Transcriptional responses of cancer cells to heat shock-inducing stimuli involve amplification of robust HSF1 binding.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
16 Nov 2023
16 Nov 2023
Historique:
received:
23
11
2022
accepted:
01
11
2023
medline:
27
11
2023
pubmed:
17
11
2023
entrez:
17
11
2023
Statut:
epublish
Résumé
Responses of cells to stimuli are increasingly discovered to involve the binding of sequence-specific transcription factors outside of known target genes. We wanted to determine to what extent the genome-wide binding and function of a transcription factor are shaped by the cell type versus the stimulus. To do so, we induced the Heat Shock Response pathway in two different cancer cell lines with two different stimuli and related the binding of its master regulator HSF1 to nascent RNA and chromatin accessibility. Here, we show that HSF1 binding patterns retain their identity between basal conditions and under different magnitudes of activation, so that common HSF1 binding is globally associated with distinct transcription outcomes. HSF1-induced increase in DNA accessibility was modest in scale, but occurred predominantly at remote genomic sites. Apart from regulating transcription at existing elements including promoters and enhancers, HSF1 binding amplified during responses to stimuli may engage inactive chromatin.
Identifiants
pubmed: 37973875
doi: 10.1038/s41467-023-43157-7
pii: 10.1038/s41467-023-43157-7
pmc: PMC10654513
doi:
Substances chimiques
DNA-Binding Proteins
0
Heat Shock Transcription Factors
0
Transcription Factors
0
Chromatin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
7420Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM104360
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM128729
Pays : United States
Informations de copyright
© 2023. The Author(s).
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