Abstract
Talaromyces marneffei is a dimorphic pathogenic fungus causing opportunistic infection in immunocompromised patients. It is a facultative intracellular pathogen and is usually found inside the host macrophages during infection. Alternative carbons and iron are the important nutrients associated with intracellular survival and pathogenesis of T. marneffei. This study reported the importance of the transcription factor AcuK in control of gluconeogenesis and iron acquisition in T. marneffei. Deletion of acuK gene in T. marneffei resulted in retardation of growth and germination in both mold and yeast phases. Microscopically, ΔacuK showed double nuclei hyphae. However, the yeast cells showed normal morphology. The ΔacuK failed to grow in iron-limiting conditions. Additionally, it could not grow in a medium containing gluconeogenic carbon sources. Moreover, ΔacuK showed higher susceptibility to macrophage killing than the wild type. These results demonstrated that AcuK controlled both iron acquisition and gluconeogenesis, and it could contribute to the pathogenicity of this fungus.
Highlights
Introduction and Gluconeogenesis in TalaromycesTalaromyces marneffei is a dimorphic pathogenic fungus causing systemic opportunistic infection in Southeast Asia
This study focused on the coupling transcriptional control of iron acquisition and gluconeogenesis as it could help to explain how the fungus act in nutrientstarvation conditions
Colony morphology was compared on T. marneffei FRR2161 wild-type (WT), ∆acuK
Summary
Talaromyces marneffei is a dimorphic pathogenic fungus causing systemic opportunistic infection in Southeast Asia. In Thailand, this infection is common in AIDS patients [1]. Infection due to T. marneffei has been reported primarily among immunocompromised people in endemic regions and travelers [2]. T. marneffei can grow either in yeast or mycelial forms, depending on the growing temperatures. In vitro cultivation on Sabauraud’s agar at 25–30 ◦ C grows as the mycelial phase, producing a green velvety colony with red diffusible pigment. The engulfed conidia initially change to yeasts to establish the infection. The pathogen is divided by fission inside the phagosome of macrophages. Multiplication inside the phagosome environment needs sufficient nutrients
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