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

Fusarium wilt of banana, caused by <i>Fusarium oxysporum</i> f. sp. <i>cubense</i> (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 <i>FoHis2</i> severely compromised histidine prototrophy, with the Δ<i>FoHis2</i> 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 Δ<i>FoHis2</i> 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 Δ<i>FoHis2</i> mutant. FoHis2 was dispensable for conidiation, cell wall integrity, and fusaric acid and beauvericin biosynthesis. Pathogenicity assays showed that the deletion of <i>FoHis2</i> 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.