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The stuA gene controls development, adaptation, stress tolerance, and virulence of the dermatophyte Trichophyton rubrum.

Abstract：

:The APSES family, comprising of the transcriptional regulators Asm1p, Phd1p, Sok2p, Efg1p, and StuA, is found exclusively in fungi and has been reported to control several cellular processes in these organisms. However, its function in dermatophytes has not yet been completely understood. Here, we generated two null mutant strains by deleting the stuA gene in the dermatophyte Trichophyton rubrum, the most common clinical isolate obtained from human skin and nail mycoses. The functional characterization of the knocked-out strains revealed the involvement of stuA in germination, morphogenesis of conidia and hyphae, pigmentation, stress responses, and virulence. Although the mutant strains could grow under several nutritional conditions, growth on the keratin medium, human nails, and skin was impaired. The co-culture of stuA mutants with human keratinocytes revealed enhanced development. Moreover, a stuA mutant grown on the keratin substrate showed a marked decrease in the transcript numbers of the hydrophobin encoding gene (hypA), suggesting the involvement of stuA in the molecular mechanisms underlying mechanosensing during the fungi-host interaction. In addition, bioinformatics analyses revealed the potential involvement of StuA in different biological processes such as oxidation-reduction, phosphorylation, proteolysis, transcription/translation regulation, and carbohydrate metabolism. Cumulatively, the present study suggested that StuA is a crosstalk mediator of many pathways and is an integral component of the infection process, implying that it could be a potential target for antifungal therapy.

journal_name

Microbiol Res

journal_title

Microbiological research

authors

Lang EAS,Bitencourt TA,Peres NTA,Lopes L,Silva LG,Cazzaniga RA,Rossi A,Martinez-Rossi NM

doi

10.1016/j.micres.2020.126592

subject

Has Abstract

pub_date

2020-12-01 00:00:00

pages

126592

eissn

0944-5013

issn

1618-0623

pii

S0944-5013(20)30460-2

journal_volume

241

pub_type

杂志文章

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