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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Published in:Molecular cell Vol. 84; no. 1; p. 80
Main Authors: Pessa, Jenny C, Joutsen, Jenny, Sistonen, Lea
Format: Journal Article
Language:English
Published: United States 04.01.2024
Subjects:
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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Abstract 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.
AbstractList 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.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.
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.
Author Sistonen, Lea
Pessa, Jenny C
Joutsen, Jenny
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  givenname: Jenny C
  surname: Pessa
  fullname: Pessa, Jenny C
  organization: Faculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland; Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland
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  givenname: Jenny
  surname: Joutsen
  fullname: Joutsen, Jenny
  organization: Department of Pathology, Lapland Central Hospital, Lapland Wellbeing Services County, Rovaniemi, Finland
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  givenname: Lea
  surname: Sistonen
  fullname: Sistonen, Lea
  email: lea.sistonen@abo.fi
  organization: Faculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland; Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland. Electronic address: lea.sistonen@abo.fi
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Keywords transcription factor
Pol II
enhancer
transcription
HSR
PTM
post-translational modification
chromatin
proteostasis
heat shock factor
HSF
heat shock response
RNA polymerase II
Language English
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