The receptor-like kinases BIR1 and BIR3 modulate antiviral resistance by different mechanisms

Abstract

The BAK1-INTERACTING RECEPTOR-LIKE KINASE (BIR) proteins, including BIR1, are negative regulators of cell death and defense in Arabidopsis. Although BIR1 is upregulated during viral infections, its role in virus defense remains unclear. Here, we demonstrate a conserved role for the BIR family as modulators of antiviral resistance in Arabidopsis. During tobacco rattle virus (TRV) infection, BIR gene expression is regulated by antagonistic interactions between salicylic acid (SA) and jasmonic acid (JA) signaling pathways. Genetic evidence shows that BIR1, BIR2, and BIR3 negatively regulate TRV resistance via distinct mechanisms. The antiviral phenotype in bir1-1 mutants is unaffected by mutations in the receptor-like kinases (RLK) BAK1, SOBIR1, or in the lipase-like PAD4. While BIR1 induction partially suppresses PTI marker gene expression, it does not affect early PTI responses such as reactive oxygen species (ROS) production or ethylene accumulation. BIR1 also inhibits plasmodesmata (PD) callose deposition and facilitates virus spread. Our data suggest that BIR1 modulates antiviral defense through mechanisms that include PTI gene expression, PD callose deposition alongside yet unidentified pathways independent of ROS or BAK1, SOBIR1, or PAD4 signaling components. In contrast, BIR3 suppresses an antiviral resistance pathway against TRV that requires BAK1 and the lipases PAD4 and EDS1. Our results suggest that BIR3 controls an NLR-dependent ETI-like response that restricts virus proliferation without triggering a hypersensitive response. These findings highlight the distinct roles of BIR family members in regulating antiviral defense in Arabidopsis.