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Thomas Wolf

About Thomas Wolf:
No description specified

SEEK ID: https://funginet.hki-jena.de/people/70

Location:  Germany

Expertise: Bioinformatics, Integrative Data Analysis, Gene Clusters, Data Management, Transcriptional Regulation, Gene Regulatory Network Inference, Secondary Metabolites

Tools: LaTeX, R, CASSIS, MEME, Python, SMIPS, FIMO, Perl, antiSMASH

ORCID: Not specified

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Project positions

INF (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI))

FungiNet total (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; A1 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; A2 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; A3 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; A4 (E) (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; A5 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; A6 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; B1 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; B2 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; B3 (E) (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; B4 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; B5 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; C1 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; C2 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; C3 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; C4 (E) (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; C5 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; C6 (E) (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; FungiNet A - Aspergillus projects (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; FungiNet B - Bioinformatics projects (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; FungiNet C - Candida projects (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; Z1 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI)) ; Z2 (Leibniz-Institute for Natural Product Research and Infection Biology Hans Knöll Institute (HKI))

Related items

FungiNet total: inactive since 2018-06-07
No description specified

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/home.html

FungiNet B - Bioinformatics projects: inactive since 2012-01-01
No description specified

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-area-b.html

FungiNet A - Aspergillus projects: inactive since 2012-01-01
No description specified

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-area-a.html

A6: inactive since 2018-06-07

Surface proteins of Lichtheimia corymbifera as virulence determinants

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: Not specified

B1: inactive since 2018-06-07

Modelling interactions between the host and fungal pathogens by combining metabolic pathway analysis and evolutionary game theory

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-b1.html

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5th Joint Meeting IMIHM XII & CRC/TR 124
FungiNet total

Programme

Creators: Thomas Wolf, Jürgen Löffler, Annika Tittelbach-Helmrich

Contributor: Thomas Wolf

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Joint Meeting IMIHM XI & CRC/TRANSREGIO 124 Schedule 2017
FungiNet total
No description specified

Creators: Annika Tittelbach-Helmrich, Jürgen Löffler

Contributor: Thomas Wolf

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[DEMO] Response of hepatocytes to rapid change in the medium composition (gene regulatory network): Model 1100 "freshMedia"
FungiNet total, FungiNet B - Bioinformatics projects

Primary hepatocytes were exposed to a stimulus by exchanging culture medium, thereby simulating changes in the blood composition. The expression of genes at different time points was recorded. Differentially expressed genes were clustered using fuzzy c-means algorithm into five groups. The arcs of the possible network were identified using the NetGenerator algorithm under the restriction of biological knowledge. The analysis was restricted to the main metabolic pathways of hepatocytes. The reverse
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Creators: Thomas Wolf, Wolfgang Schmidt-Heck, Reinhard Guthke

Contributor: Thomas Wolf

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Triple RNA-Seq Reveals Synergy in a Human Virus-Fungus Co-infection Model.
INF, A2, B5

Abstract (Expand)

High-throughput RNA sequencing (RNA-seq) is routinely applied to study diverse biological processes; however, when performed separately on interacting organisms, systemic noise intrinsic to RNA extraction, … library preparation, and sequencing hampers the identification of cross-species interaction nodes. Here, we develop triple RNA-seq to simultaneously detect transcriptomes of monocyte-derived dendritic cells (moDCs) infected with the frequently co-occurring pulmonary pathogens Aspergillus fumigatus and human cytomegalovirus (CMV). Comparing expression patterns after co-infection with those after single infections, our data reveal synergistic effects and mutual interferences between host responses to the two pathogens. For example, CMV attenuates the fungus-mediated activation of pro-inflammatory cytokines through NF-kappaB (nuclear factor kappaB) and NFAT (nuclear factor of activated T cells) cascades, while A. fumigatus impairs viral clearance by counteracting viral nucleic acid-induced activation of type I interferon signaling. Together, the analytical power of triple RNA-seq proposes molecular hubs in the differential moDC response to fungal/viral single infection or co-infection that contribute to our understanding of the etiology and, potentially, clearance of post-transplant infections.

Authors: Bastian Seelbinder, J. Wallstabe, Lothar Marischen, Esther Weiß, S. Wurster, L. Page, C. Loffler, L. Bussemer, A. L. Schmitt, Thomas Wolf, Jörg Linde, L. Cicin-Sain, J. Becker, U. Kalinke, J. Vogel, Gianni Panagiotou, Hermann Einsele, A. J. Westermann, Sascha Schäuble, Jürgen Löffler

Date Published: 17th Nov 2020

Journal: Cell Rep

Survival Strategies of Pathogenic Candida Species in Human Blood Show Independent and Specific Adaptations.
INF, B3 (E), C1, C3

Abstract (Expand)

Only four species, Candida albicans, C. glabrata, C. parapsilosis, and C. tropicalis, together account for about 90% of all Candida bloodstream infections and are among the most common causes of invasive … fungal infections of humans. However, virulence potential varies among these species, and the phylogenetic tree reveals that their pathogenicity may have emerged several times independently during evolution. We therefore tested these four species in a human whole-blood infection model to determine, via comprehensive dual-species RNA-sequencing analyses, which fungal infection strategies are conserved and which are recent evolutionary developments. The ex vivo infection progressed from initial immune cell interactions to nearly complete killing of all fungal cells. During the course of infection, we characterized important parameters of pathogen-host interactions, such as fungal survival, types of interacting immune cells, and cytokine release. On the transcriptional level, we obtained a predominantly uniform and species-independent human response governed by a strong upregulation of proinflammatory processes, which was downregulated at later time points after most of the fungal cells were killed. In stark contrast, we observed that the different fungal species pursued predominantly individual strategies and showed significantly different global transcriptome patterns. Among other findings, our functional analyses revealed that the fungal species relied on different metabolic pathways and virulence factors to survive the host-imposed stress. These data show that adaptation of Candida species as a response to the host is not a phylogenetic trait, but rather has likely evolved independently as a prerequisite to cause human infections.IMPORTANCE To ensure their survival, pathogens have to adapt immediately to new environments in their hosts, for example, during the transition from the gut to the bloodstream. Here, we investigated the basis of this adaptation in a group of fungal species which are among the most common causes of hospital-acquired infections, the Candida species. On the basis of a human whole-blood infection model, we studied which genes and processes are active over the course of an infection in both the host and four different Candida pathogens. Remarkably, we found that, while the human host response during the early phase of infection is predominantly uniform, the pathogens pursue largely individual strategies and each one regulates genes involved in largely disparate processes in the blood. Our results reveal that C. albicans, C. glabrata, C. parapsilosis, and C. tropicalis all have developed individual strategies for survival in the host. This indicates that their pathogenicity in humans has evolved several times independently and that genes which are central for survival in the host for one species may be irrelevant in another.

Authors: P. Kammer, S. McNamara, Thomas Wolf, Theresia Conrad, Stefanie Allert, F. Gerwien, Kerstin Hünniger, Oliver Kurzai, Reinhard Guthke, Bernhard Hube, Jörg Linde, S. Brunke

Date Published: 6th Oct 2020

Journal: mBio

Comparative Transcriptomic Analysis of Rhinovirus and Influenza Virus Infection.
INF, B5

Abstract (Expand)

Rhinovirus (RV) and influenza virus are the most frequently detected respiratory viruses among adult patients with community acquired pneumonia. Previous clinical studies have identified major differences … in the clinical presentations and inflammatory or immune response during these infections. A systematic transcriptomic analysis directly comparing influenza and RV is lacking. Here, we sought to compare the transcriptomic response to these viral infections. Human airway epithelial Calu-3 cells were infected with contemporary clinical isolates of RV, influenza A virus (IAV), or influenza B virus (IBV). Host gene expression was determined using RNA-seq. Differentially expressed genes (DEGs) with respect to mock-infected cells were identified using the overlapping gene-set of four different statistical models. Transcriptomic analysis showed that RV-infected cells have a more blunted host response with fewer DEGs than IAV or IBV-infected cells. IFNL1 and CXCL10 were among the most upregulated DEGs during RV, IAV, and IBV infection. Other DEGs that were highly expressed for all 3 viruses were mainly genes related to type I or type III interferons (RSAD2, IDO1) and chemokines (CXCL11). Notably, ICAM5, a known receptor for enterovirus D68, was highly expressed during RV infection only. Gene Set Enrichment Analysis (GSEA) confirmed that pathways associated with interferon response, innate immunity, or regulation of inflammatory response, were most perturbed for all three viruses. Network analysis showed that steroid-related pathways were enriched. Taken together, our data using contemporary virus strains suggests that genes related to interferon and chemokine predominated the host response associated with RV, IAV, and IBV infection. Several highly expressed genes, especially ICAM5 which is preferentially-induced during RV infection, deserve further investigation.

Authors: T. K. Dissanayake, Sascha Schäuble, Mohammad Mirhakkak, W. L. Wu, A. C. Ng, C. C. Y. Yip, A. G. Lopez, Thomas Wolf, M. L. Yeung, K. H. Chan, K. Y. Yuen, Gianni Panagiotou, K. K. To

Date Published: 28th Aug 2020

Journal: Front Microbiol

Two's company: studying interspecies relationships with dual RNA-seq.
INF

Abstract (Expand)

Organisms do not exist isolated from each other, but constantly interact. Cells can sense the presence of interaction partners by a range of receptors and, via complex regulatory networks, specifically … react by changing the expression of many of their genes. Technological advances in next-generation sequencing over the recent years now allow us to apply RNA sequencing to two species at the same time (dual RNA-seq), and thus to directly study the gene expression of two interacting species without the need to physically separate cells or RNA. In this review, we give an overview over the latest studies in interspecies interactions made possible by dual RNA-seq, ranging from pathogenic to symbiotic relationships. We summarize state-of-the-art experimental techniques, bioinformatic data analysis and data interpretation, while also highlighting potential problems and pitfalls starting from the selection of meaningful time points and number of reads to matters of rRNA depletion. A short outlook on new trends in the field of dual RNA-seq concludes this review, looking at sequencing of non-coding RNAs during host-pathogen interactions and the prediction of molecular interspecies interactions networks.

Authors: Thomas Wolf, P. Kammer, S. Brunke, Jörg Linde

Date Published: 29th Sep 2017

Journal: Curr Opin Microbiol

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

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Annual Meeting CRC/TR 124 FungiNet 2018
No description specified

Start Date: 19th Nov 2018

End Date: 20th Nov 2018

Event Website: Not specified

Country:  Germany

City: Bad Staffelstein

Joint Meeting IMIHM XII & CRC/TR 124 2018-06

This year's 12th IMIHM meeting is held for the fifth time as a Joint Meeting together with scientists from the CRC TransRegio 124 (“Pathogenic fungi and their human host: Networks of interaction – FungiNet”). This collaborative Research Centre FungiNet is a network of scientists from Jena and Wuerzburg and is funded by the Deutsche Forschungsgemeinschaft. The Consortium collaborates to better understand complex invasive mycoses by investigating the pathobiology of fungi, the response of the immune
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Start Date: 26th Jun 2018

End Date: 27th Jun 2018

Event Website: Not specified

Country:  Germany

City: Würzburg

Joint Meeting IMIHM XI & CRC/TR 124 - September 2017

This year‘s 11 th IMIHM meeting is held for the fourth time as a Joint Meeting together with scientists from the CRC TransRegio 124 (“Pathogenic fungi and their human host: Networks of interaction – FungiNet”). This Collaborative Research Centre FungiNet is a network of scientists from Jena and Wuerzburg and is funded by the Deutsche Forschungsgemeinschaft. The Consortium collaborates to better understand complex invasive mycoses by investigating the pathobiology of fungi, the response of the
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Start Date: 7th Sep 2017

End Date: 8th Sep 2017

Event Website: Not specified

Country:  Germany

City: Würzburg

SFB FungiNet: Review Meeting in Würburg
No description specified

Start Date: 9th Feb 2017

End Date: 10th Feb 2017

Event Website: Not specified

Country:  Germany

City: Würzburg

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