These phosphorylation sites seem to be important for RipBM contribution to virulence in tomato, reflecting an effector strategy to promote its own stability and contribute to bacterial virulence

This reminds me the treatments with the flg22G/A mutant peptide we did in Sun et al, Science, 2013 (doi.org/10.1126/scie...). That mutation abolishes BAK1 interaction and activation, significantly reduces ROS, but does not affect MAPK activation

Long story short, it seems that AtFLS2, when expressed in N. benthamiana, associates with NbSERKs and mediate a “partial” complex activation that leads to some downstream responses (MAPK, gene expression), but not others (ROS). Eventually, this enhances disease resistance

We did not see any gain of flg22Rso-triggered ROS burst, but…

there was MAPK activation. Surprisingly, what was supposed to be a “negative control”, even WT AtFLS2 expressed in N. benthamiana would confer MAPK activation upon flg22Rso treatment