Histidinol-Phosphate Phosphatase FoHis2 Is Essential for Growth, Stress Responses, and Full Virulence in Fusarium oxysporum f. sp. cubense

Résumé fourni par la source

Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), is a destructive vascular disease that seriously threatens global banana production. To investigate the contribution of histidine metabolism to Foc growth and pathogenicity, we functionally characterized FoHis2, a putative histidinol-phosphate phosphatase in Foc race 4 (Foc4). Targeted deletion of FoHis2 severely compromised histidine prototrophy, with the ΔFoHis2 mutant growing slowly on potato dextrose agar and even more slowly on minimal medium (MM, no histidine added). Exogenous histidine fully restored the mutant growth to wild-type (WT) levels, whereas histidinol supplementation rescued the colony size but not the reduced aerial mycelium formation. The ΔFoHis2 mutant exhibited markedly reduced vegetative growth and hyphal branching, and increased sensitivity to elevated H2O2 concentrations, compared with the WT strain. Consistent with the oxidative stress phenotype, peroxisome-associated genes were down-regulated in the ΔFoHis2 mutant. FoHis2 was dispensable for conidiation, cell wall integrity, and fusaric acid and beauvericin biosynthesis. Pathogenicity assays showed that the deletion of FoHis2 severely compromised cellophane penetration and greatly reduced disease incidence and severity on Cavendish banana plantlets, whereas genetic complementation restored the WT phenotypes. These results indicate that FoHis2-mediated histidine biosynthesis is essential for metabolic homeostasis, stress adaptation, and full virulence in Foc4, and highlight histidine metabolism as a potential target for controlling Fusarium wilt in banana.

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