Receptor-like kinases BIR1 and BIR3 modulate antiviral resistance by different mechanisms.

BRASSINOSTEROID INSENSITIVE1-ASSOCIATED RECEPTOR KINASE 1 (BAK1)-INTERACTING RECEPTOR-LIKE KINASE (BIR) proteins are negative regulators of cell death and defense against microbes in Arabidopsis thaliana. Here, we demonstrate that the members of the BIR family function as negative regulators of antiviral resistance in Arabidopsis. We show that during tobacco rattle virus (TRV) infection, BIR1 and BIR3 gene expression is antagonistically regulated by salicylic acid and jasmonic acid signaling pathways. BIR1 and BIR3 negatively regulate TRV resistance via distinct mechanisms. Our data indicate that BIR1 modulates antiviral defense through mechanisms that include pattern-triggered immune (PTI) gene expression, plasmodesmata callose deposition alongside yet unidentified defense pathways independent of the receptor-like kinases BAK1 and SUPPRESSOR OF BIR1-1 1 (SOBIR1), or the lipase-like PHYTOALEXIN DEFICIENT 4 (PAD4). BIR3 negatively regulates a pathway that involves BAK1 and ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)/PAD4, suggesting that BIR3 disrupts an immune response similar to effector-triggered immunity (ETI) driven by nucleotide-binding leucine-rich intracellular receptors. This response helps control virus proliferation without causing a hypersensitive reaction. Our findings also reveal that BIR2 represses antiviral defense against TRV, highlighting the conserved function of BIR proteins as pivotal modulators in plant-virus interactions. We propose that the induction of BIR proteins during viral infection helps maintain a balance between defense activation and suppression to prevent viral overaccumulation and plant damage.