Bax inhibitor-1 confers resistance to Phytophthora parasitica and is antagonized by RTP1 in Arabidopsis.

Abstract

Plant immunity is closely intertwined with endoplasmic reticulum (ER) stress and regulated cell death. Here, we identify the ER-localized cell death regulator Bax Inhibitor-1 (BI-1) as a critical executor of resistance against Phytophthora parasitica in Arabidopsis, whose activity is antagonized by the susceptibility factor RTP1. RTP1 negatively modulates resistance to P. parasitica via ER stress and cell death regulation, yet its downstream coordinators remain unclear. We show that BI-1 expression is significantly elevated in rtp1 mutants during early colonization. Cell viability assays reveal BI-1 is essential for RTP1-mediated cell death suppression, as rtp1 bi-1 double mutants exhibit restored cell death. Pathogenicity assays demonstrate BI-1 confers resistance required for the rtp1-mediated immunity: rtp1 bi-1 mutants show increased susceptibility, reduced expression of ER stress-responsive immune genes (WRKY33, CBP60g, MYB51) and PR1, and abolished flg22-triggered ROS burst. Mechanistically, RTP1 interacts with BI-1 and reduces its protein accumulation through a proteasome-independent pathway, thereby antagonizing BI-1 function. Conversely, activated forms of ER stress transducers bZIP60 and bZIP28 bind and co-activate the BI-1 promoter. Collectively, BI-1 serves as a key node in ER stress-associated immunity, post-translationally antagonized by RTP1 and transcriptionally driven by bZIP60/bZIP28. This study establishes the RTP1-BI-1 module as a pivotal interface linking ER stress perception to immune execution, offering a refined framework for engineering broad-spectrum disease resistance in crops.