Sample File "FungiNet_template_RNA-seq_V1.9_Ex_ID_005"
FungiNet total, A1

Cultivation of A. fumigatus in an O2-controlled fermenter and analysed its minute-scale responses to O2 limitation. Transcriptome sequencing revealed a group of genes underlying a rapid and highly dynamic regulation.

Creators: Jörg Linde, Falk Hillmann, Olaf Kniemeyer

Contributor: Maja Rey

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Serum FHR1 binding to necrotic-type cells activates monocytic inflammasome and marks necrotic sites in vasculopathies.
FungiNet total, FungiNet C - Candida projects, C4 (E)

Abstract (Expand)

Persistent inflammation is a hallmark of many human diseases, including anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) and atherosclerosis. Here, we describe a dominant trigger of … inflammation: human serum factor H-related protein FHR1. In vitro, this protein selectively binds to necrotic cells via its N-terminus; in addition, it binds near necrotic glomerular sites of AAV patients and necrotic areas in atherosclerotic plaques. FHR1, but not factor H, FHR2 or FHR3 strongly induces inflammasome NLRP3 in blood-derived human monocytes, which subsequently secrete IL-1beta, TNFalpha, IL-18 and IL-6. FHR1 triggers the phospholipase C-pathway via the G-protein coupled receptor EMR2 independent of complement. Moreover, FHR1 concentrations of AAV patients negatively correlate with glomerular filtration rates and associate with the levels of inflammation and progressive disease. These data highlight an unexpected role for FHR1 during sterile inflammation, may explain why FHR1-deficiency protects against certain diseases, and identifies potential targets for treatment of auto-inflammatory diseases.

Authors: Sarah Irmscher, S. R. Brix, Peter Zipfel, Luke Donald Halder, S. Mutluturk, S. Wulf, E. Girdauskas, H. Reichenspurner, R. A. K. Stahl, Berit Jungnickel, T. Wiech, Peter Zipfel, Christine Skerka

Date Published: 4th Jul 2019

Journal: Nat Commun

Immune modulation by complement receptor 3-dependent human monocyte TGF-beta1-transporting vesicles.
C4 (E)

Abstract (Expand)

Extracellular vesicles have an important function in cellular communication. Here, we show that human and mouse monocytes release TGF-beta1-transporting vesicles in response to the pathogenic fungus … Candida albicans. Soluble beta-glucan from C. albicans binds to complement receptor 3 (CR3, also known as CD11b/CD18) on monocytes and induces the release of TGF-beta1-transporting vesicles. CR3-dependence is demonstrated using CR3-deficient (CD11b knockout) monocytes generated by CRISPR-CAS9 genome editing and isolated from CR3-deficient (CD11b knockout) mice. These vesicles reduce the pro-inflammatory response in human M1-macrophages as well as in whole blood. Binding of the vesicle-transported TGF-beta1 to the TGF-beta receptor inhibits IL1B transcription via the SMAD7 pathway in whole blood and induces TGFB1 transcription in endothelial cells, which is resolved upon TGF-beta1 inhibition. Notably, human complement-opsonized apoptotic bodies induce production of similar TGF-beta1-transporting vesicles in monocytes, suggesting that the early immune response might be suppressed through this CR3-dependent anti-inflammatory vesicle pathway.

Authors: Luke Donald Halder, E. A. H. Jo, M. Z. Hasan, M. Ferreira-Gomes, Thomas Krüger, M. Westermann, D. I. Palme, G. Rambach, Niklas Beyersdorf, C. Speth, Ilse Jacobsen, Olaf Kniemeyer, Berit Jungnickel, Peter Zipfel, Christine Skerka

Date Published: 11th May 2020

Journal: Nat Commun

Comparison of transcriptome technologies in the pathogenic fungus Aspergillus fumigatus reveals novel insights into the genome and MpkA dependent gene expression
FungiNet A - Aspergillus projects, FungiNet B - Bioinformatics projects

Abstract

ABSTRACT:

Authors: Sebastian Müller, Clara Baldin, Marco Groth, Reinhard Guthke, Olaf Kniemeyer, Axel A Brakhage, Vito Valiante

Date Published: 2nd Oct 2012

Journal: BMC Genomics

Microevolution of Candida albicans in macrophages restores filamentation in a nonfilamentous mutant
FungiNet C - Candida projects, INF

Abstract (Expand)

Following antifungal treatment, Candida albicans, and other human pathogenic fungi can undergo microevolution, which leads to the emergence of drug resistance. However, the capacity for microevolutionary … adaptation of fungi goes beyond the development of resistance against antifungals. Here we used an experimental microevolution approach to show that one of the central pathogenicity mechanisms of C. albicans, the yeast-to-hyphae transition, can be subject to experimental evolution. The C. albicans cph1Delta/efg1Delta mutant is nonfilamentous, as central signaling pathways linking environmental cues to hyphal formation are disrupted. We subjected this mutant to constant selection pressure in the hostile environment of the macrophage phagosome. In a comparatively short time-frame, the mutant evolved the ability to escape macrophages by filamentation. In addition, the evolved mutant exhibited hyper-virulence in a murine infection model and an altered cell wall composition compared to the cph1Delta/efg1Delta strain. Moreover, the transcriptional regulation of hyphae-associated, and other pathogenicity-related genes became re-responsive to environmental cues in the evolved strain. We went on to identify the causative missense mutation via whole genome- and transcriptome-sequencing: a single nucleotide exchange took place within SSN3 that encodes a component of the Cdk8 module of the Mediator complex, which links transcription factors with the general transcription machinery. This mutation was responsible for the reconnection of the hyphal growth program with environmental signals in the evolved strain and was sufficient to bypass Efg1/Cph1-dependent filamentation. These data demonstrate that even central transcriptional networks can be remodeled very quickly under appropriate selection pressure.

Authors: A. Wartenberg, Jörg Linde, R. Martin, M. Schreiner, F. Horn, Ilse Jacobsen, S. Jenull, Thomas Wolf, K. Kuchler, Reinhard Guthke, Oliver Kurzai, A. Forche, C. d'Enfert, S. Brunke, Bernhard Hube

Date Published: 4th Dec 2014

Journal: PLoS Genet

The transcriptional stress response of Candida albicans to weak organic acids.
FungiNet total, FungiNet C - Candida projects

Abstract (Expand)

Candida albicans is the most important fungal pathogen of humans, causing severe infections, especially in nosocomial and immunocompromised settings. However, it is also the most prevalent fungus of … the normal human microbiome, where it shares its habitat with hundreds of trillions of other microbial cells. Despite weak organic acids (WOAs) being among the most abundant metabolites produced by bacterial microbiota, little is known about their effect on C. albicans. Here we used a sequencing-based profiling strategy to systematically investigate the transcriptional stress response of C. albicans to lactic, acetic, propionic, and butyric acid at several time points after treatment. Our data reveal a complex transcriptional response, with individual WOAs triggering unique gene expression profiles and with important differences between acute and chronic exposure. Despite these dissimilarities, we found significant overlaps between the gene expression changes induced by each WOA, which led us to uncover a core transcriptional response that was largely unrelated to other previously published C. albicans transcriptional stress responses. Genes commonly up-regulated by WOAs were enriched in several iron transporters, which was associated with an overall decrease in intracellular iron concentrations. Moreover, chronic exposure to any WOA lead to down-regulation of RNA synthesis and ribosome biogenesis genes, which resulted in significant reduction of total RNA levels and of ribosomal RNA in particular. In conclusion, this study suggests that gastrointestinal microbiota might directly influence C. albicans physiology via production of WOAs, with possible implications of how this fungus interacts with its host in both health and disease.

Authors: F. Cottier, A. S. Tan, J. Chen, J. Lum, F. Zolezzi, M. Poidinger, N. Pavelka

Date Published: 1st Feb 2015

Journal: G3 (Bethesda)

Template_RNA-seq_V1.9
A1
No description specified

Source: Specimen (String) *, Source: Material Type (String) , Source: Organism (String) , Source: Strain or Line (String) , Source: Organism Part (String) , Source: OrganismStatus (String) , Source: Number of fungal organisms (Integer) , Source: Unit for number of fungi (String) , Source: Sex (e.g. for mice) (String) , Source: Age (Real number) , Source: Age Time Unit (String) , Source: Sampling Time Point (Real number) , Source: Sampling Time Point Unit (String) , Source: Temperature (Real number) , Source: Temperature Unit (String) , Source: pH (Real number) , Source: Atmosphere (String) , Source: Compound (String) , Source: Media (String) , Source: Nutrients (String) , Source: Storage Protocol (String) , Source: Storage Date (Date) , Source: Storage Location (String) , RNA Extraction: Extraction Protocol (String) , RNA Extraction: Extract Name (String) , RNA Extraction: 260/280 (Real number) , RNA Extraction: 230/280 (Real number) , RNA Extraction: RIN/RNA integrity number (Real number) , RNA Extraction: Concentration (Real number) , RNA Extraction: Concentration Unit (String) , RNA Extraction: Volume (Real number) , RNA Extraction: Volume Unit (String) , RNA Extraction: Extraction Kit (String) , RNA Extraction: Material Type (String) , RNA Extraction: Extraction Date (Date) , RNA Extraction: Storage Protocol (String) , RNA Extraction: Storage Date (Date) , RNA Extraction: Storage Location (String) , Sequencing: Sequencing Protocol (String) , Sequencing: Assay Name (String) , Sequencing: Sequencing Performer (String) , Sequencing: Technology Type (String) , Sequencing: Read Length (Integer) , Sequencing: Sequencing Instrument (String) , Sequencing: Library Source (String) , Sequencing: Library Strategy (Text) , Sequencing: Library Selection (String) , Sequencing: Library Layout (String) , Sequencing: Sequencing Date (Date) , Sequencing: Storage Protocol (String) , Sequencing: Storage Date (Date) , Sequencing: Storage Location (String) , Sequencing: Data File (Text)

RNA-seq

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