Marcela Rojas-Pierce / North Carolina State University
Haustoria are critical feeding structures of many fungal and oomycete pathogens that cause plant diseases. The extrahaustorial membrane (EHM) represents the host-pathogen interface and a critical battleground, but its origin and biogenesis is poorly understood. The broad-spectrum resistance protein RPW8.2 from Arabidopsis is specifically targeted to the EHM where it activates haustorium-focused defenses. By using RPW8.2 and other RPW8 family members as tools, we demonstrated that the EHM is most likely synthesized de novo. Our recent work showed that RPW8.2 is rapidly removed mainly via the vacuole degradation pathway in uninfected cells, but accumulates at the EHM to activate defenses in haustorium-invaded cells. Forward and reverse genetic studies revealed that loss of VTI11, a Qb SNARE at the trans Golgi network compromised RPW8.2's EHM-targeting and its resistance function. Interestingly, in uninfected cells, RPW8.2's vacuole degradation seemed also compromised in the vti11 mutant. Thus, our results suggest that a VTI11-containing SNARE complex may be engaged for both deploying RPW8.2 at the EHM in infected cells and degrading RPW8.2 in the vacuole of uninfected cells. Currently, we are characterizing other SNARE components that work with VTI11 in determining the destiny of RPW8.2-vesicles.