HSFs drive transcription of distinct genes and enhancers during oxidative stress and heat shock
| العنوان: | HSFs drive transcription of distinct genes and enhancers during oxidative stress and heat shock |
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| المؤلفون: | Himanen, S. V., Puustinen, M. C., Da Silva, A. J., Vihervaara, Anniina, Sistonen, L. |
| المصدر: | Nucleic Acids Research. 50(11):6102-6115 |
| مصطلحات موضوعية: | glutathione, heat shock transcription factor, heat shock transcription factor 1, heat shock transcription factor 2, menadione, RNA polymerase II, transcription factor Nrf2, unclassified drug, DNA binding protein, heat shock protein, Article, Cacybp gene, controlled study, differential expression analysis, down regulation, enhancer region, gene, gene activation, gene expression, genetic transcription, heat stress, Hs 578T cell line, human, human cell, immunofluorescence, oxidation reduction state, oxidative stress, promoter region, temperature, transcription initiation, upregulation, Western blotting, genetics, heat shock response, metabolism, DNA-Binding Proteins, Heat Shock Transcription Factors, Heat-Shock Proteins, Heat-Shock Response |
| الوصف: | Reprogramming of transcription is critical for the survival under cellular stress. Heat shock has provided an excellent model to investigate nascent transcription in stressed cells, but the molecular mechanisms orchestrating RNA synthesis during other types of stress are unknown. We utilized PRO-seq and ChIP-seq to study how Heat Shock Factors, HSF1 and HSF2, coordinate transcription at genes and enhancers upon oxidative stress and heat shock. We show that pause-release of RNA polymerase II (Pol II) is a universal mechanism regulating gene transcription in stressed cells, while enhancers are activated at the level of Pol II recruitment. Moreover, besides functioning as conventional promoter-binding transcription factors, HSF1 and HSF2 bind to stress-induced enhancers to trigger Pol II pause-release from poised gene promoters. Importantly, HSFs act at distinct genes and enhancers in a stress type-specific manner. HSF1 binds to many chaperone genes upon oxidative and heat stress but activates them only in heat-shocked cells. Under oxidative stress, HSF1 localizes to a unique set of promoters and enhancers to trans-activate oxidative stress-specific genes. Taken together, we show that HSFs function as multi-stress-responsive factors that activate distinct genes and enhancers when encountering changes in temperature and redox state. |
| وصف الملف: | |
| الوصول الحر: | https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-326800Test https://doi.org/10.1093/nar/gkac493Test |
| قاعدة البيانات: | SwePub |
| تدمد: | 03051048 13624962 |
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| DOI: | 10.1093/nar/gkac493 |