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Trans-Generational Hormesis and the Inheritance of Aging Resistance [ChIP-seq]

ABSTRACT: Animals respond to dietary changes by adapting their metabolism to available nutrients through insulin and insulin-like growth factor signalling. Restricting calorie intake generally extends life and health span, but Drosophila fed non-ideal sugars such as galactose are stressed and have shorter life spans. Here, we report that although these flies have shorter life spans, their offspring show significant life extension if switched to a normal sugar (glucose) diet. We define this as TGH or trans-generational hormesis, a beneficial effect that comes from a mild stress. We trace the effects to changes in stress responses in parents, ROS production, effects on lipid metabolism, and changes in chromatin and gene expression. We find that this mechanism is similar to what happens to the long lived Indy mutants on normal food, but surprisingly find that Indy is required for life span extension for galactose fed flies. Indy mutant flies grown on galactose do not live longer as do their siblings grown on glucose, rather overexpression of Indy rescues lifespan for galactose reared flies. We define a process where sugar metabolism can generate epigenetic changes that are inherited by offspring, providing a mechanism for how transgenerational nutrient sensitivities are passed on.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE97162 | GEO | 2017/07/01

SECONDARY ACCESSION(S): PRJNA381045

REPOSITORIES: GEO

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Trans-Generational Hormesis and the Inheritance of Aging Resistance [RNA-seq]

Project description:Animals respond to dietary changes by adapting their metabolism to available nutrients through insulin and insulin-like growth factor signalling. Restricting calorie intake generally extends life and health span, but Drosophila fed non-ideal sugars such as galactose are stressed and have shorter life spans. Here, we report that although these flies have shorter life spans, their offspring show significant life extension if switched to a normal sugar (glucose) diet. We define this as TGH or trans-generational hormesis, a beneficial effect that comes from a mild stress. We trace the effects to changes in stress responses in parents, ROS production, effects on lipid metabolism, and changes in chromatin and gene expression. We find that this mechanism is similar to what happens to the long lived Indy mutants on normal food, but surprisingly find that Indy is required for life span extension for galactose fed flies. Indy mutant flies grown on galactose do not live longer as do their siblings grown on glucose, rather overexpression of Indy rescues lifespan for galactose reared flies. We define a process where sugar metabolism can generate epigenetic changes that are inherited by offspring, providing a mechanism for how transgenerational nutrient sensitivities are passed on.

2017-07-01 | GSE97233 | GEO

Expression Data From Dietary Restriction, p53 Knockdown and sir2 Overexpression Mutants

Project description:Expression data from four different lifespan-extending conditions: dietary restriction in two different genetic backgrounds (canton-s and a yw, w1118 combination), sir2 overexpression and p53 knockdown (+/-). Comparison of significantly over and under-expressed genes reveals a signature for dietary restriction and lifespan extension. Abstract A major challenge in translating the positive effects of dietary restriction (DR) for the improvement of human health is the development of therapeutic mimics. One approach to finding DR mimics is based upon identification of the proximal effectors of DR life span extension. Whole genome profiling of DR in Drosophila shows a large number of changes in gene expression, making it difficult to establish which changes are involved in life span determination as opposed to other unrelated physiological changes. We used comparative whole genome expression profiling to discover genes whose change in expression is shared between DR and two molecular genetic life span extending interventions related to DR, increased dSir2 and decreased Dmp53 activity. We find twenty-one genes shared among the three related life span extending interventions. One of these genes, takeout, thought to be involved in circadian rhythms, feeding behavior and juvenile hormone binding is also increased in four other life span extending conditions: Rpd3, Indy, chico and methuselah. We demonstrate takeout is involved in longevity determination by specifically increasing adult takeout expression and extending life span. These studies demonstrate the power of comparative whole genome transcriptional profiling for identifying specific downstream elements of the DR life span extending pathway. 42 samples were used in the analysis. Sir2 overexpression flies and the yw, w1118 background DR flies had the same control. Flies were collected at ages 10 and 40 days. Tissue is whole body females.

2011-01-20 | E-GEOD-26726 | biostudies-arrayexpress

Drosophila melanogaster transcriptional profiling over life span: Indy vs. Controls

2009-03-08 | GSE13872 | GEO

Drosophila melanogaster transcriptional profiling over life span: Indy vs. Controls

Project description:Transcriptional profiling of Indy long lived flies and controls over the course of their entire lifespan. Mutations in the Indy gene extend life span in Drosophila melanogaster. This study investigates the changes in gene expression over time in Indy206 flies heterozygous over Canton-S (Indy206/CS) and compares them to genetically matched heterozygous controls (2216/CS). Samples from both fly strains were collected at age: 5, 10, 20, 30, 40, 50, 70 and 80. mRNA samples were collected from the head and thorax of Indy206 and genetically matched control male adult flies at day 5, and every 10 days from day 10 to day 80 (day 60 excluded) and hybridized to two-color microarrays

2010-05-22 | E-GEOD-13872 | biostudies-arrayexpress

Expression Data From Dietary Restriction, p53 Knockdown and sir2 Overexpression Mutants

2011-01-20 | GSE26726 | GEO

chico mutant

Project description:Comparison of wild type and heterozygote and homozygote chico mutants ( Clancy, et al. Extension of Life-Span by Loss of CHICO, a Drosophila Insulin Receptor Substrate Protein. Science 292 (5514), 104.) on Affymetrix Drosophila2 GeneChip. The flies (Drosophila melanogaster) are 7 day old adult females.

2007-06-06 | E-MEXP-1099 | biostudies-arrayexpress

Drosophila melanogaster

Project description:Drosophila melanogaster transcriptional profiling over life span: Indy vs. Controls

| PRJNA110479 | ENA

Wine yeast EC1118 and CSM comparative transcriptomics during synthetic grape juice fermentation MS300 at day 6

Project description:CSM is a commercial wine yeast with a long chronological life span, while commercial strain EC1118 displays a short life span in laboratory synthetic complete medium SC. Our aim is compare their expression profile on a high sugar fermentation

2011-10-26 | GSE33068 | GEO

Significant and Systematic Expression Differentiation in Long-Lived Yeast Strains

Project description:The three yeast mutants sch9Δ, ras2Δ, tor1Δ show extended chronological life span up to three folds. This study aims to dissect the mechanisms that lead to the yeast life span extension. Keywords: Expression comparison between wild type and long-lived yeast mutant strain

2008-11-01 | GSE13420 | GEO

Deletion of the Mammalian INDY Homologue in Mice Mimics Aspects of Dietary Restriction and Protects Against Diet and Age-Induced Adiposity and Insulin Resistance

Project description:Reduction in expression of the INDY gene in Drosophila melanogaster and Caenorhabditis elegans prolongs life span, and in D. melanogaster augments mitochondrial biogenesis in a manner akin to caloric restriction. However, the cellular mechanism by which INDY does this is unknown. In order to examine the effect that INDY might have on energy metabolism and insulin sensitivity in mammals we created the first knock out mouse model of the mammalian INDY homologue SLC13A5. Here, we show that deletion of the mammalian homologue of INDY, SLC13A5 (mINDY) in mice (mINDY-/- mice) have increased mitochondrial biogenesis, hepatic lipid oxidation, and energy expenditure, but decreased hepatic de novo lipogenesis. Loss of mIndy activates hepatic AMPK, which induces PGC-1?, inhibits ACC-2, and reduces SREBP-1c levels. In contrast to wild- type mice, mINDY-/- mice have reduced body weight and are protected from insulin resistance that evolves with high-fat feeding and aging. These studies demonstrate that mIndy functions as a novel regulator of mammalian energy metabolism and suggest that mIndy might be a novel therapeutic target for the treatment of obesity and type 2 diabetes.

2011-08-04 | GSE29984 | GEO

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