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RNAi knock down of daf-16 in C. elegans over 0-192 hours

ABSTRACT: Comparison of sterile worms grown on Control Vector, daf-2 RNAi, and daf-2 + daf-16 RNAi. Synchronized fer-15(b26); fem-1(hc17) animals were grown on RNAi bacteria at 25ºC, induced with IPTG on Day 1 of adulthood, and collected from 0-48 hours (10 time points) and 0-196 hours (10 time points); RNAi bacteria was supplemented as necessary for later time points. Worms were floated off lawns with M9 buffer, centrifuged, and washed again in M9. The pelleted worms were dissolved in Trizol (Gibco) and frozen in liquid nitrogen.Time courses were compared with mixed references (collected from 1/2 of each of the time course samples)

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Andrew Fraser

PROVIDER: E-MEXP-9 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans.

Murphy Coleen T CT McCarroll Steven A SA Bargmann Cornelia I CI Fraser Andrew A Kamath Ravi S RS Ahringer Julie J Li Hao H Kenyon Cynthia C

Nature 20030629 6946

Ageing is a fundamental, unsolved mystery in biology. DAF-16, a FOXO-family transcription factor, influences the rate of ageing of Caenorhabditis elegans in response to insulin/insulin-like growth factor 1 (IGF-I) signalling. Using DNA microarray analysis, we have found that DAF-16 affects expression of a set of genes during early adulthood, the time at which this pathway is known to control ageing. Here we find that many of these genes influence the ageing process. The insulin/IGF-I pathway fun ...[more]

PMID: 12845331

Similar Datasets

RNAi knock down of daf-2, daf-3, daf-16 in C. elegans over 0-48 hours

Project description:Comparison of sterile worms grown on Control Vector, daf-2 RNAi, and daf-2 + daf-16 RNAi. Synchronized fer-15(b26); fem-1(hc17) animals were grown on RNAi bacteria at 25ºC, induced with IPTG on Day 1 of adulthood, and collected from 0-48 hours (10 time points) and 0-196 hours (10 time points); RNAi bacteria was supplemented as necessary for later time points. Worms were floated off lawns with M9 buffer, centrifuged, and washed again in M9. The pelleted worms were dissolved in Trizol (Gibco) and frozen in liquid nitrogen.Time courses were compared with mixed references (collected from 1/2 of each of the time course samples)

2003-07-17 | E-MEXP-8 | biostudies-arrayexpress

Transcription profiling of long-lived C.elegans daf-2 pathway mutants with wild type/short-lived mutants

Project description:Comparison of long-lived daf-2 pathway mutants with wild type/short-lived mutants. A: age-1 fer-15; fem-1 vs. fer-15; fem-1. B: age-1 fer-15; fem-1 vs. fer-15; fem-1. C: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. D: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. E: daf-16::gfp in daf-16(mu86);daf-2(e1370) vs. daf-16(mu86);daf-2(e1370). F: daf-2(e1368); fer-15; fem-1 vs. fer-15; fem-1. G: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. H: age-1 fer-15; fem-1 vs. fer-15; fem-1. I: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. J: daf-16::gfp in daf-2(e1370); daf-16(mu86) vs. daf-2(e1370); daf-16(mu86). K: daf-2(mu150) vs. wild type. L: daf-2(e1370) vs. daf-2(e1370); daf-16(mu86). M: daf-2(e1370) vs. daf-2(e1370); daf-16(mu86). N: daf-2(e1370) vs. daf-2(e1370); daf-16(mu86).

2003-07-17 | E-MEXP-7 | biostudies-arrayexpress

RNA-seq analysis comparing gene expression of unc-43(gf), unc-43(-) and egl-8(-) to the corresponding control strain in daf-2(+) and daf-2(-) background

Project description:To identify genes whose expression in Caenorhabditis elegans is regulated by unc-43/CamKII or egl-8/PLCbeta during adulthood, we performed an exploratory whole transcriptome RNA-sequencing (RNA-seq) study on unc-43(gf), unc-43(-), egl-8(-) and corresponding unc-43(+)/egl-8(+) control worms. To further account for potential influences of genetic background on unc-43/egl-8 function, these experiments were conducted in long-lived insulin-receptor defective [daf-2(-)], as well as in otherwise wildtype [i.e daf-2(+)] strains.

2022-10-01 | E-MTAB-11045 | biostudies-arrayexpress

RNA-seq analysis comparing gene expression between mbk-1(-) and mbk-1(+) strains in daf-2(+), daf-2(-), glp-1(+) and glp-1(-) background

Project description:To identify genes whose expression in Caenorhabditis elegans is regulated by mbk-1 (ortholog of the human protein kinase DYRK1A implicated in Down syndrome) during adulthood, we performed whole transcriptome RNA-sequencing (RNA-seq) on mbk-1(+) and mbk-1(-) worms. To further account for the influence of genetic background on mbk-1 function, these experiments were conducted in long-lived insulin-receptor defective [daf-2(-)] or germline stem cell [GSC] deficient [glp-1(-), i.e. GSC(-)] strains, as well as in corresponding [i.e daf-2(+) or glp-1(+)/GSC(+)] control strains.

2021-11-25 | E-MTAB-10898 | biostudies-arrayexpress

Defining changes in the total levels of proteins during aging of C. elegans

Project description:We performed label-free proteomics in C. elegans to define and quantify changes in the ubiquitinated (Ub)-proteome during the aging process. More specifically, we compared wild-type worms at the first day of adulthood with young (day 5), mid-age (day 10) and aged adults (day 15). Moreover, we assessed protein levels of age-matched long-lived genetic models of dietary restriction (eat-2(ad1116)) and reduced insulin/IGF-1 signaling (daf-2(e1370)).

2021-05-26 | PXD025128 | Pride

wt vs daf-2 C. elegans protein turnover

Project description:Most aging hypotheses revolve around the accumulation of some sort of damage resulting in gradual physiological decline and ultimately death. Avoiding protein damage accumulation by enhanced turnover should slow down the aging process and extend lifespan. However, lowering translational efficiency extends rather than shortens lifespan in C. elegans. We studied turnover of individual proteins in the conserved Insulin/Insulin-like Growth Factor (IGF-1) receptor mutant daf-2 by combining Stable Isotope Labeling by Nitrogen-15 in Caenorhabditis elegans and LC-MS/MS. Intriguingly, the majority of proteins displayed prolonged half-lives in daf-2, while others remained unchanged, signifying that longevity is not supported by high protein turnover. This slow-down of protein turnover was most prominent for components of the translation machinery and mitochondria. In contrast, the high turnover of lysosomal hydrolases and very low turnover of cytoskeletal proteins remained largely unchanged in daf-2. The slow-down of protein dynamics and decreased abundance of the translational machinery may point at the importance of anabolic attenuation in lifespan extension as suggested by the hyperfunction theory.

2016-09-27 | PXD002317 | Pride

Defining changes in the steady-state levels of ubiquitinated peptides in aging and longevity

Project description:We performed diGLY enrichment followed by label-free proteomics in C. elegans to define and quantify changes in the ubiquitinated (Ub)-proteome during the aging process. More specifically, we compared wild-type worms at the first day of adulthood with young (day 5), mid-age (day 10) and aged adults (day 15). Moreover, we assessed the Ub-modified proteome of age-matched long-lived genetic models of dietary restriction (eat-2(ad1116)) and reduced reduced insulin/IGF-1 signaling (daf-2(e1370)).

2021-05-27 | PXD024338 | Pride

Cathepsin B Promotes Aβ Proteotoxicity by Modulating Aging Regulating Mechanisms

Project description:While the activities of certain proteases promote proteostasis and prevent neurodegeneration-associated phenotypes, the protease cathepsin B (CTSB) enhances proteotoxicity in Alzheimer’s disease (AD) model mice, and its levels are elevated in brains of AD patients. How CTSB exacerbates the toxicity of the ADcausing Amyloid β (Aβ), is controversial. Using an activity-based probe, aging-altering interventions and the nematode C. elegans we discovered that the CTSB CPR-6 promotes Aβ proteotoxicity but mitigates the toxicity of polyQ stretches. While the knockdown of cpr-6 does not affect lifespan, it alleviates Aβ toxicity by reducing the expression of swsn-3 and elevating the level of the protein SMK-1, both involved in the regulation of aging. These observations unveil a novel mechanism by which CTSB aggravates Aβ– mediated toxicity, indicate that it plays opposing roles in the face of distinct proteotoxic insults and highlight the importance of tailoring specific remedies for distinct neurodegenerative disorders.

2024-09-04 | PXD045561 | Pride

Mechanical stress through growth on stiffer substrates has only mild impacts on animal health and longevity in C. elegans

Project description:Mechanical stress is a measure of internal resistance exhibited by a body or material when external forces, such as compression, tension, bending, etc. are applied. The study of mechanical stress on health and aging is a continuously growing field, as major changes to the extracellular matrix and cell-to-cell adhesions can result in dramatic changes to tissue stiffness during aging and diseased conditions. For example, during normal aging, many tissues including the ovaries, skin, blood vessels, and heart exhibit increased stiffness, which can result in a significant reduction in function of that organ. As such, numerous model systems have recently emerged to study the impact of mechanical and physical stress on cell and tissue health, including cell-culture conditions with matrigels and other surfaces that alter substrate stiffness and ex vivo tissue models that can apply stress directly to organs like muscle or tendons. Here, we sought to develop a novel method in an in vivo, model organism setting to study the impact of mechanical stress on aging, by increasing substrate stiffness in solid agar medium of C. elegans. To our surprise, we found shockingly limited impact of growth of C. elegans on stiffer substrates, including limited effects on cellular health, gene expression, organismal health, stress resilience, and longevity. Overall, our studies reveal that altering substrate stiffness of growth medium for C. elegans have only mild impact on animal health and longevity; however, these impacts were not nominal and open up important considerations for C. elegans biologists in standardizing agar medium choice for experimental assays.

2024-04-05 | E-MTAB-13938 | biostudies-arrayexpress

Identification of transcription factor DAF-16 binding sites in C. elegans

Project description:We identified the DNA binding sites of DAF-16 in transgenic line TJ356 (daf-16::gfp) that carries high-copy number daf-16. The expression pattern was examined through fluorescent microscopy. The binding sites were determined using chromatin immunoprecipitation with anti-GFP antibody and anti-POL II antibody followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Identification of DAF-16 binding sites at L4/Young adult stage when DAF-16 was highly overexpressed

2009-04-11 | E-GEOD-15567 | biostudies-arrayexpress

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