Necrotrophic Mycoparasites and Their Genomes
- Authors: Magnus Karlsson1, Lea Atanasova2, Dan Funck Jensen3, Susanne Zeilinger4
- Editors: Joseph Heitman5, Timothy Y. James6, Pedro W. Crous7
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VIEW AFFILIATIONS HIDE AFFILIATIONSAffiliations: 1: Department of Forest Mycology and Plant Pathology, Uppsala BioCenter, Swedish University of Agricultural Sciences, 75007, Uppsala, Sweden; 2: Institute of Microbiology, University of Innsbruck, 6020 Innsbruck, Austria; 3: Department of Forest Mycology and Plant Pathology, Uppsala BioCenter, Swedish University of Agricultural Sciences, 75007, Uppsala, Sweden; 4: Institute of Microbiology, University of Innsbruck, 6020 Innsbruck, Austria; 5: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710; 6: Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI 48109-1048; 7: CBS-KNAW Fungal Diversity Centre, Royal Dutch Academy of Arts and Sciences, Utrecht, The Netherlands
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Received 15 June 2016 Accepted 11 January 2017 Published 10 March 2017
- Correspondence: Susanne Zeilinger, [email protected]
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Abstract:
Mycoparasitism is a lifestyle where one fungus establishes parasitic interactions with other fungi. Species of the genus Trichoderma together with Clonostachys rosea are among the most studied fungal mycoparasites. They have wide host ranges comprising several plant pathogens and are used for biological control of plant diseases. Trichoderma as well as C. rosea mycoparasites efficiently overgrow and kill their fungal prey by using infection structures and by applying lytic enzymes and toxic metabolites. Most of our knowledge on the putative signals and signaling pathways involved in prey recognition and activation of the mycoparasitic response is derived from studies with Trichoderma. These fungi rely on G-protein signaling, the cAMP pathway, and mitogen-activated protein kinase cascades during growth and development as well as during mycoparasitism. The signals being recognized by the mycoparasite may include surface molecules and surface properties as well as secondary metabolites and other small molecules released from the prey. Their exact nature, however, remains elusive so far. Recent genomics-based studies of mycoparasitic fungi of the order Hypocreales, i.e., Trichoderma species, C. rosea, Tolypocladium ophioglossoides, and Escovopsis weberi, revealed not only several gene families with a mycoparasitism-related expansion of gene paralogue numbers, but also distinct differences between the different mycoparasites. We use this information to illustrate the biological principles and molecular basis of necrotrophic mycoparasitism and compare the mycoparasitic strategies of Trichoderma as a “model” mycoparasite with the behavior and special features of C. rosea, T. ophioglossoides, and E. weberi.
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Citation: Karlsson M, Atanasova L, Jensen D, Zeilinger S. 2017. Necrotrophic Mycoparasites and Their Genomes. Microbiol Spectrum 5(2):FUNK-0016-2016. doi:10.1128/microbiolspec.FUNK-0016-2016.




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References

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Abstract:
Mycoparasitism is a lifestyle where one fungus establishes parasitic interactions with other fungi. Species of the genus Trichoderma together with Clonostachys rosea are among the most studied fungal mycoparasites. They have wide host ranges comprising several plant pathogens and are used for biological control of plant diseases. Trichoderma as well as C. rosea mycoparasites efficiently overgrow and kill their fungal prey by using infection structures and by applying lytic enzymes and toxic metabolites. Most of our knowledge on the putative signals and signaling pathways involved in prey recognition and activation of the mycoparasitic response is derived from studies with Trichoderma. These fungi rely on G-protein signaling, the cAMP pathway, and mitogen-activated protein kinase cascades during growth and development as well as during mycoparasitism. The signals being recognized by the mycoparasite may include surface molecules and surface properties as well as secondary metabolites and other small molecules released from the prey. Their exact nature, however, remains elusive so far. Recent genomics-based studies of mycoparasitic fungi of the order Hypocreales, i.e., Trichoderma species, C. rosea, Tolypocladium ophioglossoides, and Escovopsis weberi, revealed not only several gene families with a mycoparasitism-related expansion of gene paralogue numbers, but also distinct differences between the different mycoparasites. We use this information to illustrate the biological principles and molecular basis of necrotrophic mycoparasitism and compare the mycoparasitic strategies of Trichoderma as a “model” mycoparasite with the behavior and special features of C. rosea, T. ophioglossoides, and E. weberi.

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Figures

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FIGURE 1
Interaction between hyphae of the mycoparasite T. atroviride and the fungal plant pathogen B. cinerea. (A) Before attack of B. cinerea (expressing cytoplasmic GFP) ( 188 ) by T. atroviride, the apical cell wall extends quickly and is only weakly stained with Congo red, a chitin-specific red fluorescent dye (arrows). (B) Mycoparasitic attack induces tip growth arrest in the prey hyphae, leading to tip swelling and increased chitin deposition in the apical cell wall (arrows). (C) Tip lysis of the prey hyphae results in cytoplasmic leakage (asterisks and inset) and use as nutrient substrate by the mycoparasite. GFP, green fluorescent protein. Scale bars: 20 μm (reprinted from FEMS Microbiology Reviews [ 189 ]).
Tables

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TABLE 1
Genome sizes and gene numbers of mycoparasites in the Hypocreales order

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TABLE 2
Predicted number of glycoside hydrolase family 18 genes in mycoparasitic and nonmycoparasitic ascomycete fungi
Supplemental Material
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