Plants respond to viruses by enhancing the expression of multiple genes that function as regulators or executors of defense programs. Among them, the receptor-like kinase (RLK) BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1) functions as a negative regulator of multiple resistance signaling pathways in Arabidopsis thaliana. BIR1 is transcriptionally upregulated during viral infections in a SA-dependent manner. A previous study from our group suggests that there is an active role of BIR1 in antiviral immunity as knockout bir1-1 mutants have increased resistance to the RNA virus Tobacco rattle virus (TRV). Here, we use a panel of Arabidopsis mutants with single and combined disruptive mutations in genes affecting different BIR family members as well as genes involved in pattern-triggered immunity (PTI) and effectortriggered immunity (ETI) signaling. We found that mutations in all three BIR genes display virusresistance phenotypes that were not rescued by mutations in other BIR1-associated RLKs, as PHYTOALEXIN DEFICIENT 4 (PAD4) or SUPPRESSOR OF BIR1-1 (SOBIR1). In contrast,mutations in ENHANCED DISEASE SUSCEPTIBILITY (EDS1), which is essential for cell death and ETI immunity, increased virus accumulation in Arabidopsis, suggesting that antiviral resistance mostly relies in R-mediated immune responses. We further use a dexamethasone(DEX)-inducible expression system to mimic the activation of BIR1 in the absence of infection or microbial elicitors, and to assess the effects of BIR1 induction on the early immune responses.We found that BIR1 induction has minimal effects on the plant transcriptome, as opposed to BIR1 overexpression or BIR1 depletion, which have constitutive defects in the immune response. We also show that BIR1 induction has negligible effects on the accumulation of reactive oxygen species (ROS) and the defense-hormone ethylene in the presence of canonical microbial PTI elicitors. However, it significantly interferes with the expression of the PTI-marker genes FLG22-INDUCED RECEPTOR-LIKE KINASE 1 (FRK1) and PATHOGENESIS RELATED 1 (PR1) in response to the bacterial peptide flg22. Interestingly, BIR1 induction also interferes with plasmodesmata callose deposition triggered by double-stranded RNA. We propose that BIR1 induction may represent a pathogen-triggered mechanism to modulate plant defenses during infection.

This work was supported by National Research grants RTI2018-096979-B-I00 and PID2021-127982NB-I00 to CL from Ministerio de Ciencia e Innovación (Spain) and UEFEDER,and grant iLINKA20415 to CL from CSIC (Spain).

Peer reviewed

2 p.