HSF-1 promotes longevity through ubiquilin-1 dependent mitochondrial remodelling
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE241558 | GEO | 2023/09/01
REPOSITORIES: GEO
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Project description:To determine the transcriptional program of HSF-1 in lifespan assurance in C. elegans, we coupled HSF-1 depletion specifically from the soma by auxin-inducible degron (AID) with RNA-seq analyses in whole animals. Depletion of HSF-1 from the soma was performed by transferring worms that express the E3 ligase TIR1 in somatic tissues and carry AID insertion to the endogenous HSF-1 onto NGM plates containing 1mM auxin (indole- 3-acetic acid, Sigma). The mock treatment was done by transferring worms to plates only containing the vehicle ethanol (EtOH). We analyzed the transcriptomic changes by RNA-seq upon soma-specific depletion of HSF-1 initiated at young adult stage for different length of time. We included the strains that only express TIR1 but do not have degron insertion at HSF-1 (CA1200) to control for the effects of auxin treatment and AID insertion into HSF-1. We performed analyses in the wild-type background (JTL611) as well as in the longlived, germline stem cell (GSC) arrested glp-1(e2141) mutant (JTL667). The AID model in fem-3(q20) mutant (JTL670) was included as a control for JTL667. JTL670 (fem-3) is sterile at 25°C as JTL667 (glp-1) but has normal lifespan.
2022-05-19 | GSE203087 | GEO
Project description:Purpose: We used RNA-Seq to compare the gene expression profiles in two long-lived C. elegans strains: (1) animals with a loss-of-function mutation in the hsb-1 gene, and (2) animals overexpressing hsf-1 under its endogenous promoter. Previous studies indicated that life span extension in both these strains is hsf-1-dependent. Methods: mRNA-Seq profiles for three biological replicates each of day 1 adult wild-type (N2 strain), hsb-1 mutant and hsf-1 overexpression strains were generated using 50 bp single-end sequencing on an Illumina HiSeq 2500 platform. The sequencing reads that passed quality control were aligned to the C. elegans reference transcriptome (WS220 release) using Bowtie 2 and splicing junctions were mapped using TopHat. Cufflinks was used to calculate FPKM values and CuffDiff 2 was used to identify differentially expressed genes based on the following two criteria: false discovery rate (FDR)-adjusted p value < 0.05 and fold-change ≥ 1.5. Results: Using our mRNA-Seq workflow, we mapped at least 14 million reads per sample to the C. elegans transcriptome at greater than 96 percent alignment rate for the raw reads. Expression of 7,478 genes was found to be significantly altered in the hsf-1 overexpression strain relative to wild-type worms, while only 1,855 genes had singnificantly different expression in the hsb-1 mutant strain relative to wild-type. Using our criterion of ≥ 1.5-fold change in gene expression, we found 1,820 and 662 genes to be differentially expressed relative to wild-type in hsf-1 overexpression and hsb-1 mutant strains, respectively. The 247 genes that were differentially expressed in both hsf-1 overexpression and hsb-1 mutant strains showed a strongly correlated expression pattern in the two strains. Conclusions: hsf-1 overexpression induces global transcriptional suppression in C. elegans. Genetic ablation of hsb-1 produces similar life span extension in worms as hsf-1 overexpression, but alters expression of a much smaller subset of the C. elegans transcriptome. Hence, HSB-1 is a specific regulator of the transactivation potential of HSF-1 that selectively modulates gene expression relevant to longevity determination in worms.
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Project description:To determine how gene expression changes in long-lived ash-2-deficient worms expressing the amyloidogenic Q40::YFP, and to assess how simultaneous depletion of hsf-1 effects these transcriptomic changes.
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Project description:To identify genes transcriptionally regulated by the nuclear hormone receptor, NHR-49, we performed RNA sequencing of wild-type and nhr-49(nr2041) loss-of-function mutant C. elegans. This transcriptomic dataset is utilized in the respective study to compare differentially regulated genes in nhr-49(nr2041) mutant worms to those treated with hsf-1 RNAi.
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Project description:To understand the roles of HSF-1 and its regulation in reproduction and heat shock response in a tissue-specific manner, we coupled tissue-specific HSF-1 depletion in C. elegans by auxin-inducible degron (AID) with genome-wide transcriptional analyses in whole animals. We used ChIP-seq to analyze the occupancy of HSF-1 (tagged with AID::GFP) and RNA Pol II in young adult (YA) animals grown at 20°C or upon heat shock (HS) at 34°C for 30 min following an acute depletion of HSF-1 by AID for 2 hours either in the somatic or in the germline cells. Depletion by AID was performed by transferring worms expressing the E3 ligase TIR1 and carrying AID insertion to endogenous HSF-1 (JTL611 or JTL621) to NGM plates containing 1mM auxin (indole- 3-acetic acid, Sigma). The mock treatment was done by transferring worms to plates only containing the vehicle ethanol (EtOH). In parallel, we used RNA-seq to analyze the heat shock respnse upon depletion of HSF-1 in the soma or the germline for 2 hours. In addition, we also analyzed the transcriptomic changes by RNA-seq upon tissue-specific depletion of HSF-1 initiated at young adult stage for different length of time. In all RNA-seq analyses, we included the strains that only express TIR1 but do not have degron insertion at HSF-1 (CA1200 and CA1199) to control for the effects of auxin treatment and AID insertion into HSF-1.
2021-07-01 | GSE162066 | GEO
Project description:To understand the roles of HSF-1 and its regulation in reproduction and heat shock response in a tissue-specific manner, we coupled tissue-specific HSF-1 depletion in C. elegans by auxin-inducible degron (AID) with genome-wide transcriptional analyses in whole animals. We used ChIP-seq to analyze the occupancy of HSF-1 (tagged with AID::GFP) and RNA Pol II in young adult (YA) animals grown at 20°C or upon heat shock (HS) at 34°C for 30 min following an acute depletion of HSF-1 by AID for 2 hours either in the somatic or in the germline cells. Depletion by AID was performed by transferring worms expressing the E3 ligase TIR1 and carrying AID insertion to endogenous HSF-1 (JTL611 or JTL621) to NGM plates containing 1mM auxin (indole- 3-acetic acid, Sigma). The mock treatment was done by transferring worms to plates only containing the vehicle ethanol (EtOH). In parallel, we used RNA-seq to analyze the heat shock respnse upon depletion of HSF-1 in the soma or the germline for 2 hours. In addition, we also analyzed the transcriptomic changes by RNA-seq upon tissue-specific depletion of HSF-1 initiated at young adult stage for different length of time. In all RNA-seq analyses, we included the strains that only express TIR1 but do not have degron insertion at HSF-1 (CA1200 and CA1199) to control for the effects of auxin treatment and AID insertion into HSF-1.
2021-07-01 | GSE162064 | GEO
Project description:To understand the roles of HSF-1 and its regulation in reproduction and heat shock response in a tissue-specific manner, we coupled tissue-specific HSF-1 depletion in C. elegans by auxin-inducible degron (AID) with genome-wide transcriptional analyses in whole animals. We used ChIP-seq to analyze the occupancy of HSF-1 (tagged with AID::GFP) and RNA Pol II in young adult (YA) animals grown at 20°C or upon heat shock (HS) at 34°C for 30 min following an acute depletion of HSF-1 by AID for 2 hours either in the somatic or in the germline cells. Depletion by AID was performed by transferring worms expressing the E3 ligase TIR1 and carrying AID insertion to endogenous HSF-1 (JTL611 or JTL621) to NGM plates containing 1mM auxin (indole- 3-acetic acid, Sigma). The mock treatment was done by transferring worms to plates only containing the vehicle ethanol (EtOH). In parallel, we used RNA-seq to analyze the heat shock respnse upon depletion of HSF-1 in the soma or the germline for 2 hours. In addition, we also analyzed the transcriptomic changes by RNA-seq upon tissue-specific depletion of HSF-1 initiated at young adult stage for different length of time. In all RNA-seq analyses, we included the strains that only express TIR1 but do not have degron insertion at HSF-1 (CA1200 and CA1199) to control for the effects of auxin treatment and AID insertion into HSF-1.
2021-07-01 | GSE162063 | GEO
Project description:Intestine-specific transcriptome of wild-type. gas-1(fc21) and gas-1(fc21); cest-2.2 OE Caenorhaditis elegans in order to gain insight into how cest-2.2 overexpression ameliorates Complex I deficiency
2021-10-01 | GSE168501 | GEO
Project description:Sequence-specific transcription factors (TFs) are critical for specifying patterns and levels of gene expression, but the DNA elements to which they can bind are not always sufficient to specify their binding in vivo. In eukaryotes, the binding of a TF is in competition with a constellation of other proteins, including histones which package DNA into nucleosomes. Here, we examine using the ChIP-seq assay, the genome-wide distribution of Drosophila Heat Shock Factor (HSF), a TF whose binding activity is mediated by heat shock-induced trimerization. We detect HSF binding to 464 sites, the vast majority of which contain HSF Sequence-binding Elements (HSEs) in Drosophila S2 cells, but these HSF-bound sites represent only a small fraction of HSEs present in the genome. We find a strong correlation of bound HSEs to active chromatin marks present prior to HSF binding, indicating an HSEM-bM-^@M-^Ys residence in open chromatin is a primary determinant of whether HSF can bind following heat shock. A single mock immunoprecipitation (IP) using the pre-innoculated animal serum was used as a background dataset for this study. For each condition (NHS and 20minute HS), we performed two independent HSF-ChIP-seq experiments. In addition, we performed two independent HSF-ChIP-seq experiments for each condition (NHS and 20minute HS) in cells that were highly depleted of HSF by RNAi.
2010-09-02 | E-GEOD-19025 | biostudies-arrayexpress