Constitutive activation of TORC1 signaling attenuates virulence in the cross-kingdom fungal pathogen Fusarium oxysporum

• Published in: bioRxiv
• Main Authors: Navarro-Velasco, Gesabel Yaneth, Antonio Di Pietro, López-Berges, Manuel S
• Format: Paper
• Language: English
• Published: Cold Spring Harbor Cold Spring Harbor Laboratory Press 08.08.2022
• Subjects: Cell walls; Fusarium oxysporum; Heat resistance; High temperature; Mutants; Nitrogen sources; Nutrient status; Pathogenicity; Pathogens; Rapamycin; TOR protein; Tuberous sclerosis; Tuberous Sclerosis Complex 2; Virulence; Wilt
• DOI: 10.1101/2022.08.08.503127

The filamentous fungus Fusarium oxysporum causes vascular wilt disease in a wide range of plant species and opportunistic infections in humans. Previous work suggested that invasive growth in this pathogen is controlled by environmental cues such as pH and nutrient status. Here we investigated the role of Target Of Rapamycin Complex 1 (TORC1), a global regulator of eukaryotic cell growth and development. Inactivation of the negative regulator Tuberous Sclerosis Complex 2 (Tsc2), but not constitutive activation of the positive regulator Gtr1, in F. oxysporum resulted in inappropriate activation of TORC1 signaling under nutrient limiting conditions. The tsc2 Δ mutants showed reduced colony growth on minimal medium with different nitrogen sources and increased sensitivity to cell wall or high temperature stress. Furthermore, these mutants were impaired in invasive hyphal growth across cellophane membranes and exhibited a marked decrease in virulence, both on tomato plants and on the invertebrate animal host Galleria mellonella. Importantly, invasive hyphal growth in tsc2 Δ strains was rescued by rapamycin-mediated inhibition of TORC1. Collectively, these results reveal a key role of TORC1 signaling in development and pathogenicity of F. oxysporum and suggest new potential targets for controlling fungal infections. Competing Interest Statement The authors have declared no competing interest.