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The transcriptional regulators SteA and StuA contribute to keratin degradation and sexual reproduction of the dermatophyte Arthroderma benhamiae

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Abstract

Most superficial fungal infections are caused by dermatophytes, a specialized group of filamentous fungi which exclusively infect keratinized host structures such as hair, skin and nails. Since little is known about the molecular basis of pathogenicity and sexual reproduction in dermatophytes, here we functionally addressed two central transcriptional regulators, SteA and StuA. In the zoophilic species Arthroderma benhamiae a strategy for targeted genetic manipulation was recently established, and moreover, the species is teleomorphic and thus allows performing assays based on mating. By comparative genome analysis homologs of the developmental regulators SteA and StuA were identified in A. benhamiae. Knock-out mutants of the corresponding genes as well as complemented strains were generated and phenotypically characterized. In contrast to A. benhamiae wild type and complemented strains, both mutants failed to produce sexual reproductive structures in mating experiments. Analysis of growth on keratin substrates indicated that loss of steA resulted in the inability of ΔsteA mutants to produce hair perforation organs, but did not affect mycelia formation during growth on hair and nails. By contrast, ΔstuA mutants displayed a severe growth defect on these substrates, but were still able to produce hair perforations. Hence, formation of hair perforation organs and fungal growth on hair per se are differentially regulated processes. Our findings on the major role of SteA and StuA during sexual development and keratin degradation in A. benhamiae provide insights into their role in dermatophytes and further enhance our knowledge of basic biology and pathogenicity of these fungi.

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Acknowledgments

This work was supported by the DFG funded excellence graduate school Jena School for Microbial Communication (JSMC; GSC 214; www.jsmc.uni-jena.de) and the Leibniz Institute for Natural Product Research and Infection Biology (HKI) (www.leibniz-hki.de).

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  1. Sandra Etzrodt

    Present address: Study and Examination Office, Faculty of Biology and Pharmacy, Friedrich Schiller University, Jena, Germany

  2. Maria Bach

    Present address: Zentrum für Diagnostik GmbH am Klinikum Chemnitz, Chemnitz, Germany

  3. Peter Staib

    Present address: Department of Research and Development, Kneipp GmbH, Würzburg, Germany

Authors and Affiliations

  1. Junior Research Group Fundamental Molecular Biology of Pathogenic Fungi, Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute (HKI), Jena, Germany

    Antje Kröber, Sandra Etzrodt, Maria Bach & Peter Staib

  2. Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute (HKI), Jena, Germany

    Antje Kröber, Olaf Kniemeyer & Axel A. Brakhage

  3. Department of Dermatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

    Michel Monod

  4. Department Microbiology and Molecular Biology, Institute of Microbiology, Friedrich Schiller University, Jena, Germany

    Olaf Kniemeyer & Axel A. Brakhage

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Correspondence to Peter Staib or Axel A. Brakhage.

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The study did not include any diagnostic procedure or therapeutic method. Furthermore, the sample collection was non-invasive (the physical integrity of the donor was maintained) and did not intrude into the privacy of the donor. Based on the regulations of the ethics commission at the Jena University Hospital, Jena (Germany), an approval of the study was not necessary in this case.

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Communicated by M. Kupiec.

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Supplementary Table S1: Primers used in this study

294_2016_608_MOESM1_ESM.docx

Supplementary Fig. S1: Multiple sequence alignments of StuA homologs of N. crassa (Asm-1, XP_960837.1), A. nidulans (StuA, AN5836), A. benhamiae (AbenStuA, ARB_07703); C. albicans (Efg1, CR_07890W_A) and S. cerevisiae (Phd1, CAA81878.1; Sok2, AAB35749.1) using EBI Clustal Omega. The APSES domain is shaded in grey (DOCX 17 kb)

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Kröber, A., Etzrodt, S., Bach, M. et al. The transcriptional regulators SteA and StuA contribute to keratin degradation and sexual reproduction of the dermatophyte Arthroderma benhamiae . Curr Genet 63, 103–116 (2017). https://doi.org/10.1007/s00294-016-0608-0

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