Pathogens utilize effectors to suppress basal plant defense known as PTI (Pathogen-associated
molecular pattern-triggered immunity). However, our knowledge of PTI suppression
by filamentous plant pathogens, i.e. fungi and oomycetes, remains fragmentary. Previous
work revealed that the co-receptor BAK1/SERK3 contributes to basal immunity against the
potato pathogen Phytophthora infestans. Moreover BAK1/SERK3 is required for the cell
death induced by P. infestans elicitin INF1, a protein with characteristics of PAMPs. The
P. infestans host-translocated RXLR-WY effector AVR3a is known to supress INF1-mediated
cell death by binding the plant E3 ligase CMPG1. In contrast, AVR3aKI-Y147del, a deletion
mutant of the C-terminal tyrosine of AVR3a, fails to bind CMPG1 and does not
suppress INF1-mediated cell death. Here, we studied the extent to which AVR3a and its
variants perturb additional BAK1/SERK3-dependent PTI responses in N. benthamiana
using the elicitor/receptor pair flg22/FLS2 as a model. We found that all tested variants of
AVR3a suppress defense responses triggered by flg22 and reduce internalization of activated
FLS2. Moreover, we discovered that AVR3a associates with the Dynamin-Related
Protein 2 (DRP2), a plant GTPase implicated in receptor-mediated endocytosis. Interestingly,
silencing of DRP2 impaired ligand-induced FLS2 internalization but did not affect
internalization of the growth receptor BRI1. Our results suggest that AVR3a associates
with a key cellular trafficking and membrane-remodeling complex involved in immune receptor-mediated endocytosis. We conclude that AVR3a is a multifunctional effector that
can suppress BAK1/SERK3-mediated immunity through at least two different pathways.