Abstract
Mycoparasitic Trichoderma species are applied as biocontrol agents in agriculture to guard plants against fungal diseases. During mycoparasitism, Trichoderma directly interacts with phytopathogenic fungi, preceded by a specific recognition of the host and resulting in its disarming and killing. In various fungal pathogens, including mycoparasites, signalling via heterotrimeric G proteins plays a major role in regulating pathogenicity-related functions. However, the corresponding receptors involved in the recognition of host-derived signals are largely unknown. Functional characterization of Trichoderma atroviride Gpr1 revealed a prominent role of this seven-transmembrane protein of the cAMP-receptor-like family of fungal G-protein-coupled receptors in the antagonistic interaction with the host fungus and governing of mycoparasitism-related processes. Silencing of gpr1 led to an avirulent phenotype accompanied by an inability to attach to host hyphae. Furthermore, gpr1-silenced transformants were unable to respond to the presence of living host fungi with the expression of chitinase- and protease-encoding genes. Addition of exogenous cAMP was able to restore host attachment in gpr1-silenced transformants but could not restore mycoparasitic overgrowth. A search for downstream targets of the signalling pathway(s) involving Gpr1 resulted in the isolation of genes encoding e.g. a member of the cyclin-like superfamily and a small secreted cysteine-rich protein. Although silencing of gpr1 caused defects similar to those of mutants lacking the Tga3 Gα protein, no direct interaction between Gpr1 and Tga3 was observed in a split-ubiquitin two-hybrid assay.
Highlights
The genus Trichoderma includes species that are potent mycoparasites, able to attack and lyse plant pathogens such as Rhizoctonia solani, Botrytis cinerea, Sclerotium sclerotiorum, Pythium spp. and Fusarium spp
We recently identified more than 50 putative G-protein-coupled receptor (GPCR) in the genome of Trichoderma reesei (Brunner et al, 2008) and, based on this analysis, isolated four genes from the mycoparasite Trichoderma atroviride encoding seven-transmembrane receptors of the cAMPreceptor-like (CRL) class
The previously isolated gpr1, gpr2, gpr3 and gpr4 genes and their deduced amino acid sequences were completely consistent with their respective counterparts in the genome database, in which Gpr1 corresponds to protein ID160995, Gpr2 to ID50902, Gpr3 to ID83166 and Gpr4 to ID81233
Summary
The genus Trichoderma includes species that are potent mycoparasites, able to attack and lyse plant pathogens such as Rhizoctonia solani, Botrytis cinerea, Sclerotium sclerotiorum, Pythium spp. and Fusarium spp. 052035 G 2012 SGM Printed in Great Britain Trichoderma as these enzymes degrade the cell wall of the host fungus to enable penetration of the mycoparasite (Hjeljord & Tronsmo, 1998). Glycoproteins (e.g. lectins) located in the host’s cell wall induce coiling of the mycoparasite around host hyphae (Inbar & Chet, 1994). Both secretion of hydrolytic enzymes and host attachment/coiling can be assumed to be induced responses triggered by hostderived molecules. Intracellular signal transduction pathways are considered to regulate the expression of pathogenicity-related genes in response to the host Examination of these pathways in Trichoderma revealed the involvement of heterotrimeric G proteins in sensing of host signals and in activating mycoparasitic host attack
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