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Braus, Gerhard H.
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Braus, Gerhard H.
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Braus, Gerhard H.
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Braus, G. H.
Braus, Gerhard
Braus, G.
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2006Conference Paper [["dc.bibliographiccitation.firstpage","S91"],["dc.bibliographiccitation.journal","Medical Mycology"],["dc.bibliographiccitation.lastpage","S94"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Krappmann, Sven"],["dc.date.accessioned","2018-11-07T09:22:02Z"],["dc.date.available","2018-11-07T09:22:02Z"],["dc.date.issued","2006"],["dc.description.abstract","Supply of all amino acids required for translation is crucial for the synthesis of new proteins. Fungal amino acid biosynthesis has to be coordinated with amino acid uptake as well as protein degradation. A global regulator that connects amino acid biosynthesis and developmental programs is the transcription factor CpcA/Gcn4p. This transcriptional activator is conserved within the fungal kingdom and the cellular levels of this protein are carefully regulated. Deletion of the encoding cpcA gene in the opportunistic pathogen Aspergillus fumigatus results in impaired virulence in immuno-compromised mice, suggesting a role of the cross-pathway control system in fungal pathogenicity."],["dc.identifier.doi","10.1080/13693780600898029"],["dc.identifier.isi","000242601400017"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29246"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.publisher.place","Abingdon"],["dc.relation.conference","2nd Advances against Aspergillosis Conference"],["dc.relation.eventlocation","Athens, GREECE"],["dc.relation.issn","1369-3786"],["dc.title","Amino acid acquisition, cross-pathway control, and virulence in Aspergillus"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2018Journal Article [["dc.bibliographiccitation.artnumber","e1007511"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLOS Genetics"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Thieme, Karl G."],["dc.contributor.author","Gerke, Jennifer"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Valerius, Oliver"],["dc.contributor.author","Thieme, Sabine"],["dc.contributor.author","Karimi, Razieh"],["dc.contributor.author","Heinrich, Antje K."],["dc.contributor.author","Finkernagel, Florian"],["dc.contributor.author","Smith, Kristina"],["dc.contributor.author","Bode, Helge B."],["dc.contributor.author","Freitag, Michael"],["dc.contributor.author","Ram, Arthur F. J."],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2019-07-09T11:45:46Z"],["dc.date.available","2019-07-09T11:45:46Z"],["dc.date.issued","2018"],["dc.description.abstract","The NF-κB-like velvet domain protein VosA (viability of spores) binds to more than 1,500 promoter sequences in the filamentous fungus Aspergillus nidulans. VosA inhibits premature induction of the developmental activator gene brlA, which promotes asexual spore formation in response to environmental cues as light. VosA represses a novel genetic network controlled by the sclB gene. SclB function is antagonistic to VosA, because it induces the expression of early activator genes of asexual differentiation as flbC and flbD as well as brlA. The SclB controlled network promotes asexual development and spore viability, but is independent of the fungal light control. SclB interactions with the RcoA transcriptional repressor subunit suggest additional inhibitory functions on transcription. SclB links asexual spore formation to the synthesis of secondary metabolites including emericellamides, austinol as well as dehydroaustinol and activates the oxidative stress response of the fungus. The fungal VosA-SclB regulatory system of transcription includes a VosA control of the sclB promoter, common and opposite VosA and SclB control functions of fungal development and several additional regulatory genes. The relationship between VosA and SclB illustrates the presence of a convoluted surveillance apparatus of transcriptional control, which is required for accurate fungal development and the linkage to the appropriate secondary metabolism."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.1371/journal.pgen.1007511"],["dc.identifier.pmid","30044771"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15315"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59309"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.subject.ddc","570"],["dc.title","Velvet domain protein VosA represses the zinc cluster transcription factor SclB regulatory network for Aspergillus nidulans asexual development, oxidative stress response and secondary metabolism."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2019Journal Article [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Biology"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Álvarez-Escribano, Isidro"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Bok, Jin Woo"],["dc.contributor.author","Na, Hyunsoo"],["dc.contributor.author","Amirebrahimi, Mojgan"],["dc.contributor.author","Lipzen, Anna"],["dc.contributor.author","Schackwitz, Wendy"],["dc.contributor.author","Martin, Joel"],["dc.contributor.author","Barry, Kerrie"],["dc.contributor.author","Gutiérrez, Gabriel"],["dc.contributor.author","Cea-Sánchez, Sara"],["dc.contributor.author","Marcos, Ana T."],["dc.contributor.author","Grigoriev, Igor V."],["dc.contributor.author","Keller, Nancy P."],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Cánovas, David"],["dc.date.accessioned","2020-12-10T18:38:58Z"],["dc.date.available","2020-12-10T18:38:58Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s12915-019-0702-0"],["dc.identifier.eissn","1741-7007"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16680"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77494"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genome sequencing of evolved aspergilli populations reveals robust genomes, transversions in A. flavus, and sexual aberrancy in non-homologous end-joining mutants"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2017Journal Article [["dc.bibliographiccitation.firstpage","398"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","International Journal of Medical Microbiology"],["dc.bibliographiccitation.lastpage","408"],["dc.bibliographiccitation.volume","307"],["dc.contributor.author","Amarsaikhan, Nansalmaa"],["dc.contributor.author","Albrecht-Eckardt, Daniela"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Ogel, Zumrut B."],["dc.contributor.author","Kniemeyer, Olaf"],["dc.date.accessioned","2020-12-10T14:24:37Z"],["dc.date.available","2020-12-10T14:24:37Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.ijmm.2017.07.011"],["dc.identifier.issn","1438-4221"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72303"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Proteomic profiling of the antifungal drug response of Aspergillus fumigatus to voriconazole"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Liu, Li"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Dirnberger, Benedict"],["dc.contributor.author","Valerius, Oliver"],["dc.contributor.author","Fekete-Szücs, Enikő"],["dc.contributor.author","Harting, Rebekka"],["dc.contributor.author","Nordzieke, Daniela E"],["dc.contributor.author","Pöggeler, Stefanie"],["dc.contributor.author","Karlovsky, Petr"],["dc.contributor.author","Gerke, Jennifer"],["dc.contributor.author","Braus, Gerhard H"],["dc.date.accessioned","2021-12-01T09:24:08Z"],["dc.date.available","2021-12-01T09:24:08Z"],["dc.date.issued","2021"],["dc.description.abstract","Fungal Hülle cells with nuclear storage and developmental backup functions are reminiscent of multipotent stem cells. In the soil, Hülle cells nurse the overwintering fruiting bodies of Aspergillus nidulans . The genome of A. nidulans harbors genes for the biosynthesis of xanthones. We show that enzymes and metabolites of this biosynthetic pathway accumulate in Hülle cells under the control of the regulatory velvet complex, which coordinates development and secondary metabolism. Deletion strains blocked in the conversion of anthraquinones to xanthones accumulate emodins and are delayed in maturation and growth of fruiting bodies. Emodin represses fruiting body and resting structure formation in other fungi. Xanthones are not required for sexual development but exert antifeedant effects on fungivorous animals such as springtails and woodlice. Our findings reveal a novel role of Hülle cells in establishing secure niches for A. nidulans by accumulating metabolites with antifeedant activity that protect reproductive structures from animal predators."],["dc.description.abstract","Fungal Hülle cells with nuclear storage and developmental backup functions are reminiscent of multipotent stem cells. In the soil, Hülle cells nurse the overwintering fruiting bodies of Aspergillus nidulans . The genome of A. nidulans harbors genes for the biosynthesis of xanthones. We show that enzymes and metabolites of this biosynthetic pathway accumulate in Hülle cells under the control of the regulatory velvet complex, which coordinates development and secondary metabolism. Deletion strains blocked in the conversion of anthraquinones to xanthones accumulate emodins and are delayed in maturation and growth of fruiting bodies. Emodin represses fruiting body and resting structure formation in other fungi. Xanthones are not required for sexual development but exert antifeedant effects on fungivorous animals such as springtails and woodlice. Our findings reveal a novel role of Hülle cells in establishing secure niches for A. nidulans by accumulating metabolites with antifeedant activity that protect reproductive structures from animal predators."],["dc.identifier.doi","10.7554/eLife.68058"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94858"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2050-084X"],["dc.title","Secondary metabolites of Hülle cells mediate protection of fungal reproductive and overwintering structures against fungivorous animals"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2015Journal Article [["dc.bibliographiccitation.artnumber","e1005205"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS Pathogens"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Lin, Chi-Jan"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Gerke, Jennifer"],["dc.contributor.author","Valerius, Oliver"],["dc.contributor.author","Irmer, Henriette"],["dc.contributor.author","Frauendorf, Holm"],["dc.contributor.author","Heinekamp, Thorsten"],["dc.contributor.author","Strassburger, Maria"],["dc.contributor.author","van Tuan Tran, Van Tuan Tran"],["dc.contributor.author","Herzog, Britta"],["dc.contributor.author","Braus-Stromeyer, Susanna A."],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2018-11-07T09:49:12Z"],["dc.date.available","2018-11-07T09:49:12Z"],["dc.date.issued","2015"],["dc.description.abstract","The transcription factor Flo8/Som1 controls filamentous growth in Saccharomyces cerevisiae and virulence in the plant pathogen Magnaporthe oryzae. Flo8/Som1 includes a characteristic N-terminal LUG/LUH-Flo8-single-stranded DNA binding (LUFS) domain and is activated by the cAMP dependent protein kinase A signaling pathway. Heterologous SomA from Aspergillus fumigatus rescued in yeast flo8 mutant strains several phenotypes including adhesion or flocculation in haploids and pseudohyphal growth in diploids, respectively. A. fumigatus SomA acts similarly to yeast Flo8 on the promoter of FLO11 fused with reporter gene (LacZ) in S. cerevisiae. FLO11 expression in yeast requires an activator complex including Flo8 and Mfg1. Furthermore, SomA physically interacts with PtaB, which is related to yeast Mfg1. Loss of the somA gene in A. fumigatus resulted in a slow growth phenotype and a block in asexual development. Only aerial hyphae without further differentiation could be formed. The deletion phenotype was verified by a conditional expression of somA using the inducible Tet-on system. A adherence assay with the conditional somA expression strain indicated that SomA is required for biofilm formation. A ptaB deletion strain showed a similar phenotype supporting that the SomA/PtaB complex controls A. fumigatus biofilm formation. Transcriptional analysis showed that SomA regulates expression of genes for several transcription factors which control conidiation or adhesion of A. fumigatus. Infection assays with fertilized chicken eggs as well as with mice revealed that SomA is required for pathogenicity. These data corroborate a complex control function of SomA acting as a central factor of the transcriptional network, which connects adhesion, spore formation and virulence in the opportunistic human pathogen A. fumigatus."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.ppat.1005205"],["dc.identifier.isi","000368332000007"],["dc.identifier.pmid","26529322"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35459"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7374"],["dc.relation.issn","1553-7366"],["dc.rights.access","openAccess"],["dc.title","Transcription Factor SomA Is Required for Adhesion, Development and Virulence of the Human Pathogen Aspergillus fumigatus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2015Journal Article [["dc.bibliographiccitation.artnumber","640"],["dc.bibliographiccitation.journal","BMC Genomics"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Irmer, Henriette"],["dc.contributor.author","Tarazona, Sonia"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Olbermann, Patrick"],["dc.contributor.author","Loeffler, Juergen"],["dc.contributor.author","Krappmann, Sven"],["dc.contributor.author","Conesa, Ana"],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2018-11-07T09:53:07Z"],["dc.date.available","2018-11-07T09:53:07Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Invasive aspergillosis is started after germination of Aspergillus fumigatus conidia that are inhaled by susceptible individuals. Fungal hyphae can grow in the lung through the epithelial tissue and disseminate hematogenously to invade into other organs. Low fungaemia indicates that fungal elements do not reside in the bloodstream for long. Results: We analyzed whether blood represents a hostile environment to which the physiology of A. fumigatus has to adapt. An in vitro model of A. fumigatus infection was established by incubating mycelium in blood. Our model allowed to discern the changes of the gene expression profile of A. fumigatus at various stages of the infection. The majority of described virulence factors that are connected to pulmonary infections appeared not to be activated during the blood phase. Three active processes were identified that presumably help the fungus to survive the blood environment in an advanced phase of the infection: iron homeostasis, secondary metabolism, and the formation of detoxifying enzymes. Conclusions: We propose that A. fumigatus is hardly able to propagate in blood. After an early stage of sensing the environment, virtually all uptake mechanisms and energy-consuming metabolic pathways are shut-down. The fungus appears to adapt by trans-differentiation into a resting mycelial stage. This might reflect the harsh conditions in blood where A. fumigatus cannot take up sufficient nutrients to establish self-defense mechanisms combined with significant growth."],["dc.identifier.doi","10.1186/s12864-015-1853-1"],["dc.identifier.isi","000360039300003"],["dc.identifier.pmid","26311470"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12535"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36263"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2164"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","RNAseq analysis of Aspergillus fumigatus in blood reveals a just wait and see resting stage behavior"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2018Journal Article [["dc.bibliographiccitation.artnumber","744"],["dc.bibliographiccitation.journal","Frontiers in Microbiology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bakti, Fruzsina"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Heinekamp, Thorsten"],["dc.contributor.author","Pócsi, István"],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2019-07-09T11:45:38Z"],["dc.date.available","2019-07-09T11:45:38Z"],["dc.date.issued","2018"],["dc.description.abstract","Most of the metal transporters in Aspergillus fumigatus are yet uncharacterized. Their role in fungal metabolism and virulence remains unclear. This paper describes the novel PIB-type cation ATPase PcaA, which links metal homeostasis and heavy metal tolerance in the opportunistic human pathogen A. fumigatus. The protein possesses conserved ATPase motif and shares 51% amino acid sequence identity with the Saccharomyces cerevisiae cadmium exporter Pca1p. A pcaA deletion, an overexpression and a gfp-pcaA complementation strain of A. fumigatus were constructed and their heavy metal susceptibilities were studied. The pcaA knock out strain showed drastically decreased cadmium tolerance, however, its growth was not affected by the exposure to high concentrations of copper, iron, zinc, or silver ions. Although the lack of PcaA had no effect on copper adaption, we demonstrated that not only cadmium but also copper ions are able to induce the transcription of pcaA in A. fumigatus wild type Af293. Similarly, cadmium and copper ions could induce the copper exporting ATPase crpA. These data imply a general response on the transcriptomic level to heavy metals in A. fumigatus through the induction of detoxification systems. Confocal microscopy of the gfp-pcaA complementation strain expressing functional GFP-PcaA supports the predicted membrane localization of PcaA. The GFP-PcaA fusion protein is located in the plasma membrane of A. fumigatus in the presence of cadmium ions. Virulence assays support a function of PcaA for virulence of A. fumigatus in the Galleria mellonella wax moth larvae model, which might be linked to the elimination of reactive oxygen species."],["dc.identifier.doi","10.3389/fmicb.2018.00744"],["dc.identifier.pmid","29706948"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59270"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1664-302X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","570"],["dc.title","Heavy Metal-Induced Expression of PcaA Provides Cadmium Tolerance to Aspergillus fumigatus and Supports Its Virulence in the Galleria mellonella Model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2008Journal Article [["dc.bibliographiccitation.firstpage","693"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Fungal Genetics and Biology"],["dc.bibliographiccitation.lastpage","704"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Sasse, Christoph"],["dc.contributor.author","Bignell, Elaine M."],["dc.contributor.author","Hasenberg, Mike"],["dc.contributor.author","Haynes, Ken"],["dc.contributor.author","Gunzer, Matthias"],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Krappmann, Sven"],["dc.date.accessioned","2018-11-07T11:15:29Z"],["dc.date.available","2018-11-07T11:15:29Z"],["dc.date.issued","2008"],["dc.description.abstract","Aspergillosis is a disease determined by various factors that influence fungal growth and fitness. A conserved signal transduction cascade linking environmental stress to amino acid homeostasis is the Cross-Pathway Control (CPC) system that acts via phosphorylation of the translation initiation factor eIF2 by a sensor kinase to elevate expression of a transcription factor. Ingestion of Aspergillus fumigatus conidia by macrophages does not trigger this stress response, suggesting that their phagosomal microenvironment is not deficient in amino acids. The cpcC gene encodes the CPC eIF2 alpha kinase, and deletion mutants show increased sensitivity towards amino acid starvation. CpcC is specifically required for the CPC response but has limited influence on the amount of phosphorylated eIF2 alpha. Strains deleted for the cpcC locus are not impaired in virulence in a murine model of pulmonary aspergillosis. Accordingly, basal expression of the Cross-Pathway Control transcriptional activator appears sufficient to support aspergillosis in this disease model. (c) 2008 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Medical Research Council [G0501164]"],["dc.identifier.doi","10.1016/j.fgb.2007.12.008"],["dc.identifier.isi","000255153600012"],["dc.identifier.pmid","18249572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54377"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1096-0937"],["dc.relation.issn","1087-1845"],["dc.title","Basal expression of the Aspergillus fumigatus transcriptional activator CpcA is sufficient to support pulmonary aspergillosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS