English

Huang Guowang,Li Yimin,Wang Yang,Fazleen Binti Idris Nur,Tu Zeng

doi:10.5897/ajmr2020.9316

Abstract

Naftifine, an antifungal drug, inhibits pigmentation in Rhodotorula mucilaginosa. However, the relative mechanism is minutely understood. In this study, regulation of gene expression by naftifine was investigated to elucidate mechanism of yeast de-pigmentation. RNA-sequencing (RNA-seq) was used to screen differentially expressed genes (DEGs), followed by quantitative PCR (qPCR). The qPCR results showed that mRNA expression of phytoene desaturase gene CAR1 was reduced to 37% of its original level, after one day’s naftifine treatment. Since CAR1 acts at the immediate upstream of carotenoid biosynthesis pathway, it was concluded that naftifine involves in the process to inhibit the activity of phytoene desaturase, and that the down-regulation of gene CAR1 by naftifine contributes to de-pigmentation in R. mucilaginosa.   Key word: Naftifine, carotenoid, Rhodotorula mucilaginosa, phytoene desaturase.

Highlights

Naftifine is a topical allylamine antifungal drug that is commonly used to treat dermatophytes infections (Carrillo-Munoz et al, 1999; Gupta et al, 2008; Ghannoum et al, 2013)
Decoloration of R. mucilaginosa was induced by low concentration of naftifine
The results suggested that the major yeast decoloration was not due to naftifine-facilitated pigment degradation

Summary

Introduction

Naftifine is a topical allylamine antifungal drug that is commonly used to treat dermatophytes infections (Carrillo-Munoz et al, 1999; Gupta et al, 2008; Ghannoum et al, 2013). In Staphylococcus aureus, naftifine at low concentrations inhibited production of the virulence factor Staphyloxanthin, a carotenoid pigment, with a IC50 = 0.088 mg/L and had no effect to inhibit bacterial growth. This inhibitory effect was not through regulating the expression of operon crtOPQMN or by inhibiting isoprenoid biosynthetic pathway, but by inhibiting CrtN enzyme directly (Chen et al, 2016).

Methods

Results

Conclusion