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Expression analysis of C. elegans wild-type N2 and rsks-1, daf-2, daf-2 rsks-1 and daf-16; daf-2 rsks-1 mutants

ABSTRACT: Investigation of whole genome gene expression level changes in C. elegans rsks-1, daf-2, daf-2 rsks-1 and daf-16; daf-2 rsks-1 mutant compared to the wild-type N2 strain. The mutants have altered longevity phenotypes. The mutants analyzed in this study are further described in Di Chen, Patrick Wai-Lun Li, Benjamin A. Goldstein, Waijiao Cai, Emma Lynn Thomas, Fen Chen, Alan E. Hubbard, Simon Melov and Pankaj Kapahi, Germline Signaling Mediates the Synergistically Prolonged Longevity by Double Mutations in daf-2 and rsks-1 in C. elegans, Cell Reports (CELL-REPORTS-D-13-00388). A 47 chip study using total RNAs from C. elegans wild-type N2 (9 replicates), rsks-1 mutant (9 replicates), daf-2 mutant (9 replicates), daf-2 rsks-1 double mutant (10 replicates) and daf-16; daf-2 rsks-1 triple mutant (10 replicates) measured gene expression levels at the whole genome level.

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Di Chen

PROVIDER: E-GEOD-52340 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression analysis of C. elegans wild-type N2 and rsks-1, daf-2, daf-2 rsks-1 and daf-16; daf-2 rsks-1 mutants

Project description:Investigation of whole genome gene expression level changes in C. elegans rsks-1, daf-2, daf-2 rsks-1 and daf-16; daf-2 rsks-1 mutant compared to the wild-type N2 strain. The mutants have altered longevity phenotypes. The mutants analyzed in this study are further described in Di Chen, Patrick Wai-Lun Li, Benjamin A. Goldstein, Waijiao Cai, Emma Lynn Thomas, Fen Chen, Alan E. Hubbard, Simon Melov and Pankaj Kapahi, Germline Signaling Mediates the Synergistically Prolonged Longevity by Double Mutations in daf-2 and rsks-1 in C. elegans, Cell Reports (CELL-REPORTS-D-13-00388).

2013-11-14 | GSE52340 | GEO

C. elegans daf-10(m79) mutants vs wild-type worms

Project description:Transcriptional profiling of whole day 1 adult C. elegans, comparing animals carrying the m79 mutation in the daf-10 gene and wild-type isogenic animals. Genes that act downstream of sensory neurons to influence longevity, dauer formation and pathogen responses in Caenorhabditis elegans Manuscript abstract: Two-condition experiments, daf-10 vs wt, 3 biological repeats of each grown in parallel, verified lifespan increase in daf-10 mutant animals

2012-11-01 | E-GEOD-41943 | biostudies-arrayexpress

daf-16/FoxO isoform-specific deletion mutants

Project description:FoxO transcription factors promote longevity across taxa. How they do so is poorly understood. In the nematode Caenorhabditis elegans, the A- and F-isoforms of the FoxO transcription factor DAF-16 extend life span in the context of reduced DAF-2 insulin-like growth factor receptor (IGFR) signaling. To elucidate the mechanistic basis for DAF-16/FoxO-dependent life span extension, we performed an integrative analysis of isoform-specific daf-16/FoxO mutants. In contrast to previous studies suggesting that DAF-16F plays a more prominent role in life span control than DAF-16A, isoform-specific daf-16/FoxO mutant phenotypes and whole transcriptome profiling revealed a predominant role for DAF-16A over DAF-16F in life span control, stress resistance, and target gene regulation. Integration of these data sets enabled the prioritization of a subset of 92 DAF-16/FoxO target genes for functional interrogation. Among 29 genes tested, two DAF-16A-specific target genes significantly influenced longevity. Our discovery of new longevity genes underscores the efficacy of our integrative strategy while providing a general framework for identifying specific downstream gene regulatory events that contribute substantially to transcription factor functions. As FoxO transcription factors have conserved functions in promoting longevity and may be dysregulated in aging-related diseases, these findings promise to illuminate fundamental principles underlying aging in animals.

2015-08-27 | GSE72426 | GEO

daf-16/FoxO isoform-specific deletion mutants

2015-08-27 | E-GEOD-72426 | biostudies-arrayexpress

Inter-species genetic regulation of longevity: Δhns E. coli activate C. elegans DAF-16 in distinct ways from IIS

Project description:We confirmed that the life span of C. elegans feeding hns mutant E. coli was increased. hns mutant E. coli was found to regulate lifespan of C. elegans through daf-16 activation in C. elegans. It is well known that daf-16 is the transcription factor of the insulin/IGF-1 signaling pathway and it is known to regulate downstream genes such as longevity, stress response, and dauer diapause regulation genes. Thus, we performed Next Generation Sequencing(NGS) to investigate the downstream genes regulated by daf-16 in C. elegans that are activated by hns mutant E. coli. N2 wild type worms and daf-16 mutant worms were fed with BW25113 wild type E. coli and hns mutant E. coli, respectively, and then NGS was performed by harvesting the worms and purifying the RNA. We investigated how the downstream genes of daf-16 of C. elegans, which is regulated by hns mutant E. coli, differs from the downstream genes of daf-16 of C. elegans, which is regulated by the insulin/IGF-1 signaling pathway. To do this, we carried out the analysis including two previous studied papers that analyzed the daf-16 downstream genes related to the insulin/IGF-1 signaling pathway. Surprisingly, only 6 genes were up-regulated in all three experiments and 288 genes were found to be dependent on daf-16 and hns mutant E. coli. This study indicated that hns mutant E. coli regulate daf-16 distinct from insulin/IGF-1 signaling pathway on C. elegans.

2020-07-29 | GSE114160 | GEO

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

Analysis of nonsense-mediated mRNA decay in daf-2 mutants

Project description:To exmine the role of nonsense-mediated mRNA decay process in the longevity regulation of daf-2 mutants, we sequenced transcriptomes from day 1 adult Caenorhabditis elegans: Bristol N2 (wild-type), and smg-2(qd101), daf-2(e1370) and smg-2(qd101); daf-2(e1370) mutants.

2017-03-17 | GSE94077 | GEO

Activation of DAF-16/FOXO by reactive oxygen species promotes longevity in long- lived mitochondrial mutants in C. elegans

Project description:Mild deficits in mitochondrial function have been shown to increase lifespan in multiple species including worms, flies and mice. Here, we study three C. elegans mitochondrial mutants (clk-1, isp-1 and nuo-6) to identify overlapping genetic pathways that contribute to their longevity. We find that genes regulated by the FOXO transcription factor DAF-16 are upregulated in all three strains, and that the transcriptional changes present in these worms overlap significantly with the long-lived insulin-IGF1 signaling pathway mutant daf-2. We show that DAF-16 and multiple DAF-16 interacting proteins (MATH-33, IMB-2, CST-1/2, BAR-1) are required for the longevity of all three mitochondrial mutants. Our results suggest that the activation of DAF-16 in these mutants results from elevated levels of reactive oxygen species. Overall, this work reveals an overlapping genetic pathway required for longevity in three mitochondrial mutants, and, combined with previous work, demonstrates that DAF-16 is a downstream mediator of lifespan extension in multiple pathways of longevity.

2018-02-26 | GSE93724 | GEO

C. elegans daf-10(m79) mutants vs wild-type worms

2012-11-01 | GSE41943 | GEO

Transcriptome profiling of sterile daf-2; mes-1 double vs. mes-1 single mutants

Project description:The germ lineage is considered to be immortal. In the quest to extend lifespan, a possible strategy is to drive germline traits in somatic cells, to try to confer some of the germ lineage’s immortality on the somatic body. Notably, a study in C. elegans suggested that expression of germline genes in the somatic cells of long-lived daf-2 mutants confers some of daf-2’s longevity. Specifically, mRNAs encoding components of C. elegans germ granules (P granules) were up-regulated in daf-2 mutant worms, and knock-down of individual P-granule and other germline genes in daf-2 young adults modestly reduced their lifespan. We investigated the contribution of a germline program to daf-2’s long lifespan, and also tested if other mutants known to express germline genes in their somatic cells are long-lived. Our key findings are: 1) We could not detect P-granule proteins in the somatic cells of daf-2 mutants by immunostaining or by expression of a P-granule transgene. 2) Whole-genome transcript profiling of animals lacking a germline revealed that germline transcripts are not up-regulated in the soma of daf-2 worms compared to the soma of control worms. 3) Simultaneous removal of multiple P-granule proteins or the entire germline program from daf-2 worms did not reduce their lifespan. 4) Several mutants that robustly express a broad spectrum of germline genes in their somatic cells are not long-lived. Taken together, our findings argue against the hypothesis that acquisition of a germ cell program in somatic cells increases lifespan and contributes to daf-2’s longevity.

2016-01-20 | GSE76946 | GEO

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