Abstract
Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4) is well-known as the causal agent of Fusarium wilt of banana and is one of the most destructive phytopathogens for banana plants. The molecular mechanisms underlying Foc TR4 virulence remain elusive. Here, we demonstrate that a cerato-platanin (CP) protein, FocCP1, functions as a virulence factor that is required by Foc TR4 for penetration and full virulence. The FocCP1 gene was expressed in every condition studied, showing a high transcript level in planta at the early stage of infection. Infiltration of the recombinant FocCP1 protein induced significant cell death and upregulated defence-related gene expression. FocCP1 knock-out strains showed a significant decrease in aerial growth rather than aqueous growth, which is reminiscent of hydrophobins. Furthermore, deletion of FocCP1 significantly reduced virulence and dramatically reduced infective growth in banana roots, likely resulting from a defective penetration ability. Taken together, the results of this study provide novel insight into the function of the recently identified FocCP1 as a virulence factor in Foc TR4.
Highlights
Fusarium oxysporum f. sp. cubense (Foc), a soil-borne hyphomycete, causes the most destructive disease to bananas
We report FocCP1 in Foc tropical race 4 (TR4), which contributes to the penetration process and virulence, as a knock-out mutant, showing reduced growth in banana plants
Based on the published Foc II5 genome sequence, more than 500 effectors are predicted to be secreted into host tissue
Summary
Fusarium oxysporum f. sp. cubense (Foc), a soil-borne hyphomycete, causes the most destructive disease to bananas. CP proteins have been shown to act as virulence factors or elicitors (acting as PAMPs) of the plant defence response. We report FocCP1 in Foc TR4, which contributes to the penetration process and virulence, as a knock-out mutant, showing reduced growth in banana plants. Results from infiltration of a recombinant FocCP1 protein into banana leaves indicate that the FocCP1 protein may function as a virulence factor in Foc TR4 pathogenesis. These findings improve our understanding of the molecular mechanism of Foc TR4 in disease development, and provide an important experimental basis for virulence research in Foc TR4
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