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Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [RNA-seq]

ABSTRACT: Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [RNA-seq]

PROVIDER: PRJNA900547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22262249_1.fastq.gz	Fastqsanger.gz
	SRR22262249_2.fastq.gz	Fastqsanger.gz
	SRR22262250_1.fastq.gz	Fastqsanger.gz
	SRR22262250_2.fastq.gz	Fastqsanger.gz
	SRR22262251_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation.

Project description:Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation.

| PRJNA900536 | ENA

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [ChIP-seq]

Project description:Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [ChIP-seq]

| PRJNA900542 | ENA

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation.

Project description:BackgroundMetformin as a first-line clinical anti-diabetic agent prolongs the lifespan of model animals and promotes cell proliferation. However, the molecular mechanisms underlying the proliferative phenotype, especially in epigenetics, have rarely been reported. The aim of this study was to investigate the physiological effects of metformin on female germline stem cells (FGSCs) in vivo and in vitro, uncover β-hydroxybutyrylation epigenetic modification roles of metformin and identify the mechanism of histone H2B Lys5 β-hydroxybutyrylation (H2BK5bhb) in Gata-binding protein 2 (Gata2)-mediated proliferation promotion of FGSCs.MethodsThe physiological effects of metformin were evaluated by intraperitoneal injection and histomorphology. The phenotype and mechanism studies were explored by cell counting, cell viability, cell proliferation assay and protein modification omics, transcriptomics, chromatin immunoprecipitation sequencing in FGSCs in vitro.ResultsWe found that metformin treatment increased the number of FGSCs, promoted follicular development in mouse ovaries and enhanced the proliferative activity of FGSCs in vitro. Quantitative omics analysis of protein modifications revealed that H2BK5bhb was increased after metformin treatment of FGSCs. In combination with H2BK5bhb chromatin immunoprecipitation and transcriptome sequencing, we found that Gata2 might be a target gene for metformin to regulate FGSC development. Subsequent experiments showed that Gata2 promoted FGSC proliferation.ConclusionOur results provide novel mechanistic understanding of metformin in FGSCs by combining histone epigenetics and phenotypic analyses, which highlight the role of the metformin-H2BK5bhb-Gata2 pathway in cell fate determination and regulation.

| S-EPMC10214601 | biostudies-literature

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [ChIP-seq]

Project description:We use ChIP-seq to report the most comprehensive survey to date of chromatin organization in female germline stem cells

2023-04-26 | GSE217782 | GEO

Sequencing of proteomic pan-β-hydroxybutyrylation in female germline stem cells

Project description:Metformin increase the number of FGSCs in mouse ovary, and the increased pan-β-hydroxylbutylated protein modification level in vitro FGSCs was detected by WB. There are the Mass spectrum original data of proteomic examination about pan-β-hydroxybutyrylation sites in female germline stem cells after merformin treatment

2022-11-11 | PXD038090 |

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation.

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

2023-04-25 | GSE217784 | GEO

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [RNA-seq]

Project description:The expression profile data was obtained by RNA-Seq data.

2023-04-26 | GSE217783 | GEO

Effect of metformin on mRNA expression in lung cancer cells

Project description:The genes whose transcription was significantly altered by metformin were investigated in H1299 cells by RNA-seq. Significantly up- or down-regulated genes were identified by cutoff value of |FC| >= 1.5. Metformin significantly downregulated mRNA levels of 499 genes while upregulating 615. KEGG (Kyoto Encyclopedia of Genes and Genomes) gene enrichment analysis revealed that the highly ranked clusters were cell cycle, apoptosis, cellular senescence and p53 signaling pathways. Multiple cell cycle checkpoint genes such as CCNA, CCNB, CCNE, CDK1, E2F2, E2F6, and E2F8 were downregulated, while certain cell cycle inhibitors such as CDKN2B (p15), CDKN1A (p21), DDIT4, and GADD45 were upregulated.

2019-11-27 | GSE141052 | GEO

Role of GATA-2 -77 enhancer in murine blood progenitor cells

Project description:We discovered enhancers that control GATA-2 expression during mouse development and in adult and generated mutant mouse strains that lack these enhancers, and these mice have very specific and important phenotypes that revealed GATA-2 mechanisms to control stem and progenitor cell transitions. In this study we aim to determine what proteins are under control of the GATA-2 -77 enhancer in a pool of heterogeneous blood progenitor cells with the specific focus on Socs2 expression.

2020-06-05 | PXD013855 | Pride

RNAseq of C. elegans cultured on metformin sensitive and resistant E. coli strains with and without 50mM metformin treatment.

Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.

2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress

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