Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity
Survival factor A (SvfA) in <i>Aspergillus nidulans</i> plays multiple roles in growth and developmental processes. It is a candidate for a novel VeA-dependent protein involved in sexual development. VeA is a key developmental regulator in <i>Aspergillus</i> species that can...
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MDPI AG
2023-01-01
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| Series: | Journal of Fungi |
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| Online Access: | https://www.mdpi.com/2309-608X/9/2/143 |
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| author | Joo-Yeon Lim Ye-Eun Jung Hye-Eun Hwang Cheol-Hee Kim Nese Basaran-Akgul Sri Harshini Goli Steven P. Templeton Hee-Moon Park |
| author_facet | Joo-Yeon Lim Ye-Eun Jung Hye-Eun Hwang Cheol-Hee Kim Nese Basaran-Akgul Sri Harshini Goli Steven P. Templeton Hee-Moon Park |
| author_sort | Joo-Yeon Lim |
| collection | DOAJ |
| description | Survival factor A (SvfA) in <i>Aspergillus nidulans</i> plays multiple roles in growth and developmental processes. It is a candidate for a novel VeA-dependent protein involved in sexual development. VeA is a key developmental regulator in <i>Aspergillus</i> species that can interact with other velvet-family proteins and enter into the nucleus to function as a transcription factor. In yeast and fungi, SvfA-homologous proteins are required for survival under oxidative and cold-stress conditions. To assess the role of SvfA in virulence in <i>A. nidulans</i>, cell wall components, biofilm formation, and protease activity were evaluated in a <i>svfA</i>-gene-deletion or an <i>AfsvfA-</i>overexpressing strain. The <i>svfA</i>-deletion strain showed decreased production of β-1,3-glucan in conidia, a cell wall pathogen-associated molecular pattern, with a decrease in gene expression for chitin synthases and β-1,3-glucan synthase. The ability to form biofilms and produce proteases was reduced in the <i>svfA</i>-deletion strain. We hypothesized that the <i>svfA</i>-deletion strain was less virulent than the wild-type strain; therefore, we performed in vitro phagocytosis assays using alveolar macrophages and analyzed in vivo survival using two vertebrate animal models. While phagocytosis was reduced in mouse alveolar macrophages challenged with conidia from the <i>svfA</i>-deletion strain, the killing rate showed a significant increase with increased extracellular signal-regulated kinase ERK activation. The <i>svfA</i>-deletion conidia infection reduced host mortality in both T-cell-deficient zebrafish and chronic granulomatous disease mouse models. Taken together, these results indicate that SvfA plays a significant role in the pathogenicity of <i>A. nidulans</i>. |
| first_indexed | 2024-03-11T08:35:51Z |
| format | Article |
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| institution | Directory Open Access Journal |
| issn | 2309-608X |
| language | English |
| last_indexed | 2024-03-11T08:35:51Z |
| publishDate | 2023-01-01 |
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| spelling | doaj.art-90e5604fdff04c9bb4b974709d234e0e2023-11-16T21:29:42ZengMDPI AGJournal of Fungi2309-608X2023-01-019214310.3390/jof9020143Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> PathogenicityJoo-Yeon Lim0Ye-Eun Jung1Hye-Eun Hwang2Cheol-Hee Kim3Nese Basaran-Akgul4Sri Harshini Goli5Steven P. Templeton6Hee-Moon Park7Department of Microbiology and Immunology, Indiana University School of Medicine-Terre Haute, Terre Haute, IN 47807, USALaboratory of Cellular Differentiation, Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Republic of KoreaLaboratory of Developmental Genetics Department of Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Republic of KoreaLaboratory of Developmental Genetics Department of Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Republic of KoreaDepartment of Microbiology and Immunology, Indiana University School of Medicine-Terre Haute, Terre Haute, IN 47807, USADepartment of Microbiology and Immunology, Indiana University School of Medicine-Terre Haute, Terre Haute, IN 47807, USADepartment of Microbiology and Immunology, Indiana University School of Medicine-Terre Haute, Terre Haute, IN 47807, USALaboratory of Cellular Differentiation, Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Republic of KoreaSurvival factor A (SvfA) in <i>Aspergillus nidulans</i> plays multiple roles in growth and developmental processes. It is a candidate for a novel VeA-dependent protein involved in sexual development. VeA is a key developmental regulator in <i>Aspergillus</i> species that can interact with other velvet-family proteins and enter into the nucleus to function as a transcription factor. In yeast and fungi, SvfA-homologous proteins are required for survival under oxidative and cold-stress conditions. To assess the role of SvfA in virulence in <i>A. nidulans</i>, cell wall components, biofilm formation, and protease activity were evaluated in a <i>svfA</i>-gene-deletion or an <i>AfsvfA-</i>overexpressing strain. The <i>svfA</i>-deletion strain showed decreased production of β-1,3-glucan in conidia, a cell wall pathogen-associated molecular pattern, with a decrease in gene expression for chitin synthases and β-1,3-glucan synthase. The ability to form biofilms and produce proteases was reduced in the <i>svfA</i>-deletion strain. We hypothesized that the <i>svfA</i>-deletion strain was less virulent than the wild-type strain; therefore, we performed in vitro phagocytosis assays using alveolar macrophages and analyzed in vivo survival using two vertebrate animal models. While phagocytosis was reduced in mouse alveolar macrophages challenged with conidia from the <i>svfA</i>-deletion strain, the killing rate showed a significant increase with increased extracellular signal-regulated kinase ERK activation. The <i>svfA</i>-deletion conidia infection reduced host mortality in both T-cell-deficient zebrafish and chronic granulomatous disease mouse models. Taken together, these results indicate that SvfA plays a significant role in the pathogenicity of <i>A. nidulans</i>.https://www.mdpi.com/2309-608X/9/2/143<i>Aspergillus nidulans</i>survival factor Apathogen-associated molecular pattern (PAMP)chronic granulomatous disease micelung immune responseinflammatory cytokines |
| spellingShingle | Joo-Yeon Lim Ye-Eun Jung Hye-Eun Hwang Cheol-Hee Kim Nese Basaran-Akgul Sri Harshini Goli Steven P. Templeton Hee-Moon Park Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity Journal of Fungi <i>Aspergillus nidulans</i> survival factor A pathogen-associated molecular pattern (PAMP) chronic granulomatous disease mice lung immune response inflammatory cytokines |
| title | Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity |
| title_full | Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity |
| title_fullStr | Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity |
| title_full_unstemmed | Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity |
| title_short | Survival Factor A (SvfA) Contributes to <i>Aspergillus nidulans</i> Pathogenicity |
| title_sort | survival factor a svfa contributes to i aspergillus nidulans i pathogenicity |
| topic | <i>Aspergillus nidulans</i> survival factor A pathogen-associated molecular pattern (PAMP) chronic granulomatous disease mice lung immune response inflammatory cytokines |
| url | https://www.mdpi.com/2309-608X/9/2/143 |
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