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C.albicans LC-MSMS lysine lactylated

ABSTRACT: C.albicans strain Ca1, retrieved from an AIDS patient, was obtained from T. C. White (School of Biological Sciences, University of Missouri at Kansas City, Kansas City, MO, USA), and was grown on yeast extract-peptone-dextrose (YPD) agar medium. For the selection of Ca1-T cells, YPD medium containing 32ug/mL fluconazole was used. For simulating human body temperature, we incubated strain Ca1 on YPD medium with and without fluconazole at 37°C for 48 hours before collecting samples.

INSTRUMENT(S):

ORGANISM(S): Candida Albicans 23r

SUBMITTER: Zhaopeng Lv

LAB HEAD: Yuying Huang

PROVIDER: PXD056982 | Pride | 2025-09-25

REPOSITORIES: Pride

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			Action	DRS
	QE_HFX_20230915_50cm_60min_E186TP-Lac_1.raw	Raw
	QE_HFX_20230915_50cm_60min_E186TP-Lac_2.raw	Raw
	QE_HFX_20230915_50cm_60min_E186TP-Lac_3.raw	Raw
	QE_HFX_20230915_50cm_60min_E186TP-Lac_4.raw	Raw
	QE_HFX_20230915_50cm_60min_E186TP-Lac_5.raw	Raw

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Project description:Azole antifungal agents such as fluconazole exhibit fungistatic activity against Candida albicans. Strategies to enhance azole antifungal activity would be therapeutically appealing. In an effort to identify transcriptional pathways that influence fluconazole susceptibility, we sought to identify transcription factors (TFs) involved in this process. From a collection of C. albicans strains disrupted for genes encoding TFs (Homann et al., PLoS Genet. 2009;5:e1000783), four exhibited a marked reduction in minimum fungicidal concentration (MFC) in both RPMI and YPD media. One of these, UPC2, has been previously characterized with regard to its role in azole susceptibility. Of mutants representing the three remaining TF genes of interest, one (CAS5) was unable to recover from fluconazole exposure at concentrations as low as 2 M-BM-5g/mL after 72 hours in YPD medium. This mutant also showed reduced susceptibility and a clear zone of inhibition by Etest, was unable to grow on solid media containing 10 M-BM-5g/mL fluconazole, and exhibited increased susceptibility by time-kill analysis. CAS5 disruption in highly azole-resistant clinical isolates exhibiting multiple resistance mechanisms did not alter susceptibility. However, CAS5 disruption in strains with specific resistance mutations in ergosterol biosynthesis or efflux pumps resulted in a moderate reduction in MIC and MFC. Genome-wide transcriptional analysis was performed in the presence of fluconazole and was consistent with the suggested role of CAS5 in cell wall organization while also suggesting a role in iron transport and homeostasis. These findings suggest that Cas5 regulates a transcriptional network that influences susceptibility of C. albicans to fluconazole. Further delineation of this transcriptional network may identify targets for potential co-therapeutic strategies to enhance the activity to the azole class of antifungals. We examined the genome-wide gene expression profiles of the wild-type parent strain SC5314 and its cas5M-NM-^T/M-NM-^T derivative in response to fluconazole in order to identify genes whose expression in response to fluconazole is influenced by Cas5.

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C.albicans LC-MSMS lysine lactylated

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