Genomic basis of longevity
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB28048 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We identified that Drosophila FoxA transcription Fork Head (FKH) function is necessary for reduced insulin signalling and rapamycin induced longevity. Furthermore, we determined that FKH function in the gut tissue alone is sufficient to extend lifespan. We carried out RNA-sequencing in gut tissue on controls (daGS;InRDN>GFP- RNAi) and reduced insulin signalling background upon control RNAi (daGS;InRDN>GFPRNAi +RU486) and upon FKH RNAi (daGS;InRDN>FKH- RNAi +RU486). InR-DN stock used: K1409A.
2017-09-23 | E-MTAB-6056 | biostudies-arrayexpress
Project description:NLRP3-inflammasome suppression improves longevity and prevents cardiac aging in mice
| PRJNA512138 | ENA
Project description:Genes controlling differences in seed longevity between two barley (Hordeum vulgare) accessions were identified by combining a quantitative genetics approach with ˈomicsˈ technologies in Near Isogenic Lines (NILs). The NILs were derived from crosses between the spring barley landraces L94 from Ethiopia and Cebada Capa from Argentina, which produce short-lived and long-lived seeds, respectively. The NILs harbor introgressions from Cebada Capa in four QTLs for seed longevity on 1H and 2H in the background of L94. A label-free proteome analysis was performed on mature, non aged seeds of the two parental lines and the L94 NILs.
2018-07-23 | PXD009464 | Pride
Project description:Our two main aims were 1) to isolate age-related changes in gene expression in females of the solitary insect, Drosophila melanogaster; and 2) to determine whether experimentally changing the shape of the fecundity-longevity relationship (by changing larvae diet) caused changes in age-related gene expression in these females. To address these aims we extracted RNA from three key tissues (fat body, head and ovary) from females at two time points (10% and 60% mortality phases). Each of these females had experienced one of two treatments: medium-quality larval diet (M) treatment (resulting in a positive fecundity-longevity relationship) and high-quality larval diet (H) treatment (resulting in a negative fecundity-longevity relationship).
2023-08-18 | GSE175623 | GEO
Project description:Aging is a multifactorial process that disturbs homeostasis, increases disease susceptibility, and ultimately results in death. Although the definitive set of molecular mechanisms responsible for aging remain to be discovered, epigenetic change over time is proving to be a promising piece of the puzzle. Several posttranslational histone modifications (PTMs) have been linked to the maintenance of longevity. Here, we focus on lysine 36 of the replication independent histone protein, H3.3 (H3.3K36). To interrogate the role of this residue in Drosophila developmental gene regulation, we generated a lysine to arginine mutant that blocks the activity of its cognate modifying enzymes. We found that an H3.3BK36R mutation causes a significant reduction in adult lifespan, accompanied by dysregulation of the genomic and transcriptomic architecture. Transgenic co-expression of wild-type H3.3B completely rescues the longevity defect. Because H3.3 is known to accumulate in nondividing tissues, we carried out transcriptome profiling of young vs aged adult fly heads. The data show that loss of H3.3K36 results in age-dependent misexpression of NF-κB and other innate immune target genes, as well as defects in silencing of heterochromatin. We propose H3.3K36 maintains the postmitotic epigenomic landscape, supporting longevity by regulating both pericentric and telomeric retrotransposition and by suppressing aberrant immune signaling.
2024-02-07 | GSE244389 | GEO
Project description:The quest to extend healthspan via pharmacological means is becoming increasingly urgent, both from a health and economic perspective. Here we show that lithium, a drug approved for human use, promotes longevity and healthspan. We demonstrate that lithium extends lifespan in female and male Drosophila, when administered throughout adulthood or only later in life. The life-extending mechanism involves the inhibition of glycogen synthase kinase-3 (GSK-3) and activation of the transcription factor nuclear factor erythroid 2-related factor (NRF-2). Combining genetic loss of the NRF-2 repressor Kelch-like ECH-associated protein 1 (Keap1) with lithium treatment revealed that high levels of NRF-2 activation conferred stress resistance, while low levels additionally promoted longevity. The discovery of GSK-3 as a new therapeutic target for aging will likely lead to more effective treatments that can modulate mammalian aging and further improve health in later life. The microarray experiment examines the transcriptional profiles of wild-type (w1118) vs. wild-type (w1118) + Lithium (LiCl, 10mM). Heads and thoraces from once mated females treated with vehicle or 10mM Li were snap frozen after 10d of treatment. RNA was Dnase treated and checked for quality by Biorad Experion. RNA was processed to cRNA, labeled and used for microarray analysis (GeneChip Drosophila Genome 2.0 Array), following manufacturer's protocol.
2016-04-07 | E-MTAB-3809 | biostudies-arrayexpress
Project description:High blood glucose level is one of the main characteristics of diabetes mellitus (DM). It is speculated that longevity families may have certain advantages in blood glucose regulation. But till now, limited information on these items is reported. In this study, a TMT- based comparative quantitative proteomics analysis was used to reveal the changes of plasma proteomics profiles between longevity subjects and non-longevity area participants in order to identify plasma proteins associated with glucose metabolism in longevity population and to explore the characteristics of blood glucose regulation in longevity population
2023-03-11 | PXD032932 | Pride
Project description:Transcriptome analysis in HEK293T transfected with plasmid carrying different isoforms of BPIFB4 gene. This gene was previously associated with exceptional longevity in a GWAS study performed on three different populations. Results indicate an up-regulation of stress response genes and proteostasis genes in HEK293T transfected with plasmid carrying the longevity-associated variant (LAV) of BPIFB4. Total RNA obtained from HEK293T over-expressing wild-type or mutated form of BPIFB4.
2015-06-12 | E-GEOD-63912 | biostudies-arrayexpress
Project description:Biomarkers of familial longevity may represent mechanisms underlying healthy aging. To identify gene expression profiles marking human familial longevity, an explorative genome-wide expression study was performed among 50 families from the Leiden Longevity Study who have a life-long survival advantage of 30%. Gene expression profiles were compared between 50 nonagenarians (mean age 93.4 years) and 50 controls (mean age 61.9 years) to investigate differential gene expression that may arise as a function of both chronological age and familial longevity. Differential expression was observed for 2953 probes (FDR≤0.05) and for 109 GO terms, which corresponded well with previously reported findings on gene expression changes associated with chronological age, such as ‘immune response’, ‘signal transduction’ and ‘regulation of gene transcription’. To explore which of the 2953 chronological age-related probes also marked familial longevity, we compared gene expression profiles of 50 offspring of the nonagenarians (mean age 60.8 years) with the same 50 controls. Since the average gene expression levels did not differ between offspring and controls, we tested for differential expression as a function of age (age range 43-79 years). We identified 360 probes (FDR≤0.1) and the ‘Rho protein signal transduction’ GO biological process (FWER = 0.079) whose expression signatures marked familial longevity already at middle-age. Of these probes, 236 were annotated and represent 244 known genes, including WRN and MYC. Interestingly, 51 genes are involved in the regulation of gene expression. Further investigation into the genes involved may be important for unraveling mechanisms underlying longevity.
2011-09-04 | GSE16717 | GEO