Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aging induces aberrant state transition kinetics in murine muscle stem cells

ABSTRACT: Aging induces aberrant state transition kinetics in murine muscle stem cells

PROVIDER: PRJNA600730 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR10874104.fastq.gz	Fastqsanger.gz
	SRR10874105.fastq.gz	Fastqsanger.gz
	SRR10874106.fastq.gz	Fastqsanger.gz
	SRR10874107.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Aging induces aberrant state transition kinetics in murine muscle stem cells.

Project description:Murine muscle stem cells (MuSCs) experience a transition from quiescence to activation that is required for regeneration, but it remains unknown if the trajectory and dynamics of activation change with age. Here, we use time-lapse imaging and single cell RNA-seq to measure activation trajectories and rates in young and aged MuSCs. We find that the activation trajectory is conserved in aged cells, and we develop effective machine-learning classifiers for cell age. Using cell-behavior analysis and RNA velocity, we find that activation kinetics are delayed in aged MuSCs, suggesting that changes in stem cell dynamics may contribute to impaired stem cell function with age. Intriguingly, we also find that stem cell activation appears to be a random walk-like process, with frequent reversals, rather than a continuous linear progression. These results support a view of the aged stem cell phenotype as a combination of differences in the location of stable cell states and differences in transition rates between them.

| S-EPMC7225128 | biostudies-literature

Aging induces aberrant state transition kinetics in murine muscle stem cells

Project description:Label retaining and non-retaining muscle stem cells from young and aged H2B-GFP+/-;rtTA+/- were profiled by single cell RNA-seq at two timepoints

2020-02-18 | GSE143476 | GEO

Granulins Regulate Aging Kinetics in the Adult Zebrafish Telencephalon

Project description:Granulins Regulate Aging Kinetics in the Adult Zebrafish Telencephalon

| PRJNA603998 | ENA

Granulins Regulate Aging Kinetics in the Adult Zebrafish Telencephalon

Project description:Granulins (GRN) are secreted factors that promote neuronal survival and regulate inflammation in various pathological conditions. However, their roles in physiological conditions in the brain remain poorly understood. To address this knowledge gap, we analysed the telencephalon in Grn-deficient zebrafish and identified morphological and transcriptional changes in microglial cells, indicative of a pro-inflammatory phenotype in the absence of any insult. Unexpectedly, activated mutant microglia shared part of their transcriptional signature with aged human microglia. Furthermore, transcriptome profiles of the entire telencephali isolated from young Grn-deficient animals showed remarkable similarities with the profiles of the telencephali isolated from aged wildtype animals. Additionally, 50% of differentially regulated genes during aging were regulated in the telencephalon of young Grn-deficient animals compared to their wildtype littermates. Importantly, the telencephalon transcriptome in young Grn-deficent animals changed only mildly with aging, further suggesting premature aging of Grn-deficient brain. Indeed, Grn loss led to decreased neurogenesis and oligodendrogenesis, and to shortening of telomeres at young ages, to an extent comparable to that observed during aging. Altogether, our data demonstrate a role of Grn in regulating aging kinetics in the zebrafish telencephalon, thus providing a valuable tool for the development of new therapeutic approaches to treat age-associated pathologies.

2020-02-18 | GSE144543 | GEO

Aberrant overexpression of TGF-β2 induces epithelial-mesenchymal transition in adenomyosis with β-catenin activation.

Project description:Aberrant activation of TGF-β2 plays an important role in the pathogenesis of adenomyosis. We used microarrays to detail the machanism underlying aberrant activation of TGF-β2 in adenomyosis

2016-10-19 | GSE88911 | GEO

Enzyme expression kinetics by Escherichia coli during transition from rich to minimal media depends on proteome reserves

Project description:Bacterial fitness depends on adaptability to changing environments. In rich growth medium, which is replete with amino acids, Escherichia coli primarily expresses protein synthesis machineries, which comprise ~40% of cellular proteins and are required for rapid growth. Upon transition to minimal medium, which lacks amino acids, biosynthetic enzymes are synthesized, eventually reaching ~15% of cellular proteins when growth fully resumes. We applied quantitative proteomics to analyse the timing of enzyme expression during such transitions, and established a simple positive relation between the onset time of enzyme synthesis and the fractional enzyme ‘reserve’ maintained by E. coli while growing in rich media. We devised and validated a coarse-grained kinetic model that quantitatively captures the enzyme recovery kinetics in different pathways, solely on the basis of proteomes immediately preceding the transition and well after its completion. Our model enables us to infer regulatory strategies underlying the ‘as-needed’ gene expression programme adopted by E. coli.

2023-02-06 | PXD035278 | Pride

De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [ATAC-seq]

Project description:Genome remethylation is essential for mammalian development. Here we examined cell fate in the absence of de novo DNA methyltransferases. We found that embryonic stem (ES) cells deficient for Dnmt3a and Dnmt3b are rapidly eliminated from chimaeras. Pluripotency progression is derailed towards extra-embryonic trophoblast. This aberrant trajectory is propelled by failure to methylate and suppress expression of Ascl2 during formative transition. Ascl2 deletion rescues transition and improves contribution to chimaeric epiblast but mutant cells are progressively lost in later development. These findings indicate that methylation constrains transcriptome trajectories during developmental transitions by silencing potentially disruptive genes. This submission is ATAC-seq.

2021-09-01 | GSE158344 | GEO

De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [RNA-seq]

2021-09-01 | GSE158310 | GEO

Gene expression - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

Project description:Dyskeratosis congenita (DKC) and idiopathic aplastic anemia (AA) are bone marrow failure syndromes that share characteristics of premature aging with severe telomere attrition. In this study, we analyzed blood samples of 62 AA and 13 DKC patients to demonstrate that their epigenetic age predictions are overall increased, albeit not directly correlated with telomere length. Aberrant DNA methylation was observed in the gene PRDM8 in DKC and AA as well as in other diseases with premature aging phenotype, such as Down syndrome, Werner syndrome and Hutchinson-Gilford-Progeria syndrome. To gain further insight into the functional relevance of PRDM8 we generated induced pluripotent stem cells (iPSCs) with heterozygous and homozygous knockout. Loss of PRDM8 impaired hematopoietic and neuronal differentiation of iPSCs, but it did not impact on epigenetic age. Taken together, aberrant DNA methylation in PRDM8 provides a biomarker for bone marrow failure syndromes, which may contribute to the hematopoietic and neuronal phenotypes of premature aging syndromes.

2020-08-31 | GSE141107 | GEO

DNA methylation - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

2020-08-31 | GSE141106 | GEO