6/1/2023 0 Comments Spike growth 5eIn summary, we systemically demonstrated that FgTem1 and its GAP FgBub2-FgBfa1 complex are required for fungal development and pathogenicity in F. Double deletion of FgBUB2/FgBFA1 genes showed that FgBUB2 and FgBFA1 have little functional redundancy in F. Deletion of FgBUB2 and FgBFA1 genes caused fewer perithecia and immature asci formations, and dramatically down-regulated trichothecene biosynthesis (TRI) gene expressions. We further demonstrated that a direct interaction exists between FgBub2 and FgBfa1 which crucially promotes conidiation, pathogenicity and DON production, and negatively regulates septum formation and nuclear division in F. The cell cycle arrest protein FgBub2-FgBfa1 complex was shown to act as the GTPase-activating protein (GAP) for FgTem1. The septins FgCdc10 and FgCdc11 were demonstrated to interact with the dominant negative form of FgTem1, and FgCdc11 was found to regulate the localization of FgTem1. Furthermore, the regulatory mechanisms of FgTem1 have been further investigated by high-throughput co-immunoprecipitation and genetic strategies. ![]() FgTem1 localizes to both the inner nuclear periphery and the spindle pole bodies, and negatively regulates mitotic exit in F. graminearum pathogenicity and functions in regulating the formation of infection structures and invasive hyphal growth on wheat spikelets and wheat coleoptiles, but plays only little roles in vegetative growth and conidiation of the phytopathogen. In this study, we found that a small GTPase FgTem1 plays an important role in F. graminearum infects wheat spikelets and colonizes the entire head by growing through the rachis node at the bottom of each spikelet. ![]() The mitotic exit is a key step in cell cycle, but the mechanism of mitotic exit network in the wheat head blight fungus Fusarium graminearum remains unclear.
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