM3OS lncRNA, thereby promoting DNM3OS stability. The current study identifies a mechanism in which the interplay between splicing versus microprocessor complex dictates the serum-induced expression of lnc-MIRHG MIR222HG for efficient cell cycle re-entry.

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

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

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

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