Candida glabrataencodes a longer variant of the mating type (MAT) alpha2 gene in the mating type-likeMTL3locus, which can form homodimers

Robledo-Márquez, Karina; Gutiérrez-Escobedo, Guadalupe; Yáñez-Carrillo, Patricia; Vidal-Aguiar, Yamile; Briones-Martin-del-Campo, Marcela; Orta-Zavalza, Emmanuel; Peñas, Alejandro De Las; Castaño, Irene

doi:10.1093/femsyr/fow082

Cited by 9 publications

(9 citation statements)

References 27 publications

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“…The MAT locus in S. cerevisiae , consisting of the active MAT locus, and silent HMLα and HMRa loci, resides on the chromosome III (Figure 2), and the mating type is determined by the presence of MATa or MATα allele [75]. However, unlike S. cerevisiae , the MAT loci are present on different chromosomes in C. glabrata with CgMTL1 and CgMTL3 on chromosome B, and Cg MTL2 on chromosome E (Figure 2) [76]. CgMTL1 locus encodes either ‘a’ ( Cga1 gene) or ‘alpha’ ( Cgα1 or Cgα2 genes) information while CgMTL2 and CgMTL3 code for ‘a’ and ‘α’ information, respectively [74,76].…”

Section: Salient Pathobiological Featuresmentioning

confidence: 99%

“…However, unlike S. cerevisiae , the MAT loci are present on different chromosomes in C. glabrata with CgMTL1 and CgMTL3 on chromosome B, and Cg MTL2 on chromosome E (Figure 2) [76]. CgMTL1 locus encodes either ‘a’ ( Cga1 gene) or ‘alpha’ ( Cgα1 or Cgα2 genes) information while CgMTL2 and CgMTL3 code for ‘a’ and ‘α’ information, respectively [74,76]. While CgMTL1 and CgMTL2 are transcriptionally active, CgMTL3 is subjected to subtelomeric silencing [77].…”

Section: Salient Pathobiological Featuresmentioning

confidence: 99%

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Candida glabrata: A Lot More Than Meets the Eye

et al. 2019

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Candida glabrata is an opportunistic human fungal pathogen that causes superficial mucosal and life-threatening bloodstream infections in individuals with a compromised immune system. Evolutionarily, it is closer to the non-pathogenic yeast Saccharomyces cerevisiae than to the most prevalent Candida bloodstream pathogen, C. albicans. C. glabrata is a haploid budding yeast that predominantly reproduces clonally. In this review, we summarize interactions of C. glabrata with the host immune, epithelial and endothelial cells, and the ingenious strategies it deploys to acquire iron and phosphate from the external environment. We outline various attributes including cell surface-associated adhesins and aspartyl proteases, biofilm formation and stress response mechanisms, that contribute to the virulence of C. glabrata. We further discuss how, C. glabrata, despite lacking morphological switching and secreted proteolytic activity, is able to disarm macrophage, dampen the host inflammatory immune response and replicate intracellularly.

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Section: Salient Pathobiological Featuresmentioning

confidence: 99%

Section: Salient Pathobiological Featuresmentioning

confidence: 99%

Candida glabrata: A Lot More Than Meets the Eye

et al. 2019

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“…glabrata mating‐type combinations did not exert any significant effects on the MICs of the tested antifungals, except for CAS and AFG, indicating that discovering spontaneous mating‐type switching, especially clinical isolates might be challenging. Robledo‐Marquez et al observed no changes in growth phenotype (colony size or morphology) under different stress conditions, that is FLU, NaCl, H 2 O 2 and metals, compared to C . glabrata strains expressing the a and α alleles generated in the laboratory, and MTL1 , MTL2 and MTL3 mutant isolates.…”

Section: Discussionmentioning

confidence: 98%

Mating genotypes and susceptibility profiles of clinical isolates of Candida glabrata from Turkey

Kaplan

Aktas

Önder

et al. 2019

Mycoses

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Summary The sexual cycle of Candida glabrata is not known; however, genomic evidence is indicative of recombination among subpopulations and the genome harbours genes necessary for undergoing mating and meiosis, which may increase fitness. The relationship between specific mating type‐like (MTL) loci and antifungal susceptibility is not well understood in C. glabrata. We investigated different combinations of clinical C. glabrata isolate mating types and their antifungal susceptibility profiles. Allele profiles of the mating genes of 103 clinical C. glabrata isolates were identified, and their antifungal susceptibility to azoles, echinocandins and amphotericin B were compared. The majority (88.3%) of screened isolates harboured the a allele in the locus. The MTL1, MTL2 and MTL3 loci harboured a (88.3%), a (95.1%), and α (71.8%) alleles, respectively. The C. glabrata isolates were susceptible to echinocandins but displayed high minimal inhibitory concentrations (MICs) for azoles. The MIC ranges and MIC90 values of all isolates were 1.0 to ≥64 and 8.0 μg mL−1 for fluconazole, 0.06 to ≥16.0 and 0.5 μg mL−1 for voriconazole, 0.06 to ≥16.0 and 1.0 μg mL−1 for posaconazole, ≤0.015 to 0.06, and 0.03 μg mL−1 for caspofungin, ≤0.015 to 0.06 and 0.015 μg mL−1 for anidulafungin and 0.5‐2 and 2.0 μg mL−1 for amphotericin B, respectively. The mating gene alleles of the clinical C. glabrata isolates were not associated with differences in the MICs of the tested antifungals, except for the MTL3 α‐allele and echinocandins. The mating genotypes of the clinical C. glabrata isolates had no recognisable common effect on antifungal susceptibility.

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“…The strains were grown in YPD at 30°and harvested in stationary phase. The protein extraction and western blot assays were done as previously described with minor modifications (Orta-Zavalza et al 2013;Robledo-Márquez et al 2016). Briefly, cells were resuspended in lysis buffer [45 mM HEPES, 400 mM potassium acetate, 0.5% Nonidet P-40, 1 mM EDTA, 1 mM DTT, 1 mM PMSF, and 13 Complete protease inhibitor cocktail (Roche)], 100 ml of zirconia beads were added, and cells were broken using FastPrep-24 (MP Biomedicals) equipment, with three pulses for 60 sec at 6 m/sec.…”

Section: Western Blot Assaymentioning

confidence: 99%

Chromatin Loop Formation Induced by a Subtelomeric Protosilencer Represses EPA Genes in Candida glabrata

et al. 2018

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Adherence, an important virulence factor, is mediated by the (Epithelial Adhesin) genes in the opportunistic pathogen Expression of adhesin-encoding genes requires tight regulation to respond to harsh environmental conditions within the host. The majority of genes are localized in subtelomeric regions regulated by subtelomeric silencing, which depends mainly on Rap1 and the Sir proteins. adhesion to epithelial cells is primarily mediated by Epa1. forms a cluster with and in the right telomere of chromosome E (E). This telomere contains a -acting regulatory element, the protosilencer Sil2126 between and the telomere. Interestingly, Sil2126 is only active in the context of its native telomere. Replacement of the intergenic regions between genes in E revealed that -acting elements between and are required for Sil2126 activity when placed 32 kb away from the telomere (Sil@-32kb). Sil2126 contains several putative binding sites for Rap1 and Abf1, and its activity depends on these proteins. Indeed, Sil2126 binds Rap1 and Abf1 at its native position and also when inserted at -32 kb, a silencing-free environment in the parental strain. In addition, we found that Sil@-32kb and Sil2126 at its native position can physically interact with the intergenic regions between and respectively, by chromosome conformation capture assays. We speculate that Rap1 and Abf1 bound to Sil2126 can recruit the Silent Information Regulator complex, and together mediate silencing in this region, probably through the formation of a chromatin loop.

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Candida glabrataencodes a longer variant of the mating type (MAT) alpha2 gene in the mating type-likeMTL3locus, which can form homodimers

Cited by 9 publications

References 27 publications

Candida glabrata: A Lot More Than Meets the Eye

Candida glabrata: A Lot More Than Meets the Eye

Mating genotypes and susceptibility profiles of clinical isolates of Candida glabrata from Turkey

Chromatin Loop Formation Induced by a Subtelomeric Protosilencer Represses EPA Genes in Candida glabrata

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