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Updated: Dec 13, 2025

Whole Genome Sequencing of Candida glabrata for Detection of Markers of Antifungal Drug Resistance
Published on: December 28, 2017
Chromatin Structure and Drug Resistance in Candida spp
Callum J O'Kane1, Rachel Weild1, Edel M Hyland1
1School of Biological Sciences, Queen's University Belfast, BT9 5DL Belfast, Northern Ireland.
Abstract:
Anti-microbial resistance (AMR) is currently one of the most serious threats to global human health and, appropriately, research to tackle AMR garnishes significant investment and extensive attention from the scientific community. However, most of this effort focuses on antibiotics, and research into anti-fungal resistance (AFR) is vastly under-represented in comparison. Given the growing number of vulnerable, immunocompromised individuals, as well as the positive impact global warming has on fungal growth, there is an immediate urgency to tackle fungal disease, and the disturbing rise in AFR. Chromatin structure and gene expression regulation play pivotal roles in the adaptation of fungal species to anti-fungal stress, suggesting a potential therapeutic avenue to tackle AFR. In this review we discuss both the genetic and epigenetic mechanisms by which chromatin structure can dictate AFR mechanisms and will present evidence of how pathogenic yeast, specifically from the Candida genus, modify chromatin structure to promote survival in the presence of anti-fungal drugs. We also discuss the mechanisms by which anti-chromatin therapy, specifically lysine deacetylase inhibitors, influence the acquisition and phenotypic expression of AFR in Candida spp. and their potential as effective adjuvants to mitigate against AFR.
Insights
Antifungal resistance (AFR) is a growing threat, especially in immunocompromised patients. This review explores how fungal chromatin structure impacts AFR and discusses anti-chromatin therapies as a potential solution.
Area of Science:
- Mycology
- Molecular Biology
- Genetics
Background:
- Antimicrobial resistance (AMR) receives significant attention, but antifungal resistance (AFR) is under-represented despite rising global health concerns.
- Increased numbers of immunocompromised individuals and climate change contribute to the urgent need to address fungal diseases and AFR.
- Fungal adaptation to antifungal stress is significantly influenced by chromatin structure and gene expression regulation.
Purpose of the Study:
- To review the genetic and epigenetic mechanisms of chromatin structure in antifungal resistance (AFR).
- To present evidence of chromatin modification in *Candida* species for survival against antifungal drugs.
- To discuss the potential of anti-chromatin therapies, like lysine deacetylase inhibitors, as adjuvants to combat AFR.
Main Methods:
- Review of existing literature on chromatin structure, gene expression, and antifungal resistance mechanisms.
- Analysis of genetic and epigenetic factors influencing fungal adaptation to antifungal agents.
- Examination of the role of lysine deacetylase inhibitors in modulating AFR in *Candida* species.
Main Results:
- Pathogenic yeasts, particularly *Candida* species, alter chromatin structure to survive antifungal drug exposure.
- Epigenetic modifications of chromatin play a crucial role in the development and expression of antifungal resistance.
- Lysine deacetylase inhibitors demonstrate potential in influencing the acquisition and phenotypic expression of AFR.
Conclusions:
- Chromatin structure is a key determinant of antifungal resistance (AFR) in pathogenic fungi.
- Targeting chromatin modification presents a promising therapeutic strategy to combat AFR.
- Anti-chromatin therapies, such as lysine deacetylase inhibitors, may serve as effective adjuvants in treating fungal infections and mitigating AFR.
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