Application of Deoxyribonucleic Acid Microarray Analysis to the Study of Azole Antifungal Resistance in Candida albicans

2005 ◽  
pp. 045-056
Author(s):  
Katherine S. Barker ◽  
P. David Rogers
Keyword(s):  
Candida Albicans ◽  
Microarray Analysis ◽  
Deoxyribonucleic Acid ◽  
Antifungal Resistance

Antifungal resistance-modifying multiplexing action of Momordica charantia protein and phosphorylated derivatives on the basis of growth-dependent gene coregulation in Candida albicans

2020 ◽  
Author(s):  
Qiao Yuan-Biao ◽  
Zhang Lan-Fang ◽  
Qiao Qi ◽  
Niu Jia-Hui ◽  
Ren Ze-Mei ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Translation Initiation ◽  
Low Dose ◽  
Fungal Growth ◽  
Momordica Charantia ◽  
Antifungal Resistance ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
High Dose ◽  
Rrna Processing

Abstract Fungal growth-dependent gene coregulation is strongly implicated in alteration of gene-encoding target proteases ruling with an antifungal resistance niche and biology of resistant mutants. On the basis of multi-alterative processes in this platform, the resistance-modifying strategy is designed in ketoconazole resistant Candida albicans and evaluated with less selective Momordica charantia protein and allosterically phosphorylated derivatives at the Thr102, Thr24 and Thr255 sites, respectively. We demonstrate absolutely chemo-sensitizing efficacy regarding stepwise-modifying resistance in sensitivity, by a load of only 26.23–40.00 μg/l agents in Sabouraud's dextrose broth. Five successive modifying-steps realize the decreasing of ketoconazole E-test MIC50 from 11.10 to a lower level than 0.10 mg/l. With the ketoconazole resistance-modifying, colony undergoes a high-frequency morphological switch between high ploidy (opaque) and small budding haploid (white). A cellular event in the first modifying-step associates with relatively slow exponential growth (ie, a 4-h delay)-dependent action, mediated by agents adsorption. Moreover, multiple molecular roles are coupled with intracellularly and extracellularly binding to ATP-dependent RNA helicase dbp6; the 0.08–2.45 fold upregulation of TATA-box-binding protein, rRNA-processing protein and translation initiation factor 5A; and the 7.52–55.33% decrease of cytochrome P450 lanosterol 14α-demethylase, glucan 1, 3-β glucosidase, candidapepsin-1 and 1-acylglycerol-3-phosphate O-acyltransferase. Spatial and temporal gene coregulation, in the transcription and translation initiation stages with rRNA-processing, is a new coprocessing platform enabling target protease attenuations for resistance-impairing. An updated resistance-modifying measure of these agents in the low-dose antifungal strategic design may provide opportunities to a virtually safe therapy that is in high dose-dependency. Lay Summary A new platform to modify resistance is fungal growth-dependent gene coregulation. MAP30 and phosphorylated derivatives are candidate resistance-modifying agents. Low-dose stepwise treatment absolutely modifies azole resistance in model fungus.

The yeast, the antifungal, and the wardrobe: a journey into antifungal resistance mechanisms of Candida tropicalis

2020 ◽  
Vol 66 (6) ◽  
pp. 377-388
Author(s):  
Jonathas Sales de Oliveira ◽  
Vandbergue Santos Pereira ◽  
Débora de Souza Collares Maia Castelo-Branco ◽  
Rossana de Aguiar Cordeiro ◽  
José Júlio Costa Sidrim ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Intensive Care ◽  
Candida Tropicalis ◽  
Clinical Management ◽  
Candida Species ◽  
Genetic Basis ◽  
Antifungal Susceptibility ◽  
Resistance Mechanisms ◽  
Antifungal Resistance ◽  
Resistant Strains

Candida tropicalis is a prominent non-Candida albicans Candida species involved in cases of candidemia, mainly causing infections in patients in intensive care units and (or) those presenting neutropenia. In recent years, several studies have reported an increase in the recovery rates of azole-resistant C. tropicalis isolates. Understanding C. tropicalis resistance is of great importance, since resistant strains are implicated in persistent or recurrent and breakthrough infections. In this review, we address the main mechanisms underlying C. tropicalis resistance to the major antifungal classes used to treat candidiasis. The main genetic basis involved in C. tropicalis antifungal resistance is discussed. A better understanding of the epidemiology of resistant strains and the mechanisms involved in C. tropicalis resistance can help improve diagnosis and assessment of the antifungal susceptibility of this Candida species to improve clinical management.

scholarly journals TOS9 Regulates White-Opaque Switching in Candidaalbicans

2006 ◽  
Vol 5 (10) ◽  
pp. 1674-1687 ◽  
Author(s):  
Thyagarajan Srikantha ◽  
Anthony R. Borneman ◽  
Karla J. Daniels ◽  
Claude Pujol ◽  
Wei Wu ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Gene Product ◽  
Expression Pattern ◽  
Microarray Analysis ◽  
White Phase ◽  
Corepressor Complex ◽  
Its Gene ◽  
Analysis Strategy ◽  
Mass Conversion ◽  
Switching Locus

ABSTRACTInCandida albicans, thea1-α2 complex represses white-opaque switching, as well as mating. Based upon the assumption that thea1-α2 corepressor complex binds to the gene that regulates white-opaque switching, a chromatinimmunoprecipitation-microarray analysis strategy was used to identify 52 genes that bound to the complex. One of these genes,TOS9, exhibited an expression pattern consistent with a “master switch gene.”TOS9was only expressed in opaque cells, and its gene product, Tos9p, localized to the nucleus. Deletion of the gene blocked cells in the white phase, misexpression in the white phase caused stable mass conversion of cells to the opaque state, and misexpression blocked temperature-induced mass conversion from the opaque state to the white state. A model was developed for the regulation of spontaneous switching between the opaque state and the white state that includes stochastic changes of Tos9p levels above and below a threshold that induce changes in the chromatin state of an as-yet-unidentified switching locus.TOS9has also been referred to asEAP2andWOR1.

scholarly journals Ras1 involved in the antifungal resistance of Candida albicans and the inhibition of farnesol on the resistance of biofilms

2019 ◽  
Author(s):  
Xin Wei ◽  
Lulu Zuo ◽  
Shengyan Chen ◽  
Zhenzhen Zhang ◽  
Liuliu Jiang
Keyword(s):  
Candida Albicans ◽  
Molecular Mechanisms ◽  
Hyphal Growth ◽  
Antifungal Resistance ◽  
Morphological Observation ◽  
Inhibitory Effects ◽  
Wild Strains ◽  
Almost All ◽  
Candida Albicans Biofilms

Abstract Background: Farnesol enhances the susceptibility of Candida albicans biofilms to antifungals, while the molecular mechanisms of this behavior are poorly understood. RAS1 regulates the hyphal growth of C. albicans, and farnesol inhibited hyphal growth by RAS1 regulation, while the role of RAS1 in the resistance of C. albicans biofilms and the molecular mechanism of the RAS1 in the farnesol-relevant antifungal capacity to C. albicans biofilms is still unknown. The study hypothesized that Ras1 involved in the antifungal resistance of C. albicans and the inhibition of farnesol on the resistance of biofilms. Results: The susceptibility assays showed that RAS1 over-expressing strain (RAS1OE) increased the resistance of C.albicans in both planktonic and biofilm form to antifungals, while RAS1 deletion strain (ras1Δ/Δ) reduced that to antifungals. The SMIC50 of the antifungals were increased with the mature of the biofilms formed from the mutant and the wild strains. Exogenous farnesol decreased the resistance of RAS1OE to antifungals, including fluconazole, amphotericin B, itraconazole, caspofungin, terbinafine, 5-flurocytosine and nystatin. The inhibitory effects of farnesol on the antifungal resistance of the biofilms from the RAS1OE were in accordance to almost all of the growth phases. Moreover, exogenous farnesol decreased the resistance of biofilms from RAS1OE more obviously than that from the wild strains (P<0.05). In addition, Morphological observation showed that that RAS1OE increased hyphal growth the biofilms, while ras1Δ/Δ reduced that of the biofilms. Compare to the wild-type strain, the inhibitory effects of farnesol on hyphal growth were more obvious to the RAS1OE, while less obvious to the ras1Δ/Δ. Furthermore, farnesol reduced the level of Ras1 and the expression of RAS1 of the biofilms formed from the RAS1OE strain compared with those of the untreated controls at all studied phases. Moreover, farnesol reduced the level of Ras1 and the expression of RAS1 of the biofilms formed from RAS1OE more obviously than that from the wild strains. Conclusions: Ras1 involved in the antifungal resistance of Candida albicans, and the inhibition of farnesol on the resistance of biofilm.

scholarly journals Deoxyribonucleic acid-deficient strains of Candida albicans.

1980 ◽  
Vol 141 (3) ◽  
pp. 1284-1290 ◽  
Author(s):  
A F Olaiya ◽  
J R Steed ◽  
S J Sogin
Keyword(s):  
Candida Albicans ◽  
Deoxyribonucleic Acid
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