Genes involved in coiling and appressorium formation

Trichoderma atroviride has been shown to act as a mycoparasite and is therefore commercially applied as biocontrol agent against a number of plant pathogenic fungi. The mycoparasitic interaction relies on host- recognition and is not merely a contact response. It is thus likely that Trichoderma recognizes multiple signals from the host such as lectins and/or diffusible low molecular-weight substances, which trigger the attack of the host fungus. The mycoparasitic attack is accompanied by morphological changes, like coiling around the host hyphae and the formation of appressorium-like structures, but also by secretion of hydrolytic enzymes and production of secondary metabolites such as antibiotics. In contrast to the current knowledge about the different stages passed through the antagonism of Trichoderma against their fungal hosts, still only little is known about the genes expressed. Furthermore, the information on the impact of diverse plant-pathogenic host fungi on the gene transcription during the mycoparasitic interaction is still insufficient. For this reason, the aim of the presented project is the identification of genes differentially expressed during T. atroviride - host - interactions. These results provide a basis for the elucidation of genes involved in specific steps of the mycoparasitic response especially morphological changes. The strategy embarked on this project to find the genes responsible for coiling is suppression subtractive hybridization in combination with the design of an especially extended microarray for T. atroviride mycoparasitism. An additional and important tool to isolate the respective genes is represented by mutant strains, lacking the gene encoding the T. atroviride mitogen-activated protein kinase (MAPK) Tmk1, since these knockout mutants were characterized by permanent and host-independent coiling around the own hyphae.