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DAF-16 stabilizes the aging transcriptome and is activated in mid-aged C. elegans to cope with internal stress

ABSTRACT: DAF-16 stabilizes the aging transcriptome and is activated in mid-aged C. elegans to cope with internal stress

PROVIDER: PRJNA506829 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8240860_1.fastq.gz	Fastqsanger.gz
	SRR8240860_2.fastq.gz	Fastqsanger.gz
	SRR8240870_1.fastq.gz	Fastqsanger.gz
	SRR8240870_2.fastq.gz	Fastqsanger.gz
	SRR8240880_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

DAF-16 stabilizes the aging transcriptome and is activated in mid-aged C. elegans to cope with internal stress

Project description:The roles and regulatory mechanisms of transcriptome changes during aging are unclear. It has been proposed that the transcriptome suffers decay during aging owing to age-associated down-regulation of transcription factors. In this study, we characterized the role of a transcription factor DAF-16, which is a highly conserved lifespan regulator, in the normal aging process of Caenorhabditis elegans. We found that DAF-16 translocates into the nucleus in aged wild-type worms and activates the expression of hundreds of genes in response to age-associated cellular stress. Most of the age-dependent DAF-16 targets are different from the canonical DAF-16 targets downstream of insulin signaling. This and other evidence suggest that activation of DAF-16 during aging is distinct from activation of DAF-16 due to reduced signaling from DAF-2. Further analysis showed that it is due in part to a loss of proteostasis during aging, at least in part. We also found that without daf-16, dramatic gene expression changes occur as early as on adult day 2, indicating that DAF-16 acts to stabilize the transcriptome during normal aging. Our results thus reveal that normal aging is not simply a process in which the gene expression program descends into chaos due to loss of regulatory activities; rather, there is active transcriptional regulation during aging.

2018-11-26 | GSE122892 | GEO

DAF-16 stabilizes the aging transcriptome and is activated in mid-aged Caenorhabditis elegans to cope with internal stress.

Project description:The roles and regulatory mechanisms of transcriptome changes during aging are unclear. It has been proposed that the transcriptome suffers decay during aging owing to age-associated down-regulation of transcription factors. In this study, we characterized the role of a transcription factor DAF-16, which is a highly conserved lifespan regulator, in the normal aging process of Caenorhabditis elegans. We found that DAF-16 translocates into the nucleus in aged wild-type worms and activates the expression of hundreds of genes in response to age-associated cellular stress. Most of the age-dependent DAF-16 targets are different from the canonical DAF-16 targets downstream of insulin signaling. This and other evidence suggest that activation of DAF-16 during aging is distinct from activation of DAF-16 due to reduced signaling from DAF-2. Further analysis showed that it is due in part to a loss of proteostasis during aging. We also found that without daf-16, dramatic gene expression changes occur as early as on adult day 2, indicating that DAF-16 acts to stabilize the transcriptome during normal aging. Our results thus reveal that normal aging is not simply a process in which the gene expression program descends into chaos due to loss of regulatory activities; rather, there is active transcriptional regulation during aging.

| S-EPMC6516157 | biostudies-literature

N2, daf-1(m40), and daf-1(m40);daf-3(mgDf90) adult, gravid hermaphrodites

Project description:total RNA from N2, daf-1(m40), and daf-1(m40);daf-3(mgDf90) adult, gravid hermaphrodites were extracted and sequenced.

2020-05-28 | GSE131997 | GEO

RNAseq of dauer-forming C. elegans L2d in daf-2 and daf-2;daf-42

Project description:Under adverse environmental conditions, nematodes arrest into dauer, an alternative developmental stage for diapause. Dauers endure unfavorable environment and interact with host animals to access favorable environments, thus playing a critical role in the survival of both free-living and parasitic nematodes. Here, we discovered that in Caenorhabditis elegans, daf-42 is essential for development into dauer stage, as the null mutant shows lethal phenotype during dauer entry. To examine the transcriptional changes accompanied by the absence of DAF-42 during dauer entry, we performed RNA-sequencing on daf-2 and daf-2; daf-42 worms at 52 hours after egg laying (HAE) and 60 HAE, the time at which 0% and about 40% of daf-2; daf-42 mutants form dead dauer at 25 degrees Celcius, respectively. daf-2 control worms develop into dauer stage after 60 HAE, and half of its population develop into dauer by 72 HAE, when raised at 25 degrees Celcius.

2023-04-23 | GSE230353 | GEO

Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.

2007-02-08 | GSE5801 | GEO

DAF-16/FoxO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage [N2, daf-2, daf-16, daf-2;daf-16]

Project description:Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature aging. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with aging. Here we show that the FoxO transcription factor DAF-16 is activated in response to DNA damage during development while the DNA damage responsiveness of DAF-16 declines with aging. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA damage induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16 mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists.

2014-11-18 | GSE51162 | GEO

C. elegans microarrays: daf-2(-) vs. daf-2(-) xbp-1(-)

Project description:Transcriptional profiling of day 1 animals comparing untreated daf-2(-) animals and daf-2(-) xbp-1(-) animals. Goal was to identify genes whose expression in daf-2 mutants is dependent (directly or indirectly) on xbp-1.

2010-02-03 | GSE20148 | GEO

Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi

Project description:Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals.

2010-01-01 | GSE18561 | GEO

Transcription profiling of C. elegans mutants daf-2(e1368) and daf-2(e1368);pmk-1(km25), between daf-2(e1368), daf-2(e1368);daf-16(mgDf47)

Project description:Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Experiment Overall Design: Three independent biological replicates were isolated for each strain. All strains in a replicate were grown and harvested in parallel.

2008-06-14 | E-GEOD-5801 | biostudies-arrayexpress

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

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