Cu transporter protein CrpF protects against Cu-induced toxicity inFusarium oxysporum

Cu is an essential trace element for cell growth and proliferation. However, excess of Cu accumulation leads to cellular toxicity. Thus, precise and tight regulation of Cu homeostasis processes, including transport, delivery, storage, detoxification, and efflux machineries, is required. Moreover, the maintenance of Cu homeostasis is critical for the survival and virulence of fungal pathogens. Cu homeostasis has been extensively studied in mammals, bacteria, and yeast, but it has not yet been well documented in filamentous fungi. In the present work, we investigated Cu tolerance in the filamentous fungusFusarium oxysporumby analysing the Cu transporter coding genecrpF, previously studied inAspergillus fumigatus. The expression studies demonstrated thatcrpFis upregulated in the presence of Cu and its deletion leads to severe sensitivity to low levels of CuSO(4)inF. oxysporum. Targeted deletion ofcrpFdid not significantly alter the resistance of the fungus to macrophage killing, nor its pathogenic behaviour on the tomato plants. However, the targeted deletion mutant Delta crpFshowed increased virulence in a murine model of systemic infection compared to wild-type strain (wt).