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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 [scRNA-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 [scBS-seq]

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

Project description: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

Project description: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.

2019-08-22 | GSE121437 | GEO

Aging affects expression and variability of genes in the human liver

Project description:Aging affects expression and variability of genes in the human liver

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Label-free single-cell RNA Multiplexing leveraging genetic variability [scRNA-seq]

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NF-κB activation impairs somatic cell reprogramming in ageing [NGPS_iPSCs]

Project description:Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) fibroblasts and induced pluripotent stem cells (iPSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. However, the regulatory mechanisms that constitute age-associated barriers for cell reprogramming remain largely unknown. Here, by using cells from patients with premature ageing, we demonstrate that NF-κB activation is a critical barrier for the generation of induced pluripotent stem cells (iPSCs) in ageing. We show that NF-κB repression occurs during cell reprogramming towards a pluripotent state. Conversely, ageing-associated NF-κB hyperactivation impairs generation of iPSCs by eliciting reprogramming repressors DOT1L and YY1, reinforcing cell senescence signals and down-regulating pluripotency genes. We also show that genetic and pharmacological NF-κB inhibitory strategies significantly increase the reprogramming efficiency of fibroblasts from Néstor-Guillermo Progeria Syndrome (NGPS) and Hutchinson-Gilford Progeria Syndrome (HGPS) patients, as well as from normal aged donors. Finally, we demonstrate that DOT1L inhibition in vivo ameliorates the accelerated ageing phenotype and extends lifespan in a progeroid animal model. Collectively, our results provide evidence for a novel role of NF-κB in the control of cell fate transitions and reinforce the interest of studying age-associated molecular impairments to implement cell reprogramming methodologies, and to identify new targets of rejuvenation strategies. Control and NGPS fibroblasts were reprogrammed. RNA was extracted and transcriptional profiling was obtained with GeneChip Human Exon 1.0 ST Arrays.

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