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

Hindawi Publishing Corporation Journal of Signal Transduction Volume 2010, Article ID 123126, 8 pages doi:10.1155/2010/123126 Review Article How a Mycoparasite Employs G-Protein Signaling: Using the Example of Trichoderma Markus Omann and Susanne Zeilinger 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 Correspondence should be addressed to Markus Omann, omann@mail.tuwien.ac.at Received 20 May 2010; Revised 6 July 2010; Accepted 20 July 2010 Academic Editor: Terry Hebert Copyright © 2010 M. Omann and S. 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 Gα subunits and G-protein-coupled receptors were recently shown to play crucial roles