Transcriptional reprogramming at the intersection of the heat shock response and proteostasis

Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to prote...

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Vydáno v:Molecular cell Ročník 84; číslo 1; s. 80
Hlavní autoři: Pessa, Jenny C, Joutsen, Jenny, Sistonen, Lea
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 04.01.2024
Témata:
transcription factor
Pol II
enhancer
transcription
HSR
PTM
post-translational modification
chromatin
proteostasis
heat shock factor
HSF
heat shock response
RNA polymerase II
ISSN:1097-4164, 1097-4164
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Shrnutí:Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to proteotoxic stress. The HSR encompasses a dual regulation of transcription, characterized by rapid activation of genes encoding molecular chaperones and concomitant global attenuation of non-chaperone genes. Recent genome-wide approaches have delineated the molecular depth of stress-induced transcriptional reprogramming. The dramatic rewiring of gene and enhancer networks is driven by key transcription factors, including heat shock factors (HSFs), that together with chromatin-modifying enzymes remodel the 3D chromatin architecture, determining the selection of either gene activation or repression. Here, we highlight the current advancements of molecular mechanisms driving transcriptional reprogramming during acute heat stress. We also discuss the emerging implications of HSF-mediated stress signaling in the context of physiological and pathological conditions.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1097-4164
1097-4164
DOI:10.1016/j.molcel.2023.11.024