Table of Contents
Journal of Signal Transduction
Volume 2010 (2010), Article ID 123126, 8 pages
Review Article

How a Mycoparasite Employs G-Protein Signaling: Using the Example of Trichoderma

Research Area of Gene Technology and Applied Biochemistry, Working Group Molecular Biochemistry of Fungi, Institute for Chemical Engineering, Vienna University of Technology, Getreidemarkt 9, 1060 Vienna, Austria

Received 20 May 2010; Revised 6 July 2010; Accepted 20 July 2010

Academic Editor: Terry Hebert

Copyright © 2010 Markus Omann and Susanne Zeilinger. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mycoparasitic Trichoderma spp. act as potent biocontrol agents against a number of plant pathogenic fungi, whereupon the mycoparasitic attack includes host recognition followed by infection structure formation and secretion of lytic enzymes and antifungal metabolites leading to the host's death. Host-derived signals are suggested to be recognized by receptors located on the mycoparasite's cell surface eliciting an internal signal transduction cascade which results in the transcription of mycoparasitism-relevant genes. Heterotrimeric G proteins of fungi transmit signals originating from G-protein-coupled receptors mainly to the cAMP and the MAP kinase pathways resulting in regulation of downstream effectors. Components of the G-protein signaling machinery such as G š›¼ subunits and G-protein-coupled receptors were recently shown to play crucial roles in Trichoderma mycoparasitism as they govern processes such as the production of extracellular cell wall lytic enzymes, the secretion of antifungal metabolites, and the formation of infection structures.