期刊
MOLECULAR PLANT PATHOLOGY
卷 24, 期 4, 页码 289-301出版社
WILEY
DOI: 10.1111/mpp.13292
关键词
fungal pathogenicity; Fusarium oxysporum; Gtr1; TORC1; Tsc2
This study reveals the critical role of TORC1 signaling in the development and pathogenicity of F. oxysporum. Inactivation of the negative regulator TSC2 leads to inappropriate activation of TORC1, resulting in impaired invasive growth and decreased virulence. These findings suggest new potential targets for the control of fungal infections.
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 signalling under nutrient-limiting conditions. The tsc2 Delta 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 Delta strains was rescued by rapamycin-mediated inhibition of TORC1. Collectively, these results reveal a key role of TORC1 signalling in the development and pathogenicity of F. oxysporum and suggest new potential targets for controlling fungal infections.
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