Abstract
Talaromyces marneffei is an opportunistic, dimorphic fungal pathogen that causes a disseminated infection in people with a weakened immunological status. The ability of this fungus to acquire nutrients inside the harsh environment of the macrophage phagosome is presumed to contribute to its pathogenicity. The transcription factors AcuM and AcuK are known to regulate gluconeogenesis and iron acquisition in Aspergillus fumigatus. This study demonstrated that they are also involved in both of these processes in the dimorphic fungus T. marneffei. Expression of acuM and acuK genes was determined by real time-polymerase chain reaction (RT-PCR) on the cells grown in media containing gluconeogenic substrates and various iron concentrations. We found that the acuM and acuK transcript levels were sequentially reduced when growing the fungus in increasing amounts of iron. The acuM transcript was upregulated in the gluconeogenic condition, while the acuK transcript showed upregulation only in the acetate medium in the yeast phase. These results suggest the involvement of acuM and acuK in gluconeogenesis and iron homeostasis in T. marneffei.
Highlights
Talaromyces marneffei is an opportunistic fungus that causes a disseminated infection in immunocompromised patients in Southeast Asian countries and people who travel into this area of endemicity [1,2]
Upregulation of acuK was only observed in the yeast phase in the acetate medium (Figure 5B). These results suggest that acuM, and possibly acuK, play a conservative role in the control of gluconeogenesis like they do in A. nidulans and A. fumigatus
Control of gluconeogenesis by acuM and acuK has been reported in A. nidulans [20,21]
Summary
Talaromyces marneffei is an opportunistic fungus that causes a disseminated infection in immunocompromised patients in Southeast Asian countries and people who travel into this area of endemicity [1,2]. Infection due to T. marneffei is presumed to begin with multiple factors affecting the growth of the fungus inside the host immune cells. After the inhaled conidia reach the alveoli, they are phagocytosed by the alveolar macrophages. The conidia can resist the weakened killing mechanism and convert the growth pattern into a yeast phase. T. marneffei yeast cells can replicate and survive within the alveolar macrophages. Intracellular pathogen, a T. marneffei infection requires the ability to obtain the nutrients necessary for growth and replication under the nutrient-deprived conditions inside the host cells for successful establishment
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