ArticleMolecular and cellular biology2015
Heat stress-induced Cup9-dependent transcriptional regulation of SIR2.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- A Saccharomyces cerevisiae knockout screen for genes critical for growth under sulfur- and nitrogen-limited conditions reveals intracellular sorting via vesicular transport systems.G3 (Bethesda, Md.) · 2025Article
- Saccharomyces cerevisiae as a tool for deciphering Hsp90 molecular chaperone function.Essays in biochemistry · 2023Article
- DNA damage-induced nuclear import of HSP90α is promoted by Aha1.Molecular biology of the cell · 2022Article
- Heat Shock Protein 90 Regulates the Activity of Histone Deacetylase Sir2 in Plasmodium falciparum.mSphere · 2022Article
- Biologia futura: combinatorial stress responses in fungi.Biologia futura · 2022Review
- Yeast epigenetics: the inheritance of histone modification states.Bioscience reports · 2019Review
- Glu-108 in Saccharomyces cerevisiae Rad51 Is Critical for DNA Damage-Induced Nuclear Function.mSphere · 2019Article
- Article
- Hsp90 induces increased genomic instability toward DNA-damaging agents by tuning down RAD53 transcription.Molecular biology of the cell · 2016Article
- Hsp90, the concertmaster: tuning transcription.Frontiers in oncology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epigenetic writer Sir2 maintains the heterochromatin state of chromosome in three chromosomal regions, namely, the silent mating type loci, telomeres, and the ribosomal DNA (rDNA). In this study, we demonstrated the mechanism by which Sir2 is regulated under heat stress. Our study reveals that a transient heat shock causes a drastic reduction in the SIR2 transcript which results in sustained failure to initiate silencing for as long as 90 generations. Hsp82 overexpression, which is the usual outcome of heat shock treatment, leads to a similar downregulation of SIR2 transcription. Using a series of genetic experiments, we have established that heat shock or Hsp82 overexpression causes upregulation of CUP9 that, in turn, represses SIR2 transcription by binding to its upstream activator sequence. We have mapped the cis regulatory element of SIR2. Our study shows that the deletion of cup9 causes reversal of the Hsp82 overexpression phenotype and upregulation of SIR2 expression in heat-induced Hsp82-overexpressing cells. On the other hand, we found that Cup9 overexpression represses SIR2 transcription and leads to a failure in the establishment of heterochromatin. The results of our study highlight the mechanism by which environmental factors amend the epigenetic configuration of chromatin.
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