Characterization of FgUgtD reveals its impact on cell wall integrity and virulence in Fusarium graminearum, suggesting antifungal target potential.
Fusarium graminearum , the predominant causal agent of Fusarium head blight (FHB) in wheat, severely impacts global food security by reducing crop yields and contaminating grains with health-threatening mycotoxins. Galactofuranose (Galf), a critical cell wall component, is vital for fungal cellular integrity, virulence, and stress tolerance. Notably, the activated form UDP-Galf is synthesized in the cytoplasm but requires translocation to the Golgi lumen, implying the existence of an unidentified transporter. This study identified and characterized FgUgtD, a putative UDP-Galf transporter from F . graminearum belonging to the nucleotide-sugar transporter family. Through subcellular localization, gene knockout, and functional complementation assays, we investigated its role in fungal biology and virulence. FgUgtD localized to the Golgi and endoplasmic reticulum. Its disruption caused severe phenotypic defects: (1) impaired hyphal growth and asexual reproduction, (2) complete loss of ascospore formation, (3) cell wall disorganization with chitin depletion, (4) hypersensitivity to galactose, and (5) > 80% reduction in virulence on wheat and maize—all rescued by genetic complementation. Crucially, the absence of UDP-Galf biosynthesis in plants and animals highlights FgUgtD as a promising antifungal target for controlling FHB.
No takes yet. Share an insight, caveat, or question.
Liu et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: