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Mus musculus

ABSTRACT: Unprecedented life- and healthspan extension and genome preservation by diet restriction in DNA repair deficient progeroid Ercc1∆/- mice [RNA-seq]

PROVIDER: PRJNA310638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3139921.fastq.gz	Fastqsanger.gz
	SRR3139922.fastq.gz	Fastqsanger.gz
	SRR3139923.fastq.gz	Fastqsanger.gz

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Similar Datasets

Unprecedented life- and healthspan extension and genome preservation by diet restriction in DNA repair deficient progeroid Ercc1 Δ/- mice

Project description:Unprecedented life- and healthspan extension and genome preservation by diet restriction in DNA repair deficient progeroid Ercc1 Δ/- mice

| PRJNA310633 | ENA

Disentangling mTOR signalling from the lifespan extending effect of dietary restriction in progeroid DNA-repair deficient mice

Project description:Dietary restriction (DR) and rapamycin, the best-known DR-mimetic, are two intervention that extend health- and lifespan across multiple species. We have recently shown that DR works extremely well in progeroid DNA repair deficient mice and dramatically extend their lifespan by ~200%. We next questioned the applicability of rapamycin in these mouse mutants. Here we show that treatments with rapamycin did significantly lower mTOR-signalling but did not improve the lifespan of DNA repair deficient Ercc1{delta}/- mice. These data are an extended version of the data in GEO Series GSE77321

2021-01-25 | GSE149029 | GEO

Mus musculus

Project description:Lifespan extension by diet restriction in DNA repair deficient progeroid Ercc1Δ/- mice [mRNA]

| PRJNA310020 | ENA

Mus musculus

Project description:Lifespan extension by diet restriction in DNA repair deficient progeroid Ercc1Δ/- mice [miRNA]

| PRJNA309778 | ENA

Effect of methione restriction in the liver of WT and Lmna G609G KI mice

Project description:Dietary intervention constitutes a feasible approach for modulating metabolism and improving healthspan and lifespan. Methionine restriction (MR) delays the appearance of age-related diseases and increases longevity in normal mice. However, the effect of MR on premature aging remains to be elucidated. Here, we describe that MR extends lifespan in two different mouse models of Hutchinson-Gilford progeria syndrome (HGPS) by reversing the transcriptome alterations in inflammation and DNA-damage response genes present in this condition. Further, MR improves the lipid profile and alters the levels of bile acids, both in wild-type and in progeroid mice. Notably, treatment with the bile acid cholic acid improves healthspan and lifespan in vivo. These results suggest the existence of a metabolic pathway involved in the longevity extension achieved by MR and support the possibility of dietary interventions for treating progeria.

2018-08-27 | GSE117188 | GEO

Identify the protein partners of Ercc1 in DNA damage progeria in MEFs

Project description:ERCC1 is a DNA endonuclease participating in the Nucleotide Excision Repair (NER) pathway. Its functionality is related to XPF; the two proteins work as a heterodimer to incise the 5 of a 30-mer that contains the damaged nucleotide and remove the fragment together with XPG. Apart from NER deficiency, mutated Ercc1 in mice and humans causes a series of progeroid symptoms (premature ageing). We hypothesize that there are undescribed functions of ERCC1, possibly in transcriptional regulation that contribute to the development of the striking phenotypes observed. The aim is to identify previously uncharacterized protein partners of ERCC1 that might contribute to our understanding of its differential roles during DNA damage-driven progeria.

2023-10-04 | PXD017063 | Pride

Microbiota from mice

Project description:Healthspan and lifespan extension by fecal microbiota transplantation in progeroid mice

| PRJEB34214 | ENA

Expression data for hematopoietic stem cells (lin- sca1+ ckit+) isolated from the bone marrow of Ercc1-deficient and proficient littermates

Project description:To identify cellular and genetic abnormalities involved in interstrand cross link repair-deficient bone marrow failure and its transformation to leukemia, we used an Ercc1 hypomorphic mouse model (Ercc1 -/d). Gene expression profiling was done to determine which genes are differentially expressed

2015-03-24 | GSE47700 | GEO

Systemic lipolysis promotes healthspan in Drosophila melanogaster

Project description:Since healthspan-extending interventions such as caloric restriction or fasting robustly promote lipid catabolism, we investigated how lifespan and healthspan were affected by increased lipid catabolism via bmm (brummer, FBgn0036449), the major triglyceride hydrolase in Drosophila. Global overexpression of bmm strongly promoted lifespan extension as well as numerous markers of healthspan, including increased female fecundity, fertility maintenance, preserved locomotion activity, increased mitochondrial biogenesis and oxidative metabolism. Increased Bmm robustly upregulated the heat shock protein 70 (Hsp70) family of proteins, which equipped the flies with higher resistance to heat, cold, and ER stress via improved proteostasis. Overexpression of bmm recapitulated major physiological changes associated with dietary restriction (DR) and conveyed its effects through dSir2. Taken together, these data show that bmm overexpression has broad beneficial effects on healthspan, and implicate lipolysis as a key node underlying the beneficial effects of dietary interventions known to improve healthspan.

2022-09-27 | GSE178816 | GEO

Tissue-infiltrating macrophages mediate an exosome-based metabolic reprogramming upon DNA damage

Project description:DNA damage and metabolic disorders are intimately linked with premature disease onset but the underlying mechanisms remain poorly understood. Here, we show that persistent DNA damage accumulation in tissue-infiltrating macrophages carrying an ERCC1-XPF DNA repair defect (Er1F/-) riggers Golgi dispersal, dilation of endoplasmic reticulum, autophagy and exosome biogenesis leading to the secretion of extracellular vesicles (EVs) in vivo and ex vivo. Macrophage-derived EVs accumulate in Er1F/- animal sera and are secreted in macrophage media after DNA damage. The Er1F/- EV cargo is taken up by recipient cells leading to an increase in insulin-independent glucose transporter levels, enhanced cellular glucose uptake, higher cellular oxygen consumption rate and greater tolerance to glucose challenge in mice. We find that high glucose in EV-targeted cells triggers pro-inflammatory stimuli via mTOR activation. This, in turn, establishes chronic inflammation and tissue pathology in mice with important ramifications for DNA repair-deficient, progeroid syndromes and aging.

2019-11-06 | PXD015727 | Pride

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