TY - JOUR
T1 - Transcriptional responses of cancer cells to heat shock-inducing stimuli involve amplification of robust HSF1 binding
AU - Dastidar, Sayantani Ghosh
AU - De Kumar, Bony
AU - Lauckner, Bo
AU - Parrello, Damien
AU - Perley, Danielle
AU - Vlasenok, Maria
AU - Tyagi, Antariksh
AU - Koney, Nii Koney Kwaku
AU - Abbas, Ata
AU - Nechaev, Sergei
N1 - Publisher Copyright:
© 2023, The Author(s).
PY - 2023/12
Y1 - 2023/12
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85177088913&partnerID=8YFLogxK
U2 - 10.1038/s41467-023-43157-7
DO - 10.1038/s41467-023-43157-7
M3 - Article
C2 - 37973875
AN - SCOPUS:85177088913
SN - 2041-1723
VL - 14
JO - Nature Communications
JF - Nature Communications
IS - 1
M1 - 7420
ER -