The root invading pathogen Fusarium oxysporum targets pattern-triggered immunity using both cytoplasmic and apoplastic effectors

- Plant pathogens use effector proteins to promote host colonization. The mode of action of effectors from root invading pathogens, such as Fusarium oxysporum (Fo), is poorly understood. Here, we investigated whether Fo effectors suppress pattern-triggered immunity (PTI), and whether they enter host cells during infection.
- Eight candidate effectors of an Arabidopsis-infecting Fo strain were expressed with and without signal peptide in Nicotiana benthamiana and their effect on flg22- and chitin-triggered ROS burst was monitored. To detect uptake, effector biotinylation by an intracellular Arabidopsis-produced biotin ligase was examined following root infection.
- Four effectors suppressed PTI signaling; two act intracellularly and two apoplastically. Heterologous expression of a PTI-suppressing effector in Arabidopsis enhanced bacterial susceptibility. Consistent with an intracellular activity, host cell uptake of five effectors, but not of the apoplastically acting ones, was detected in Fo infected Arabidopsis roots.
- Multiple Fo effectors target PTI signaling, uncovering a surprising overlap in infection strategies between foliar- and root pathogens. Extracellular targeting of flg22 signaling by a microbial effector provides a new mechanism on how plant pathogens manipulate their host. Effector translocation appears independent of protein size, charge, presence of conserved motifs or the promoter driving its expression.