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Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells [scRNA-seq]

ABSTRACT: Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells [scRNA-seq]

PROVIDER: PRJNA497128 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8066860_1.fastq.gz	Fastqsanger.gz
	SRR8066860_2.fastq.gz	Fastqsanger.gz
	SRR8066870_1.fastq.gz	Fastqsanger.gz
	SRR8066870_2.fastq.gz	Fastqsanger.gz
	SRR8066880_1.fastq.gz	Fastqsanger.gz

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Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells

Project description:Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells

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Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells [scBS-seq]

Project description:Age-related tissue alterations have been associated with a decline in stem cell number and function. Increased cell-to-cell variability in transcription or epigenetic marks has been proposed to be a major hallmark of ageing. Here, using parallel single-cell transcriptome and DNA methylome profiling, we find a global increase of uncoordinated transcriptional heterogeneity and context-dependent alterations of DNA methylation heterogeneity in ageing mouse muscle stem cells. Importantly, promoters with increased methylation heterogeneity are associated with increased transcriptional heterogeneity of the genes they drive. Notably, old cells diverging from young cells revealed alterations in the transcription of multiple extracellular matrix related genes. These findings show linked increases in heterogeneity between the epigenome and the transcriptome, with attendant degradation of coherent transcriptional networks and stem cell functional decline during ageing.

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Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells [scRNA-seq]

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Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells [scBS-seq]

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Ageing affects DNA methylation drift and transcriptional cell-to-cell variability in mouse muscle stem cells.

Project description:Age-related tissue alterations have been associated with a decline in stem cell number and function. Although increased cell-to-cell variability in transcription or epigenetic marks has been proposed to be a major hallmark of ageing, little is known about the molecular diversity of stem cells during ageing. Here we present a single cell multi-omics study of mouse muscle stem cells, combining single-cell transcriptome and DNA methylome profiling. Aged cells show a global increase of uncoordinated transcriptional heterogeneity biased towards genes regulating cell-niche interactions. We find context-dependent alterations of DNA methylation in aged stem cells. Importantly, promoters with increased methylation heterogeneity are associated with increased transcriptional heterogeneity of the genes they drive. These results indicate that epigenetic drift, by accumulation of stochastic DNA methylation changes in promoters, is associated with the degradation of coherent transcriptional networks during stem cell ageing. Furthermore, our observations also shed light on the mechanisms underlying the DNA methylation clock.

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Cyclophilin A supports translation of intrinsically disordered proteins and affects haematopoietic stem cell ageing

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Ageing affects DNA methylation and transcriptional cell-to-cell variability in muscle stem cells

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

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Aging affects expression and variability of genes in the human liver

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Stem cell competition orchestrates skin homeostasis and ageing

Project description:Stem cells underlie tissue homeostasis, but their dynamics during ageing—and the relevance of these dynamics to organ ageing—remain unknown. Here we report that the expression of the hemidesmosome component collagen XVII (COL17A1) by epidermal stem cells fluctuates physiologically through genomic/oxidative stress-induced proteolysis, and that the resulting differential expression of COL17A1 in individual stem cells generates a driving force for cell competition. In vivo clonal analysis in mice and in vitro 3D modelling show that clones that express high levels of COL17A1, which divide symmetrically, outcompete and eliminate adjacent stressed clones that express low levels of COL17A1, which divide asymmetrically. Stem cells with higher potential or quality are thus selected for homeostasis, but their eventual loss of COL17A1 limits their competition, thereby causing ageing. The resultant hemidesmosome fragility and stem cell delamination deplete adjacent melanocytes and fibroblasts to promote skin ageing. Conversely, the forced maintenance of COL17A1 rescues skin organ ageing, thereby indicating potential angles for anti-ageing therapeutic intervention.

2019-04-05 | GSE111825 | GEO

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