ArticleMolecular and cellular biology2015
The Set3 Complex Antagonizes the MYST Acetyltransferase Esa1 in the DNA Damage Response.
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 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Histone Acetylation Dynamics Regulate Fungal Development, Pathogenicity, and Mycotoxin Biosynthesis.Journal of fungi (Basel, Switzerland) · 2026Review
- The Direct and Individual Transcriptional Function of the Human Homodimeric and Heterodimeric Basic Helix-Loop-Helix Transcription Factors E47 and Scleraxis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Research Progress on the Mechanism and Function of Histone Acetylation Regulating the Interaction between Pathogenic Fungi and Plant Hosts.Journal of fungi (Basel, Switzerland) · 2024Review
- Regulatory Roles of Histone Modifications in Filamentous Fungal Pathogens.Journal of fungi (Basel, Switzerland) · 2022Review
- Histone Acetyltransferases and Deacetylases Are Required for Virulence, Conidiation, DNA Damage Repair, and Multiple Stresses Resistance ofFrontiers in microbiology · 2021Article
- Set3 Is Required for Asexual Development, Aflatoxin Biosynthesis, and Fungal Virulence inFrontiers in microbiology · 2019Article
- NuA4 acetyltransferase is required for efficient nucleotide excision repair in yeast.DNA repair · 2019Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Acetylation is a dynamic posttranslational modification that contributes to chromatin-regulated processes, including DNA replication, repair, recombination, and gene expression. Acetylation is controlled by complexes containing opposing lysine and histone acetyltransferase (KAT and HAT) and deacetylase (KDAC and HDAC) activities. The essential MYST family Esa1 KAT acetylates core histones and many nonhistone substrates. Phenotypes of esa1 mutants include transcriptional silencing and activation defects, impaired growth at high temperatures, and sensitivity to DNA damage. The KDAC Rpd3 was previously identified as an activity opposing Esa1, as its deletion suppresses growth and silencing defects of esa1 mutants. However, loss of Rpd3 does not suppress esa1 DNA damage sensitivity. In this work, we identified Hos2 as a KDAC counteracting ESA1 in the damage response. Deletion of HOS2 resulted in changes of esa1's transcriptional response upon damage. Further, loss of HOS2 or components of the Set3 complex (Set3C) in which it acts specifically suppressed damage sensitivity and restored esa1 histone H4 acetylation. This rescue was mediated via loss of either Set3C integrity or of its binding to dimethylated histone H3K4. Our results thus add new insight into the interactions of an essential MYST acetyltransferase with diverse deacetylases to respond specifically to environmental and physiological challenges.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.