Fig. 6: A simplified model for BcSSP2 action.

Upon B. cinerea infection, WT plants accumulate immune regulator MPK3, which is transported from cytoplasm into nucleus via NPC central barrier phase separation to activate expression of downstream genes essential for plant resistance. To combat plant immunity, B. cinerea (B05.10 wild-type strain) accumulates BcSSP2 and secrets it into the plant cells of the edge area to target plant NPC central barrier (NUP62, NUP58 and NUP54), disrupt their phase separation (NUP62 is representatively indicated), and attenuate NTR-aided nuclear transport of MPK3, thereby suppressing plant defense responses for effective pathogen infection (as indicated by an infected plant) (first panel). When infected by the bcssp2 mutant, the NPC phase separation-mediated defense response of WT plants is not suppressed due to the absence of BcSSP2, which allows efficient nuclear transport of MPK3 essential for plant defense (a healthy plant) (second panel). However, NPC phase separation-mediated plant defense responses are suppressed by the ectopically expressed BcSSP2 in estradiol-treated iBcSSP2 transgenic plants (ES-iBcSSP2), which leads to attenuated plant defense and severe disease symptoms (a susceptible plant) (third panel).