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Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

ABSTRACT: Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

PROVIDER: PRJNA151765 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR413510.fastq.gz	Fastqsanger.gz
	SRR413511.fastq.gz	Fastqsanger.gz
	SRR413512.fastq.gz	Fastqsanger.gz
	SRR413513.fastq.gz	Fastqsanger.gz
	SRR413514.fastq.gz	Fastqsanger.gz

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Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

Project description:Transcriptome profiling of three models with impaired insulin/IGF1 signaling. 1. Deep sequencing of endogenous mRNA from Caenorhabditis elegans N2 var. Bristol (wildtype) and daf-2(e1370) mutant; 2. Deep sequencing of endogenous mRNA from murine embryonic fibroblasts (MEF) wildtype and irs1-/- knockout; 3. Deep sequencing of endogenous mRNA from murine embryoinic fibroblast (MEF) insr+/- -lox and insr+/- knockout 14 samples examined: C. elegans N2 var. Bristol (wildtype) vs. daf-2(e1370) mutant; MEF wildtype vs. irs1-/- knockout; MEF insr+/- -lox vs. insr +/- knockout

2012-02-25 | E-GEOD-36041 | biostudies-arrayexpress

Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

Project description:Transcriptome profiling of three models with impaired insulin/IGF1 signaling. 1. Deep sequencing of endogenous mRNA from Caenorhabditis elegans N2 var. Bristol (wildtype) and daf-2(e1370) mutant; 2. Deep sequencing of endogenous mRNA from murine embryonic fibroblasts (MEF) wildtype and irs1-/- knockout; 3. Deep sequencing of endogenous mRNA from murine embryoinic fibroblast (MEF) insr+/- -lox and insr+/- knockout Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)

2012-02-25 | GSE36041 | GEO

Impaired insulin/IGF1 signaling extends life span by promoting mitochondrial L-proline catabolism to induce a transient ROS signal.

Project description:Impaired insulin and IGF-1 signaling (iIIS) in C. elegans daf-2 mutants extends life span more than 2-fold. Constitutively, iIIS increases mitochondrial activity and reduces reactive oxygen species (ROS) levels. By contrast, acute impairment of daf-2 in adult C. elegans reduces glucose uptake and transiently increases ROS. Consistent with the concept of mitohormesis, this ROS signal causes an adaptive response by inducing ROS defense enzymes (SOD, catalase), culminating in ultimately reduced ROS levels despite increased mitochondrial activity. Inhibition of this ROS signal by antioxidants reduces iIIS-mediated longevity by up to 60%. Induction of the ROS signal requires AAK-2 (AMPK), while PMK-1 (p38) and SKN-1 (NRF-2) are needed for the retrograde response. IIIS upregulates mitochondrial L-proline catabolism, and impairment of the latter impairs the life span-extending capacity of iIIS while L-proline supplementation extends C. elegans life span. Taken together, iIIS promotes L-proline metabolism to generate a ROS signal for the adaptive induction of endogenous stress defense to extend life span.

| S-EPMC4844853 | biostudies-literature

Loss of mitochondrial proline catabolism depletes FAD, impairing sperm function, and male reproductive advantage

Project description:Exposure to environmental stress has a clinically established influence on male reproductive health, but the impact of normal cellular metabolism on sperm quality and function is less well-defined. Here we show that homeostatic changes in mitochondrial dynamics driven by defective mitochondrial proline catabolism result in pleiotropic consequences on sperm quality and competitive fitness. Disruption of alh-6, which converts 1-pyrroline-5-carboxylate (P5C) to glutamate, results in P5C accumulation that drives oxidative stress, activation of the cytoprotective transcription factor SKN-1, and a reduction of energy-storing flavin adenine dinucleotide (FAD) levels. These molecular changes lead to premature male reproductive senescence by reducing sperm quality. These sperm-specific defects are suppressed by abating P5C metabolism, by treatment with antioxidants to combat reactive oxygen species (ROS), or by feeding diets that restore FAD levels. Our results define a role for mitochondrial proline catabolism and FAD homeostasis on sperm function and specify strategies to pharmacologically reverse unintended outcomes from SKN-1/Nrf transcriptional activation.

2020-02-17 | GSE121920 | GEO

Loss of mitochondrial proline catabolism depletes FAD, impairing sperm function, and male reproductive advantage

Project description:Loss of mitochondrial proline catabolism depletes FAD, impairing sperm function, and male reproductive advantage

| PRJNA499069 | ENA

Rapamycin extends life span, but has limited effects on aging in mice

Project description:Rapamycin extends life span in mice, but it remains unclear if this compound also delays mammalian aging. Here, we present results from a comprehensive large-scale assessment of a wide rage of structural and functional aging phenotypes in mice. Rapamycin extended life span but showed few effects on a large number of systemic aging phenotypes, suggesting that rapamycin's effects on aging are largely limited to the regulation of age-related mortality and carcinogenesis. Total RNA obtained from 2-4 male mice of each analysed group (25 weeks old controls, 25 month old controls, 25 month old rapamycin treated)

2013-07-29 | E-GEOD-41018 | biostudies-arrayexpress

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

Project description:Insight into the role of Insulin-like Growth Factor (IGF) in development of lungs has come from the study of genetically modified mice. IGF1 is a key factor during lung development. IGF1 deficiency in the neonatal mouse causes respiratory failure collapsed alveoli and altered alveolar septa. To further characterize IGF1 function during lung development we analyzed Igf1-/- mouse prenatal lungs in a C57Bl/6 genetic background. Mutant lungs showed disproportional hypoplasia, disorganized extracellular matrix and dilated alveolar capillaries. IGF1 target genes during lung maturation were identified by analyzing RNA differential expression in Igf1-/- lungs using microarrays. Lungs from E18.5 were isolated from both Igf1+/+ wild type and Igf1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos at embrionic (E) stage 18.5 days post coitum (E18.5). 3 biological replicates per genotype.

2014-03-31 | E-GEOD-17157 | biostudies-arrayexpress

Rapamycin extends life span, but has limited effects on aging in mice

2013-07-29 | GSE41018 | GEO

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

2014-03-31 | GSE17157 | GEO

Generating IGF1 signatures in human melanoma cell lines by activation of IGF1 or ihibition of IGF1R

Project description:To generate IGF1 signatures in human melanoma cell lines. Recombinant human IGF1 (rhIGF1) was added to WM35, known to be responsive to rhIGF1, whereas constitutive IGF1 signaling in Mel-624 was abrogated by siRNA directed against the IGF1 receptor (siIGF1R). Experiments were performed in triplicate in normoxia (O2 concentration, 21%) and hypoxia (1% O2), because hypoxia has been suspected to play an adverse role in melanoma. After generating GEP data, we created signatures of genes significantly (p ≤0.0001, q ≤0.05) and consistently upregulated in rhIGF1-treated WM35 cells, or similarly downregulated in siIGF1R-treated Mel-624 cells, as compared to control cells at the same O2 concentration.

2018-01-01 | GSE59343 | GEO

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