Neuronal HSF-1 activity coordinates fat desaturation across tissues in C. elegans via TGF-b/BMP signalling
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ABSTRACT:
PROVIDER: PRJNA606076 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11068823.fastq.gz | Fastqsanger.gz | |||
| SRR11068824.fastq.gz | Fastqsanger.gz | |||
| SRR11068825.fastq.gz | Fastqsanger.gz | |||
| SRR11068826.fastq.gz | Fastqsanger.gz | |||
| SRR11068827.fastq.gz | Fastqsanger.gz |
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Project description:To survive elevated temperatures, ectotherms adjust the fluidity of membranes by fine-tuning lipid desaturation levels in a process that has been previously described to be cell-autonomous. We have discovered that, in Caenorhabditis elegans, the neuronal over-expression of the master regulator of the conserved heat shock response (HSR), Hsf-1, causes extensive fat remodelling in peripheral tissues. These changes include a decrease in fat desaturase expression in the gut, and a shift in the saturation levels of fatty acids in the plasma membrane, in line with ectothermic adaptive responses. We have identified the cGMP receptor TAX-2/TAX-4 and TGF-β/BMP signalling, as key players in signalling across tissues. We also find that gradual increments in ambient temperature result in HSR activation exclusively in wild-type head neurons. This is the first study to suggest that a thermostat-based mechanism can non-cell autonomously coordinate membrane fluidity in response to warm temperatures across tissues in multicellular animals.
2021-10-19 | GSE145123 | GEO
Project description:Impaired protein homeostasis promotes age-associated tissue dysregulation, presenting a need for therapeutic approaches that can restore proteome integrity. The heat shock factor HSF-1 is the master transcriptional regulator of proteostasis and regulates the expression of heat shock proteins (HSPs), which facilitate proper protein folding, localisation, and degradation. Increased HSF-1 activity can suppress proteotoxicity and enhance longevity across species. Studies into the mechanisms behind these beneficial effects have mostly focused on HSPs; however, the precise mechanisms by which increased HSF-1 activity extends lifespan are not known. To address this, we conducted an RNAi screen for genes that promote longevity, in C. elegans over expressing HSF-1 (hsf-1 OE). We found that ubiquilin-1 (ubql-1), a multifaceted shuttle protein that functions in protein degradation pathways is necessary for full lifespan extension in hsf-1OE worms. Surprisingly, we find that lack of ubql-1 does not impact proteostasis capacity, but does alter mitochondrial dynamics, in hsf-1 OE worms. These effects are independent of mitophagy or the mitochondrial unfolded protein response (mitoUPR) suggesting enhanced turnover of mitochondrial outer membrane proteins may be important for increased longevity via the HSF-1-ubiquilin-1 axis. Additionally, we reveal a role for ubql-1, a protein quality control regulator in regulating lipid homeostasis in hsf-1 OE animals. Lack of ubql-1 in hsf-1 OE animals supresses the expression of a key mitochondrial β-oxidation and lipid mobilization gene regulated by NHR-49 - acyl-CoA synthetase-2, ACS-2 amongst other genes. We propose that ubql-1 is required for mito-fusion and metabolic modulations that promote longevity in hsf-1 OE by interacting with NHR-49.
2024-10-17 | PXD044595 | Pride
Project description: Not available
| S-EPMC8585009 | biostudies-literature
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
Project description:In order to recover nuclei with two active X chromosomes (class I), we developed a reprogramming strategy by supplementing hESC media with the small molecules sodium butyrate, and 3-deazaneplanocin A (DZNep). In order to determine how B+D affects global gene expression, we performed microarray analysis in triplicate in the HSF-6 (8) C and HSF-6 (8) B+D treated cultures. We also evaluated HSF-6 (S9) B+D in triplicate and identified no statistically significant changes in gene expression in HSF-6 (S9) B+D compared to HSF-6 (8) B+D treated cultures. This suggests that global transcriptional differences are more strongly modulated by presence or absence of B+D and not the percentage of class I, II or III nuclei.
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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 HSE’s residence in open chromatin is a primary determinant of whether HSF can bind following heat shock.
2010-09-02 | GSE19025 | GEO
Project description:In order to recover nuclei with two active X chromosomes (class I), we developed a reprogramming strategy by supplementing hESC media with the small molecules sodium butyrate, and 3-deazaneplanocin A (DZNep). In order to determine how B+D affects global gene expression, we performed microarray analysis in triplicate in the HSF-6 (8) C and HSF-6 (8) B+D treated cultures. We also evaluated HSF-6 (S9) B+D in triplicate and identified no statistically significant changes in gene expression in HSF-6 (S9) B+D compared to HSF-6 (8) B+D treated cultures. This suggests that global transcriptional differences are more strongly modulated by presence or absence of B+D and not the percentage of class I, II or III nuclei. We performed gene expression profiling on hESC HSF-6 (8, S9) in absent (control) and presence of butyrate and DZNep. All cell were collected after 11 passages in absent and presence of butyrate and DZNep.
2011-11-22 | E-GEOD-33864 | biostudies-arrayexpress
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:In this experiment, we aimed to determine the gene expression changes associated with loss of UBQL-1 in wildtype and in worms overexpressing HSF-1 (hsf-1 OE).
2023-09-01 | GSE241558 | GEO
Project description:Stutzerimonas nitrititolerans strain:HSF Genome sequencing
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