ArticleNucleic acids research2019
Gcn5-mediated acetylation at MBF-regulated promoters induces the G1/S transcriptional wave.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- SIRT6 overexpression counteracts chromatin aging in the male murine liver.Nature communications · 2026Article
- TORC2 coordinates MBF-dependent transcription and restrains oxidative stress responses during DNA replication stress in fission yeast.The Journal of biological chemistry · 2026Article
- Article
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- The SAGA histone acetyltransferase module targets SMC5/6 to specific genes.Epigenetics & chromatin · 2023Article
- Expression of Huntingtin and TDP-43 Derivatives in Fission Yeast Can Cause Both Beneficial and Toxic Effects.International journal of molecular sciences · 2022Article
- TOR and MAP kinase pathways synergistically regulate autophagy in response to nutrient depletion in fission yeast.Autophagy · 2022Article
- TOR complex 2 contributes to regulation of gene expression via inhibiting Gcn5 recruitment to subtelomeric and DNA replication stress genes.PLoS genetics · 2022Article
- SWI/SNF and RSC remodeler complexes bind to MBF-dependent genes.Cell cycle (Georgetown, Tex.) · 2021Article
- Spatial sequestration of misfolded proteins as an active chaperone-mediated process during heat stress.Current genetics · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In fission yeast, MBF-dependent transcription is inactivated at the end of S phase through a negative feedback loop that involves the co-repressors, Yox1 and Nrm1. Although this repression system is well known, the molecular mechanisms involved in MBF activation remain largely unknown. Compacted chromatin constitutes a barrier to activators accessing promoters. Here, we show that chromatin regulation plays a key role in activating MBF-dependent transcription. Gcn5, a part of the SAGA complex, binds to MBF-regulated promoters through the MBF co-activator Rep2 in a cell cycle-dependent manner and in a reverse correlation to the binding of the MBF co-repressors, Nrm1 or Yox1. We propose that the co-repressors function as physical barriers to SAGA recruitment onto MBF promoters. We also show that Gcn5 acetylates specific lysine residues on histone H3 in a cell cycle-regulated manner. Furthermore, either in a gcn5 mutant or in a strain in which histone H3 is kept in an unacetylated form, MBF-dependent transcription is downregulated. In summary, Gcn5 is required for the full activation and correct timing of MBF-regulated gene transcription.
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