Plant endomembrane system in plant-microbe interaction: favorite target of pathogen and major venue for plant immunity

In plant-pathogen interactions, pathogens secrete small proteins, broadly termed effectors, into host plant cells. Effectors are diverse and interact with various host proteins, manipulating key biological processes to suppress plant defenses and facilitate successful colonization. In response, plant cytoplasmic receptors (NLRs) recognize corresponding effector proteins, triggering robust immunity associated with hypersensitive response-programmed cell death (HR-PCD). 

Several effectors target the plant endomembrane system, highlighting its critical role in plant defense. Here, we present findings on two RXLR effectors from Phytophthora species, which interact with key proteins involved in plant vesicle trafficking, leading to distinct outcomes in plant immunity. The effector Pc12, secreted by Phytophthora capsici, directly interacts with Rab13-2, a protein primarily localized to the ER and Golgi apparatus. Pc12 inhibits Rab13-2 dynamics at the Golgi, perturbing the localization of ER-resident proteins and confining secretory proteins within the ER, ultimately inducing necrotic cell death. Conversely, AvrVnt1, an effector from Phytophthora infestans, the causal agent of potato late blight, is recognized by the potato NLR Rpi-vnt1 from Solanum venturii, triggering HR-PCD. AvrVnt1 exhibits multiple localizations within plant cells, including the cytoplasm, nucleus, and plasma membrane (PM). Our findings indicate that the PM-localized AvrVnt1 is critical for initiating HR-PCD. Furthermore, immunoprecipitation coupled with mass spectrometry identified DRP1 as a novel interacting protein of AvrVnt1. DRP1, essential for endocytosis, plays a key role in plant defense by mediating the trafficking of PM-resident pathogen recognition receptors and facilitating reactive oxygen species (ROS) bursts. 

Together, these findings illustrate the distinct yet critical involvement of endomembrane system employed by Pc12 and AvrVnt1 to modulate plant immunity—one by subverting vesicle trafficking to suppress plant defense and the other by leveraging it to enhance immune responses. These insights advance our understanding of how pathogens target vesicle trafficking and the endomembrane system to influence the outcome of plant-pathogen interactions.