Abstract
Mycoparasites, e.g. fungi feeding on other fungi, are prominent within the genus Trichoderma and represent a promising alternative to chemical fungicides for plant disease control. We previously showed that the seven-transmembrane receptor Gpr1 regulates mycelial growth and asexual development and governs mycoparasitism-related processes in Trichoderma atroviride. We now describe the identification of genes being targeted by Gpr1 under mycoparasitic conditions. The identified gene set includes a candidate, sfp2, encoding a protein of the fungal-specific Sur7 superfamily, whose upregulation in T. atroviride upon interaction with a fungal prey is dependent on Gpr1. Sur7 family proteins are typical residents of membrane microdomains such as the membrane compartment of Can1 (MCC)/eisosome in yeast. We found that GFP-labeled Gpr1 and Sfp2 proteins show partly overlapping localization patterns in T. atroviride hyphae, which may point to shared functions and potential interaction during signal perception and endocytosis. Deletion of sfp2 caused heavily altered colony morphology, defects in polarized growth, cell wall integrity and endocytosis, and significantly reduced mycoparasitic activity, whereas sfp2 overexpression enhanced full overgrowth and killing of the prey. Transcriptional activation of a chitinase specific for hyphal growth and network formation and strong downregulation of chitin synthase-encoding genes were observed in Δsfp2. Taken together, these findings imply crucial functions of Sfp2 in hyphal morphogenesis of T. atroviride and its interaction with prey fungi.
Highlights
Fungal pathogens causing plant disease and thereby losses in natural resources pose a common problem in agriculture
The top ten genes that were most robustly identified as differently regulated encode proteins involved in protein synthesis and cell detoxification (Table S1), including a putative RTA1-like protein whose family comprises fungal proteins with multiple transmembrane regions that may be involved in the efflux of xenobiotics[37]; a putative mitochondrial endoribonuclease of the isochorismatase superfamily presumably involved in processing and turnover of mitochondrial RNAs; translation elongation factor 2; a putative monooxygenase involved in ubiquinone biosynthesis; a glutathione S-transferase catalyzing the conjugation of the reduced form of glutathione to xenobiotic substrates for the purpose of detoxification[38]; a GH3 family protein; a mitochondrial/plastidial beta-ketoacyl-carrier protein reductase; and two proteins with unknown function
Several such mycoparasitism-relevant genes were differently regulated in the prey responses of wild type (WT) and mutants, including aspartyl proteases, protein kinases, nonribosomal peptide synthases (NRPSs), methyl- and acetyltransferases, heat shock proteins (HSP), glutathione S-transferases, glutathione synthetase, small secreted cysteine rich proteins (SSCRP), chitinases (GH18), glycoside hydrolase family 16 (GH16) proteins, N-acetylglucosamine transferases, MFS superfamily members, and carbon binding module 50/LysM domain (CBM50) proteins
Summary
Fungal pathogens causing plant disease and thereby losses in natural resources pose a common problem in agriculture. Trichoderma spp. may recognize plant-pathogenic prey fungi via small molecules that are released by the pathogen already before contact These molecules are supposed to bind Trichoderma receptors such as seven-transmembrane G protein-coupled receptors (GPCRs), thereby eliciting a signaling cascade that triggers www.nature.com/scientificreports/. Sur7-containing MCC domains are important for plasma membrane organization, sphingolipid homeostasis, and cell wall morphogenesis (for review see[15]). While S. cerevisiae SUR7 deletion mutants showed reduced sporulation but had no obvious macroscopic growth phenotype[14,20], CaSur[7] of the opportunistic human pathogen Candida albicans promoted proper spatial organization of cell wall synthesis and plasma membrane organization as well avirulence[17,21], and the mutants showed a clear growth phenotype resembling the one caused by the inhibition of β-glucan synthesis[22]. The yeast Sur[7] paralogs Fmp[45], Pun[1], and YNL194C affect the response to nitrogen stress, cell wall integrity, and survival in stationary phase[15,24,25]
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