Stress-driven emergence of heritable non-genetic drug resistance DOI Open Access
Jinglin Lucy Xie,

Sifei Yin,

Theodore S. Yang

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Дек. 21, 2024

Abstract Drug resistance is the chief cause of treatment failure for therapies targeting chronic and infectious diseases. Whether emergence accelerated by environmental exposure to low levels therapeutics remains controversial. Here, we report a non-genetic mechanism stress adaptation that promotes heritable widely used antifungal drug fluconazole. In human fungal pathogen Candida albicans, transient subtherapeutic fluconazole doses induces protective response term para-resistance. Like conventional mechanisms, para-resistance heritable. However, it does not arise from genetic mutations can revert spontaneously. Systematic analyses para-resistant isolates suggest its key regulators include stress-activated MAP kinase Hog1, histone deacetylase subunit Snt1, chromatin regulator Rap1, Sko1 transcriptional factor. Notably, molecules disrupt biomolecular condensation prion propagation – crucial inheritance protein assemblies block induction para-resistance, whereas inhibiting deacetylases facilitates induction. We find common in clinical and, remarkably, passage through mammalian gut triggers acquisition, compromising fluconazole’s therapeutic efficacy. Our work defines pervasive, prion-like epigenetic highlights potential strategies mitigate rapid resistance.

Язык: Английский

Advancing Microbial Comparative Genomics Through Tumor-Normal Inspired Framework DOI Creative Commons
Junjie Yang, Sheng Yang

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Фев. 5, 2025

Abstract Comparative genomics has emerged as a pivotal methodology for elucidating genetic variations in microbial studies. However, conventional analytical approaches diploid and polyploid microorganisms have demonstrated limited efficacy discriminating new mutations from background heterozygosity. This study presents an innovative comparative framework adapted tumor-normal sequencing methodology. Our approach establishes the original strain “normal sample” derived “tumor sample”, enabling precise identification of (“somatic variants”) while filtering pre-existing heterozygous sites (“germline variations”). The pipeline also includes assessment loss-of-heterozygosity (LOH) events genome-wide detection copy number (CNVs) with resolution to identify both regional CNV whole-chromosome aneuploidy through integrated variant allele frequency analysis. We validated this using Saccharomyces cerevisiae strains before successfully extending its application Kluyveromyces marxianus , Candida spp., Hortaea werneckii encompassing haploid, diploid, polyploid, aneuploid states. revealed previously undetected across experimental evolution studies, demonstrating superior compared approaches. adaptable platform paradigm genome particularly organisms or states where traditional methods prove inadequate.

Язык: Английский

Процитировано

0

Tolerance and heteroresistance to echinocandins in Candida auris : conceptual issues, clinical implications, and outstanding questions DOI Creative Commons
Erika Shor, David S. Perlin, Dimitrios P. Kontoyiannis

и другие.

mSphere, Год журнала: 2025, Номер unknown

Опубликована: Апрель 16, 2025

ABSTRACT Candida auris is a significant public health threat due to its environmental persistence and multidrug resistance, with echinocandins being the preferred treatment. However, in addition echinocandin tolerance heteroresistance may contribute treatment challenges. Echinocandin involves reduced drug-mediated killing, while ability of small cell subset grow at high drug concentrations. These phenomena facilitate emergence full resistance complicate clinical outcomes. The significance these mechanisms remains unclear, limited data correlating them failures. Research needed understand their impact, develop streamlined robust methods detect settings, explore mitigation strategies. pathogen’s range adaptations demands innovative approaches like spatial transcriptomics dissect complex responses improve patient

Язык: Английский

Процитировано

0

Hotspot gene conversion between FKS1 and FKS2 in echinocandin resistant Candida glabrata serial isolates DOI Creative Commons

Christopher Zajac,

Nancy E. Scott, Susan L. Kline

и другие.

npj Antimicrobials and Resistance, Год журнала: 2025, Номер 3(1)

Опубликована: Апрель 17, 2025

Candida glabrata (Nakaseomyces glabratus) is the most common cause of drug-resistant candidemia and associated with a high mortality rate. Only few mechanisms drug resistance are known in C. glabrata, predominantly involving recurrent single nucleotide polymorphisms. The importance structural variation acquired not understood. We performed comparative phenotypic genomic analyses six serial bloodstream isolates identified novel mutations to echinocandins. Critically, we gene conversion event between hotspot 2 regions FKS1 FKS2 that was increased micafungin. further analyzed 621 publicly available genomes found three additional examples FKS2. Ultimately, involves variants missed current diagnostic methods need be considered when designing implementing more effective antifungal management strategies.

Язык: Английский

Процитировано

0

Understanding adaptation to fluconazole: comparative insights into tolerance and resistance in Saccharomyces cerevisiae and Candida albicans DOI Creative Commons
Lijun Zheng, Yubo Dong, Jing Wang

и другие.

Frontiers in Cellular and Infection Microbiology, Год журнала: 2025, Номер 15

Опубликована: Май 5, 2025

Introduction Antifungal resistance and tolerance are distinct responses exhibited by fungi when exposed to drugs. While considerable research has focused on azole in the human pathogen Candida albicans , studies other fungal species remain limited. Objective This study aims conduct a comparative investigation of adaptation model organism Saccharomyces cerevisiae C. fluconazole vitro . Methods We performed experiments using laboratory strains S. evaluate their under varying temperature conditions. High concentrations were administered, subsequent changes phenotypes analyzed through techniques such as transcriptome analysis monitoring petite formation. Results Our results revealed that is present wild-type influenced temperature, albeit manner opposite observed Importantly, subjected high fluconazole, developed without displaying tolerance; all resistant adaptors identified petites. Chemical induction formation led an increase accompanied decrease tolerance. Conclusion Transcriptome indicated petites up-regulated efflux mechanisms while down-regulating most ERG genes. suggests that, unlike petite-negative petite-positive swiftly transitions phenotype upon exposure resulting enhanced but diminished evolutionary divergence emphasizes need for additional pathogenic fungi.

Язык: Английский

Процитировано

0

Targeted loss of heterozygosity in Candida albicans using CRISPR-Cas9 DOI Creative Commons
Philippe C Després, Nicholas C. Gervais, Meea Fogal

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Май 13, 2025

The diploid genome of the fungal pathogen Candida albicans is highly heterozygous, with most allele pairs diverging at either coding or regulatory level. When faced selection pressure like antifungal exposure, this hidden genetic diversity can provide a reservoir adaptive mutations through loss heterozygosity (LOH) events. Validating potential phenotypic impact LOH events observed in clinical experimentally evolved strains be difficult due to challenge precisely targeting one over other. Here, we show that CRISPR-Cas9 system used overcome challenge. By designing allele-specific guide RNA sequences, induce targeted, directed events, which validate by whole-genome long-read sequencing. Using approach, efficiently recapitulate recently described event increases resistance fluconazole. Additionally, find recombination tracts these induced have similar lengths those naturally. To facilitate future use method, database sgRNA sequences for Cas9 near genome-wide coverage heterozygous sites direct indirect targeting. This approach will useful probing role important human pathogen.

Язык: Английский

Процитировано

0

Stress-driven emergence of heritable non-genetic drug resistance DOI Open Access
Jinglin Lucy Xie,

Sifei Yin,

Theodore S. Yang

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Дек. 21, 2024

Abstract Drug resistance is the chief cause of treatment failure for therapies targeting chronic and infectious diseases. Whether emergence accelerated by environmental exposure to low levels therapeutics remains controversial. Here, we report a non-genetic mechanism stress adaptation that promotes heritable widely used antifungal drug fluconazole. In human fungal pathogen Candida albicans, transient subtherapeutic fluconazole doses induces protective response term para-resistance. Like conventional mechanisms, para-resistance heritable. However, it does not arise from genetic mutations can revert spontaneously. Systematic analyses para-resistant isolates suggest its key regulators include stress-activated MAP kinase Hog1, histone deacetylase subunit Snt1, chromatin regulator Rap1, Sko1 transcriptional factor. Notably, molecules disrupt biomolecular condensation prion propagation – crucial inheritance protein assemblies block induction para-resistance, whereas inhibiting deacetylases facilitates induction. We find common in clinical and, remarkably, passage through mammalian gut triggers acquisition, compromising fluconazole’s therapeutic efficacy. Our work defines pervasive, prion-like epigenetic highlights potential strategies mitigate rapid resistance.

Язык: Английский

Процитировано

0