ArticleProceedings of the National Academy of Sciences of the United States of America2010
Histone acetyltransferase Rtt109 is required for Candida albicans pathogenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
84 citing papers in PubMed, 132 citations in OpenAlex.
- Epigenetic maintenance of PRC2-repressed chromatin requires RTT109 but not H3K56 acetylation.PLoS genetics · 2026Article
- Histone Acetylation Dynamics Regulate Fungal Development, Pathogenicity, and Mycotoxin Biosynthesis.Journal of fungi (Basel, Switzerland) · 2026Review
- Ergosterol remodeling by the MARVEL protein Mrv6 links genotoxic stress adaptation to virulence in Candida albicans.The Journal of biological chemistry · 2026Article
- Antifungal resistance: from classical mechanisms to the expanding role of acetyltransferases.Journal of biomedical science · 2026Review
- Article
- Lysine crotonylation enhances fungal effector activity and promotes invasion of host plants.Plant communications · 2026Article
- Rad53 orchestrates divergent pathways governing genotoxic resistance, morphogenesis, and virulence inVirulence · 2025Article
- Core histones govern echinocandin susceptibility inMicrobiology spectrum · 2025Article
- Targeting epigenetic regulators to overcome drug resistance in the emerging human fungal pathogen Candida auris.Nature communications · 2025Article
- Is a Fungal Apocalypse Inevitable or Just a Hallucination? An Overview of the Antifungal Armamentarium Used in the Fight against Pathogenic Fungi.ACS medicinal chemistry letters · 2025Review
- Protein lysine acetylation regulates oral microorganisms.Frontiers in cellular and infection microbiology · 2025Review
- DNA damage repair factor Rad18 controls virulence partially via transcriptional suppression of genesVirulence · 2024Article
- Repurposing Plant-Based Histone Acetyltransferase Inhibitors: A Review of Novel Therapeutic Strategies Against Drug-Resistant Fungal Biofilms.Current microbiology · 2024Review
- DNA Damage Checkpoints Govern Global Gene Transcription and Exhibit Species-Specific Regulation onJournal of fungi (Basel, Switzerland) · 2024Article
- Mec1-Rad53 Signaling Regulates DNA Damage-Induced Autophagy and Pathogenicity inJournal of fungi (Basel, Switzerland) · 2023Article
- Post-translational modifications confer amphotericin B resistance inFrontiers in immunology · 2023Article
- Nicotinamide potentiates amphotericin B activity againstVirulence · 2022Article
- Epigenetic Regulation of Antifungal Drug Resistance.Journal of fungi (Basel, Switzerland) · 2022Review
- Transcriptional Profiling of theInternational journal of molecular sciences · 2022Article
- Fun30 and Rtt109 Mediate Epigenetic Regulation of the DNA Damage Response Pathway inJournal of fungi (Basel, Switzerland) · 2022Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Candida albicans is a ubiquitous opportunistic pathogen that is the most prevalent cause of hospital-acquired fungal infections. In mammalian hosts, C. albicans is engulfed by phagocytes that attack the pathogen with DNA-damaging reactive oxygen species (ROS). Acetylation of histone H3 lysine 56 (H3K56) by the fungal-specific histone acetyltransferase Rtt109 is important for yeast model organisms to survive DNA damage and maintain genome integrity. To assess the importance of Rtt109 for C. albicans pathogenicity, we deleted the predicted homolog of Rtt109 in the clinical C. albicans isolate, SC5314. C. albicans rtt109(-/-) mutant cells lack acetylated H3K56 (H3K56ac) and are hypersensitive to genotoxic agents. Additionally, rtt109(-/-) mutant cells constitutively display increased H2A S129 phosphorylation and elevated DNA repair gene expression, consistent with endogenous DNA damage. Importantly, C. albicans rtt109(-/-) cells are significantly less pathogenic in mice and more susceptible to killing by macrophages in vitro than are wild-type cells. Via pharmacological inhibition of the host NADPH oxidase enzyme, we show that the increased sensitivity of rtt109(-/-) cells to macrophages depends on the host's ability to generate ROS, providing a mechanistic link between the drug sensitivity, gene expression, and pathogenesis phenotypes. We conclude that Rtt109 is particularly important for fungal pathogenicity, suggesting a unique target for therapeutic antifungal compounds.
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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.