News

The Final ImResFun Scientific Conference of the EC-funded Marie-Curie Initial Training Network ImResFun is now announced.

Publication: Candidalysin is a fungal peptide toxin critical for mucosal infection

ITN Practical Course "C2a", Barcelona, Spain (May 10-15, 2015)

ITN Meeting, La Colle sur Loup, France (May 16, 2015)

HPF2015, La Colle sur Loup, France (May 16-22, 2015)

ITN Practical Course "S3" & "C3", Madrid, Spain (July 6-10, 2015)

ITN Mid-Term Review Meeting, Vienna, Austria (November 3, 2015)

ITN Practical Course "S5" & "C5", Tübingen, Germany (May 9-11, 2016)

ITN Lecture Course "S4" & "C4", Szeged, Hungary (July 2-8, 2016)

ITN Practical Course "S6" & "C6", Göttingen, Germany (October 26-28, 2016)

ITN Symposium "S7" & Final Consortium Meeting, Innsbruck, Austria (January 28-30, 2017)

 

Name & Address

Karl Kuchler - Portrait

Karl KuchlerProfessor of Molecular GeneticsCoordinator ImResFun
Medical University Vienna, Max F. Perutz Laboratories
Department of Medical Biochemistry, Campus Vienna Biocenter
Dr. Bohr-Gasse 9/2; A-1030 - Vienna, Austria
Phone: +43-1-4277-61807 FAX: +43-1-4277-9618
e-mail:
Web: http://www.mfpl.ac.at/index.php?cid=77 & http://www.cdl.univie.ac.at/

ESR-MUW Project: (Start November/December 2013)

Genomic adaptations in Candida spp during host colonization

The ESR will study the genetic and genomic adaptations occurring during host niche colonization by Candida spp (i.e. organ-specific) and/or and genes implicated in host dissemination exploiting infection models in vitro / in vivo. Fungal dissemination routes will be studied exploiting infections in mouse animal models and gene deletion approaches. RNA-Seq approaches on infected organs will identify genetic alterations in fungal pathogens and hosts.

ER-MUW Project: (Start January / February 2014)

Host response in innate immune cells and mice invaded by Candida spp

This ER will test the hypothesis that the host signaling immune response drives sepsis-related signaling networks, and activates the recruitment of inflammatory immune cells migration (MPHs). Dual-RNA-Seq in vivo will identify / predict interspecies networks. RNA-Seq of primary innate immune cells (macrophages / dendritic cells, PBMCs) and animal models shall identify genetic alterations in the host and pathogen and proteomics will identify signaling networks activated during host dissemination.

Main Research Interests

Our research interests focus on host-fungus relationships. Hence, my group uses genomics methodologies necessary for studies aimed at a better understanding of host-pathogen interactions and drug resistance in prevalent human fungal pathogens such as Candida spp. The aim is to improve our understanding of the molecular mechanisms underlying fungal virulence. Most if not all host-pathogen interactions are characterized by highly dynamic and interdependent relationships due to alternating attack and defense mechanisms. Thus, we decipher fungal virulence by studying the simultaneous molecular processes occuring both in the pathogen and in its host. Our work stretches from functional and mechanistic studies on single genes and signaling pathways to genome-wide approaches through quantitative transcriptomics, functional genomics and/or reverse-genetics. Finally, interdisciplinary systems biology approaches enable us to predict and identify gene regulatory networks modulating the molecular cross-talk of signaling pathways in fungal pathogen-host interactions. The major goal is to unravel the molecular basis of fungal virulence and host immune response, including a better understanding of host tolerogenic mechanisms, which enable microbial pathogens to evade immune surveillance. As for fungal pathogens, we: i) identify fungal virulence and genes implicated in antifungal resistance, ii) decipher the role of histone-modificating enzymes such as histone deacetylases / histone acetyl transferases (HDAC/HAT) in morphogenetic switching or cell fate determination, iii) study the genetic and genomic adaptation processes occurring in fungal pathogens during specific host niche colonization, and On the host immune signaling response, we: (i) study the signaling mechanisms in primary innate immune cells, as well as in mouse models infected with fungal pathogens, (ii) the signaling cross-talk of adaptive and innate immunity during immune surveillance, (iii) the signaling mechanisms by which innate phagocytes provide instructions for the adaptive immune response, but also how signaling drives the recruitment of inflammatory phagocytes and controls the outcome of fungal infections.

Selected Recent Publications

Hnisz, D., O. Majer, I.E. Frohner, V. Komnenovic, & K. Kuchler (2010). The Set3/Hos2 histone deacetylase complex attenuates cAMP/PKA signaling to regulate morphogenesis and virulence of C. albicans. PLoS Pathogens 13: e1000889doi: 10.1371

Tierney, L., L. Rizzetto, D. Cavalieri* & K. Kuchler* (2012). Systems biology of host-fungus interactions: turning complexity into simplicity? Curr Opin Microbiol. 15: 440-446

Majer, O., Bourgeois, C., F. Zwolanek, M. Mack, C. Lassing, D. Kerjaschki, M. Müller & K. Kuchler (2012). Type I interferon signaling promotes fatal immunopathology through the recruitment of inflammatory monocytes and neutrophils. PLoS Pathogens 8: e1002811