ArticlePLoS genetics2020
Histone H4 dosage modulates DNA damage response in the pathogenic yeast Candida glabrata via homologous recombination pathway.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanism of azole resistance inJournal of medical microbiology · 2025Article
- Comparative Proteomic Analysis of Non-Bleached and Bleached Fragments of the HydrocoralBiology · 2025Article
- Core histones govern echinocandin susceptibility inMicrobiology spectrum · 2025Article
- Proteomic characterization of clinical Candida glabrata isolates with varying degrees of virulence and resistance to fluconazole.PloS one · 2025Article
- The Hog1 MAPK substrate governs Candida glabrata-epithelial cell adhesion via the histone H2A variant.PLoS genetics · 2024Article
- SWI/SNF complex-mediated chromatin remodeling iniScience · 2024Article
- The regulatory subunits of CK2 complex mediate DNA damage response and virulence in Candida Glabrata.BMC microbiology · 2023Article
- An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae.Epigenetics & chromatin · 2022Article
- GSTpi reduces DNA damage and cell death by regulating the ubiquitination and nuclear translocation of NBS1.Cellular and molecular life sciences : CMLS · 2021Article
- Two Functionally Redundant FK506-Binding Proteins Regulate Multidrug Resistance Gene Expression and Govern Azole Antifungal Resistance.Antimicrobial agents and chemotherapy · 2021Article
- An aspartyl protease-mediated cleavage regulates structure and function of a flavodoxin-like protein and aids oxidative stress survival.PLoS pathogens · 2021Article
- Genome protection: histone H4 and beyond.Current genetics · 2020Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Candida glabrata, a nosocomial fungal bloodstream pathogen, causes significant morbidity and mortality in hospitals worldwide. The ability to replicate in macrophages and survive a high level of oxidative stress contributes to its virulence in the mammalian host. However, the role of DNA repair and recombination mechanisms in its pathobiology is still being discovered. Here, we have characterized the response of C. glabrata to the methyl methanesulfonate (MMS)-induced DNA damage. We found that the MMS exposure triggered a significant downregulation of histone H4 transcript and protein levels, and that, the damaged DNA was repaired by the homologous recombination (HR) pathway. Consistently, the reduced H4 gene dosage was associated with increased HR frequency and elevated resistance to MMS. The genetic analysis found CgRad52, a DNA strand exchange-promoter protein of the HR system, to be essential for this MMS resistance. Further, the tandem-affinity purification and mass spectrometry analysis revealed a substantially smaller interactome of H4 in MMS-treated cells. Among 23 identified proteins, we found the WD40-repeat protein CgCmr1 to interact genetically and physically with H4, and regulate H4 levels, HR pathway and MMS stress survival. Controlling H4 levels tightly is therefore a regulatory mechanism to survive MMS stress in C. glabrata.
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