Heat Shock Protein Genes Undergo Dynamic Alteration in Their Three-Dimensional Structure and Genome Organization in Response to Thermal Stress

Chowdhary, Surabhi; Kainth, Amoldeep S.; Gross, David S.

doi:10.1128/mcb.00292-17

Cited by 49 publications

(94 citation statements)

References 68 publications

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“…Transcriptional reprogramming upon stress co-occurs with global changes in chromatin landscape at genes, enhancers and untranscribed regions 11,27,29 . Moreover, heat-induced changes in connectivity and organization of the genome have been reported in yeast 91 and fly 92 .…”

Section: Chromatin Remodelling Upon Stressmentioning

confidence: 99%

Molecular mechanisms driving transcriptional stress responses

Vihervaara¹,

Duarte²,

Lis³

2018

Nat Rev Genet

212

224

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Proteotoxic stress, that is, stress caused by protein misfolding and aggregation, triggers the rapid and global reprogramming of transcription at genes and enhancers. Genome-wide assays that track transcriptionally-engaged RNA polymerase II (Pol II) at nucleotide resolution have provided key insights into the underlying molecular mechanisms that regulate transcriptional responses to stress. In addition, recent kinetic analyses on transcriptional control under heat stress have shown how cells ‘prewire’ and rapidly execute genome-wide changes in transcription while concurrently becoming poised for recovery. The regulation of Pol II at genes and enhancers in response to heat stress is coupled to chromatin modification and compartmentalization, as well as to co-transcriptional RNA processing. These mechanistic features seem to apply broadly to other coordinated genome-regulatory responses.

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Section: Chromatin Remodelling Upon Stressmentioning

confidence: 99%

Molecular mechanisms driving transcriptional stress responses

Vihervaara¹,

Duarte²,

Lis³

2018

Nat Rev Genet

212

224

View full text Add to dashboard Cite

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“…Enhancerpromoter loops, typically 10-100 kb in mammals, are stabilized by Mediator, cohesin, and the sequence-specific factor YY1 (Beagan et al, 2017;Kagey et al, 2010;Weintraub et al, 2017). Analogous, albeit smaller, enhancer (UAS)-promoter loops have been observed in S. cerevisiae (Chowdhary et al, 2017;Dobi and Winston, 2007).…”

Section: Introductionmentioning

confidence: 96%

Heat Shock Factor 1 Drives Intergenic Association of Its Target Gene Loci Upon Heat Shock

Chowdhary

Kainth

Pincus

et al. 2018

Preprint

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Transcriptional induction of Heat Shock Protein (HSP) genes in yeast is accompanied by dynamic changes in their 3D structure and spatial organization, yet the molecular basis for these phenomena remains unknown. Using chromosome conformation capture and single cell imaging, we show that genes transcriptionally activated by Heat Shock Factor 1 (Hsf1) specifically interact across chromosomes and coalesce into diffraction-limited intranuclear foci. Genes activated by the alternative stress regulators Msn2 and Msn4, in contrast, do not interact among themselves nor with Hsf1 targets.Likewise, constitutively expressed genes, even those interposed between HSP genes, show no detectable interaction. Hsf1 forms discrete subnuclear puncta when stressactivated, and these puncta dissolve in concert with transcriptional attenuation, paralleling the kinetics of HSP gene coalescence and dissolution. Nuclear Hsf1 and RNA Pol II are both necessary for intergenic HSP gene interactions, while DNA-bound Hsf1 is necessary and sufficient to drive coalescence of a heterologous gene. Our findings demonstrate that Hsf1 can dynamically restructure the yeast genome.

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“…HS-induced dynamic chromatin looping to bring the distal regulatory elements closure has been well established by earlier studies (49). Recent studies also suggest that HSP genes undergo extensive transcriptiondependent intragenic folding interactions (crumpling) during the thermal stress (24,50). To test this possibility in the TNF-a gene, we performed the 3C assay.…”

Section: Hsf1 Acts Through An Hse Located At the 39-utr Of The Tnf-a mentioning

confidence: 93%

“…The chromatin conformation capture (3C) assay was executed by following a previously described protocol (24,25), with slight modification. In brief, after treatment with HS or not, the HEK293 cells were cross-linked with 1% formaldehyde.…”

Section: Chromatin Conformation Capture Assaymentioning

confidence: 99%

HSF1 mediated TNF‐α production during proteotoxic stress response pioneers proinflammatory signal in human cells

2018

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The proteotoxic stress response that safeguards the cellular proteome from various stressors was shown to activate NF‐κB signaling pathways (NκBS) with an underlying mechanism that is poorly understood. We show here that the TNFα gene, a pleiotropic NκBS inducer, is a direct target of heat shock factor 1 (HSF1). Human HSF1 drives this process by assembling a multiprotein activation complex at a heat shock element (HSE) located at the 3′‐UTR of the TNF‐α gene (HSE5). HSF1 associated with the HSE5 at the TNF‐α 3′‐UTR communicates with the promoter through chromatin looping by recruiting lymphoid enhancer–binding factor 1 at an adjacent Wnt‐responsive element through its transactivation domain. TNF‐α thus produced guides the activation of NκBS by acting through TNF‐α receptor 1 (TNFR1). Notably, cells with TNFR1−/− background or masked HSE5 through Clustered Regularly Interspaced Short Palindromic Repeats/dead CRISPR‐associated protein 9 were defective in NκBS and exhibited marked alteration in cellular biology, which includes loss of ability of cancer cells to migrate, to clear the protein aggregates, and associated toxicity upon heat shock. For the first time, our results suggest that TNF‐α thus produced pioneers the proinflammatory signal during proteotoxic stress response with an important implication for inflammation and cancer.—Ali, A., Biswas, A., Pal, M. HSF1 mediated TNF‐α production during proteotoxic stress response pioneers proinflammatory signal in human cells. FASEB J. 33, 2621–2635 (2019). http://www.fasebj.org

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Heat Shock Protein Genes Undergo Dynamic Alteration in Their Three-Dimensional Structure and Genome Organization in Response to Thermal Stress

Cited by 49 publications

References 68 publications

Molecular mechanisms driving transcriptional stress responses

Molecular mechanisms driving transcriptional stress responses

Heat Shock Factor 1 Drives Intergenic Association of Its Target Gene Loci Upon Heat Shock

HSF1 mediated TNF‐α production during proteotoxic stress response pioneers proinflammatory signal in human cells

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