Schematic Representation of Arabidopsis Nonhost Resistance to Bgh.
After germination of spores (Sp), formation of appressoria (Ap), and breaching of the host cell wall (CW) by the fungal penetration peg (Pp), ∼90% of penetrations are stopped in cell wall extensions called papillae (Pa). This resistance is dependent on unidentified cargo molecules (green circles) delivered by a PEN1-mediated vesicle (Ves)–based secretion system and on postulated toxin(s) (dark blue circles) synthesized in peroxisomes (Per) in a PEN2-mediated pathway and delivered by a PEN3-encoded ABC transporter in the plasma membrane (PM) to the apoplast and pathogen invasion site. These events are components of prehaustorial resistance. The activation of the dynamic prehaustorial resistance, dependent on cytoskeleton function, may be induced by mechanical or chemical signals resulting from cell wall penetration and/or PAMPs (yellow circles) produced by the pathogen and detected by host PAMP receptors (PAMP-R). Approximately 10% of infections (increased to ∼30 to 90% in pen1, pen2, and pen3 single and double mutants) form haustoria (H) and are stopped (post-haustorial resistance) by basal resistance possibly contributed to by PEN2 pathway products (dark blue circles) and hypersensitive host cell death (HR) dependent on EDS1, SAG101, and PAD4. Because these genes and the HR are also associated with gene-for-gene R genes, it is possible that R proteins could also function to perceive effector molecules (light blue circles) secreted by Bgh haustoria.