Pathogens use effector proteins to manipulate their hosts. During infection of tomato, the fungus Fusarium oxysporum secretes the effectors Avr2 and Six5. Whereas Avr2 suffices to trigger I-2-mediated cell death in heterologous systems, both effectors are required for I-2-mediated disease resistance in tomato. How Six5 participates in triggering resistance is unknown. Using bimolecular fluorescence complementation assays we found that Avr2 and Six5 interact at plasmodesmata. Single-cell transformation revealed that a 2xRFP marker protein and Avr2-GFP only move to neighboring cells in the presence of Six5. Six5 alone does not alter plasmodesmatal transduction as 2xRFP was only translocated in the presence of both effectors. In SIX5-expressing transgenic plants, the distribution of virally expressed Avr2-GFP, and subsequent onset of I-2-mediated cell death, differed from that in wild-type tomato. Taken together, our data show that in the presence of Six5, Avr2 moves from cell to cell, which in susceptible plants contributes to virulence, but in I-2 containing plants induces resistance. Plasmodesmata are gated junctions regulating symplastic transport between adjacent plant cells. Two secreted proteins from the tomato pathogen Fusarium oxysporum were found to manipulate plasmodesmatal selectivity. This manipulation allows the proteins to move from one cell to neighboring cells to suppress immune responses, signifying a new mechanism of host manipulation by fungal pathogens.
Cao, L., Blekemolen, M. C., Tintor, N., Cornelissen, B. J. C., & Takken, F. L. W. (2018). The Fusarium oxysporum Avr2-Six5 Effector Pair Alters Plasmodesmatal Exclusion Selectivity to Facilitate Cell-to-Cell Movement of Avr2. Molecular Plant, 11(5), 691–705. https://doi.org/10.1016/j.molp.2018.02.011