Formation of new chromosomes as a virulence mechanism in yeast Candida glabrata
Open accessAbstract
In eukaryotes, the number and rough organization of chromosomes is well preserved within isolates of the same species. Novel chromosomes and loss of chromosomes are infrequent and usually associated with pathological events. Here, we analyzed 40 pathogenic isolates of a haploid and asexual yeast, Candida glabrata, for their genome structure and stability. This organism has recently become the second most prevalent yeast pathogen in humans. Although the gene sequences were well conserved among different strains, their chromosome structures differed drastically. The most frequent events reshaping chromosomes were translocations of chromosomal arms. However, also larger segmental duplications were frequent and occasionally we observed novel chromosomes. Apparently, this yeast can generate a new chromosome by duplication of chromosome segments carrying a centromere and subsequently adding novel telomeric ends. We show that the observed genome plasticity is connected with antifungal drug resistance and it is likely an advantage in the human body, where environmental conditions fluctuate a lot.
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C. glabrata can undergo genomic re-arrangements as an adaptive survival mechanism.
“Previous studies found that C. glabrata can undergo genomic re-arrangements as an adaptive survival mechanism (Shin et al., 2007; Muller et al., 2009; Poláková et al., 2009).”
From Genome Comparisons of Candida glabrata Serial Clinical Isolates Reveal Patterns of Genetic Variation in Infecting Clonal Populations (2019) · cites this paper as Poláková et al., 2009
Genetic instability in Candida glabrata results in segmental duplications, chromosomal rearrangements, and extra chromosomes at high frequency.
“According to Poláková et al. [90], the genetic instability results in segmental duplications, chromosomal rearrangements, and extra chromosomes occurring in C. glabrata at high frequency.”
From Candida glabrata: pathogenicity and resistance mechanisms for adaptation and survival (2021) · cites this paper as [90]
Duplicated segments of ChrFL encode an ATP-binding cassette transporter (CAGL0F01419g) that is very similar to Saccharomyces cerevisiae AUS1.
“Duplicated segments of ChrFL encode a transporter of the ATP-binding cassette family (CAGL0F01419g) that is very similar to S. cerevisiae AUS1.”
From Candida glabrata: pathogenicity and resistance mechanisms for adaptation and survival (2021) · cites this paper as [90]
Aneuploidy gain of a small chromosome segment on the left arm of chromosome F that encodes ABC transporters AUS1 and PDH1 is observed in C. glabrata-resistant isolates.
“Aneuploidy gain of small chromosome segment on the left arm of chromosome F that encodes ABC transporter AUS1 and PDH1 is also observed in C. glabrata-resistant isolates [90].”
From Candida glabrata: pathogenicity and resistance mechanisms for adaptation and survival (2021) · cites this paper as [90]
Small chromosome F encodes an ortholog of Saccharomyces cerevisiae ABC transporter PDR5 (CAGL0F02717g), known in C. glabrata as PDH1.
“The small chromosome F encodes an ortholog of S. cerevisiae ABC transporter PDR5 (CAGL0F02717g) known in C. glabrata as PDH1.”
From Candida glabrata: pathogenicity and resistance mechanisms for adaptation and survival (2021) · cites this paper as [90]
Several genes on chromosomes ChrEL and ChrFL potentially mediate interactions between C. glabrata and the susceptible host.
“Several genes on chromosomes (ChrEL and ChrFL) potentially mediate interactions between C. glabrata and the susceptible host.”
From Candida glabrata: pathogenicity and resistance mechanisms for adaptation and survival (2021) · cites this paper as [90]
For haploid C. glabrata, genome rearrangements underlying azole resistance include chromosomal translocations, segmental duplications, and occasionally formation of de novo minichromosomes.
“For the haploid yeast C. glabrata, genome rearrangements underlying azole resistance include chromosomal translocations, segmental duplications, and occasionally, the formation of de novo minichromosomes70.”
From Molecular mechanisms governing antifungal drug resistance (2023) · cites this paper as [70]
Genome plasticity has been connected with antifungal drug resistance in C. glabrata.
“Since genome plasticity has been connected with antifungal drug resistance in C. glabrata (Shin et al., 2007; Polakova et al., 2009)”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Polakova et al., 2009
The most frequent genome rearrangements identified in C. glabrata were translocations of chromosomal arms and inter-chromosomal duplications, but formation of novel chromosomes was also reported.
“the most frequent genome rearrangements identified were translocations of chromosomal arms and inter-chromosomal duplications, but formation of novel chromosomes was also reported (Muller et al., 2009; Polakova et al., 2009).”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Polakova et al., 2009
C. glabrata genome organization varies significantly among different isolates.
“Karyotyping using pulsed-field gel electrophoresis (PFGE), which separates whole chromosomes, revealed that C. glabrata genome organization varies significantly among different isolates (Muller et al., 2009; Polakova et al., 2009).”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Polakova et al., 2009
High karyotypic variability among C. glabrata strains prevents using the reference strain CBS138 genomic sequence as a template for assembling sequences of other strains, including clinical isolates.
“Indeed, while the genome of a reference C. glabrata laboratory strain (CBS138) has been sequenced, we were not able to use that strain's genomic sequence as a template for assembling the sequences of other strains, e.g., various clinical isolates, due to the high karyotypic variability among strains (Muller et al., 2009; Polakova et al., 2009; Bader et al., 2012; Figure 1B).”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Polakova et al., 2009
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- Authors
- Poláková, S., Blume, C., Zárate, J. Á., Mentel, M., Jørck-Ramberg, D., Stenderup, J., & Piškur, J.
- Affiliations
- Lund University (SE)
- Technical University of Denmark (DK)
- Regionshospitalet Herning (DK)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-02-24
- Volume
- 106
- Issue
- 8
- Pages
- 2688-2693
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2637908
- OpenAlex
- W2105649156
- Cited by
- 206
- References
- 35
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 12 · 2023: 10 · 2022: 12 · 2021: 11 · 2020: 11 · 2019: 9 · 2018: 13 · 2017: 8 · 2016: 7 · 2015: 13 · 2014: 15 · 2013: 14 · 2012: 15
- FWCI
- 8.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Technical University of Denmark, DTU Orbit (Technical University of Denmark, DTU) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Yeasts and Rust Fungi Studies
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Keywords
- Candida glabrata, chromosomal translocation, segmental duplication, genome plasticity, antifungal resistance, virulence, telomeres, centromere, haploid yeast, asexual reproduction, fungal pathogens
- MeSH terms
- Antifungal Agents, Base Sequence, Phylogeny, Virulence, Blotting, Southern, Chromosomes, Fungal, Polymerase Chain Reaction, Electrophoresis, Gel, Pulsed-Field, DNA Primers, Candida glabrata
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