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Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [Germline - Timecourse]

ABSTRACT: Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [Germline - Timecourse]

PROVIDER: PRJNA680495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13125229_1.fastq.gz	Fastqsanger.gz
	SRR13125229_2.fastq.gz	Fastqsanger.gz
	SRR13125230_1.fastq.gz	Fastqsanger.gz
	SRR13125230_2.fastq.gz	Fastqsanger.gz
	SRR13125231_1.fastq.gz	Fastqsanger.gz

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Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [Germline - Timecourse]

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

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [HS response]

2021-07-01 | GSE162064 | GEO

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [ChIP-Seq]

2021-07-01 | GSE162063 | GEO

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Lifespan Assurance [HSF-1 transcriptome in the soma]

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

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [ChIP-Seq]

Project description:Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [ChIP-Seq]

| PRJNA680485 | ENA

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction, Lifespan Assurance and Heat Shock Response.

Project description:Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction, Lifespan Assurance and Heat Shock Response.

| PRJNA680487 | ENA

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [HS response]

Project description:Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction and Heat Shock Response. [HS response]

| PRJNA680496 | ENA

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Lifespan Assurance [HSF-1 transcriptome in the soma]

Project description:Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Lifespan Assurance [HSF-1 transcriptome in the soma]

| PRJNA838551 | ENA

Using Auxin-inducible-degradation System to Interrogate Tissue-specific Transcriptional Programs of HSF-1 in Reproduction, Lifespan Assurance and Heat Shock Response.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-01 | GSE162067 | GEO

HSF-1 promotes longevity through ubiquilin-1 dependent mitochondrial remodelling

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

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