Survival Factor A (SvfA) Contributes to Aspergillus nidulans Pathogenicity

dc.contributor.authorLim, Joo-Yeon
dc.contributor.authorJung, Ye-Eun
dc.contributor.authorHwang, Hye-Eun
dc.contributor.authorKim, Cheol-Hee
dc.contributor.authorBasaran-Akgul, Nese
dc.contributor.authorGoli, Sri Harshini
dc.contributor.authorTempleton, Steven P.
dc.contributor.authorPark, Hee-Moon
dc.contributor.departmentMicrobiology and Immunology, School of Medicine
dc.date.accessioned2023-10-24T17:20:06Z
dc.date.available2023-10-24T17:20:06Z
dc.date.issued2023-01-21
dc.description.abstractSurvival factor A (SvfA) in Aspergillus nidulans 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 Aspergillus 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 A. nidulans, cell wall components, biofilm formation, and protease activity were evaluated in a svfA-gene-deletion or an AfsvfA-overexpressing strain. The svfA-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 svfA-deletion strain. We hypothesized that the svfA-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 svfA-deletion strain, the killing rate showed a significant increase with increased extracellular signal-regulated kinase ERK activation. The svfA-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 A. nidulans.
dc.eprint.versionFinal published version
dc.identifier.citationLim JY, Jung YE, Hwang HE, et al. Survival Factor A (SvfA) Contributes to Aspergillus nidulans Pathogenicity. J Fungi (Basel). 2023;9(2):143. Published 2023 Jan 21. doi:10.3390/jof9020143
dc.identifier.urihttps://hdl.handle.net/1805/36618
dc.language.isoen_US
dc.publisherMDPI
dc.relation.isversionof10.3390/jof9020143
dc.relation.journalJournal of Fungi
dc.rightsAttribution 4.0 Internationalen
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.sourcePMC
dc.subjectAspergillus nidulans
dc.subjectSurvival factor A
dc.subjectPathogen-associated molecular pattern (PAMP)
dc.subjectChronic granulomatous disease mice
dc.subjectLung immune response
dc.subjectInflammatory cytokines
dc.titleSurvival Factor A (SvfA) Contributes to Aspergillus nidulans Pathogenicity
dc.typeArticle
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