Are1-mediated nitrogen metabolism is associated with iron regulation in the mycoparasite Trichoderma atroviride.

Trichoderma atroviride is a mycoparasitic fungus with antagonistic activity against fungal pathogens and is used as a pathogen control agent alternative to synthetic fungicides. Sensing nutrient availability in the environment and adjusting metabolism for optimal growth, development and reproduction is essential for adaptability and is relevant to its mycoparasitic activity. During mycoparasitism, secondary metabolites are produced to weaken the fungal prey and support the attack.

The TOR kinase pathway is relevant for nitrogen signaling and antagonism of the mycoparasite Trichoderma atroviride.

Trichoderma atroviride (Ascomycota, Sordariomycetes) is a well-known mycoparasite applied for protecting plants against fungal pathogens. Its mycoparasitic activity involves processes shared with plant and human pathogenic fungi such as the production of cell wall degrading enzymes and secondary metabolites and is tightly regulated by environmental cues. In eukaryotes, the conserved Target of Rapamycin (TOR) kinase serves as a central regulator of cellular growth in response to nutrient availability.