The siderophore biosynthetic gene SID1, but not the ferroxidase gene FET3, is required for full Fusarium graminearum virulence.

SUMMARY: To acquire iron from plant hosts, fungal pathogens have evolved at least two pathways for iron uptake. One system is hinged on the secretion and subsequent uptake of low-molecular-weight iron chelators termed siderophores, while the other uses cell-surface reductases to solubilize ferric iron by reducing it to ferrous iron for uptake. We identified five iron uptake-related genes from the head blight pathogen Fusarium graminearum and showed that they were transcribed in response to iron limitation. To examine the relative contribution of the reductive and siderophore pathways of iron uptake, we created mutants disrupted at the ferroxidase gene FET3 (Deltafet3) or the siderophore biosynthetic gene SID1 (Deltasid1). The Deltafet3 mutants produced wild-type amounts of siderophores and grew at the same rate as the wild-type under iron limitation, but accumulated high levels of free intracellular iron. The Deltasid1 mutants did not produce siderophores and grew slowly under low iron conditions. Transcription of the iron uptake-related genes was induced in the Deltasid1 mutant regardless of the growth medium iron content, whereas these genes were transcribed normally in the Deltafet3 mutant. Finally, the Deltasid1 mutants could infect single, inoculated spikelets, but were unable to spread from spikelet-to-spikelet through the rachises of wheat spikes, while the Deltafet3 mutants behaved as wild-type throughout infection. Together, our data suggest that siderophore-mediated iron uptake is the major pathway of cellular iron uptake and is required for full virulence in F. graminearum.