Applied and Environmental Microbiology (2019) 85 (2 - e01825-18)

Karina Atriztán-Hernández, Abigail Moreno-Pedraza, Robert Winkler, Therese Markow and Alfredo Herrera-Estrella (2019)
Trichoderma atroviride from predator to prey: Role of the mitogen-activated protein kinase Tmk3 in fungal chemical defense against fungivory by Drosophila melanogaster larvae
Applied and Environmental Microbiology 85 (2 - e01825-18)
Abstract: The response to injury represents an important strategy for animals and plants to survive mechanical damage and predation. Plants respond to injury by activating a defense response that includes the production of an important variety of compounds that help them withstand predator attack and recover from mechanical injury (MI). Similarly, the filamentous fungus Trichoderma atroviride responds to MI by strongly modifying its transcriptional profile and producing asexual reproduction structures (conidia). Here, we analyzed whether the response to MI in T. atroviride is related to a possible predator defense mechanism from a metabolic perspective. We found that the production of specific groups of secondary metabolites increases in response to MI but is reduced after fungivory by Drosophila melanogaster larvae. We further show that fungivory results in repression of the expression of genes putatively involved in the regulation of secondary metabolite production in T. atroviride. Activation of secondary metabolite production appears to depend on the mitogen-activated protein kinase (MAPK) Tmk3. Interestingly, D. melanogaster larvae preferred to feed on a tmk3 gene replacement mutant rather than on the wild-type strain. Consumption of the mutant strain, however, resulted in increased larval mortality.
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Research topic(s) for pests/diseases/weeds:
biocontrol - natural enemies
Research topic(s) for beneficials or antagonists:
general biology - morphology - evolution
molecular biology - genes

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Pest and/or beneficial records:

Beneficial	Pest/Disease/Weed	Crop/Product	Country	Quarant.
Trichoderma atroviride (antagonist)