Biology subjects

Guzman-Benito, I.

Publications and source records attributed to Guzman-Benito, I..

2 recordsLinked to original sources

bioRxiv2026

Dual regulation of the receptor-like kinase BIR1 involves site-directed transcript cleavage and 5-leader-mediated translational control

In Arabidopsis, receptor-like kinase BRASSINOSTEROID INSENSITIVE1-ASSOCIATED RECEPTOR KINASE 1 (BAK1)-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1) is a negative regulator of plant immunity and cell death. BIR1 was earlier described as a target of epigenetic and post-transcriptional silencing. Degradome analysis mapped predominant mRNA cleavage sites at the 5-untranslated leader region (site A) and the protein-coding sequence (sites B and C). Here, we identified another cleavage site (D) within the BIR1 coding region and investigated the contribution of site-directed mRNA cleavage to BIR1 regulation. Mutations at B, C, and D sites enhanced mRNA stability by impairing transcript cleavage, resulting in increased BIR1 mRNA and protein accumulation. This regulation is disrupted in RNA silencing mutants, supporting a model of cis-directed small interfering RNA (siRNA)-mediated degradation. Cleavage events are highly localized, occurring at a limited number of sites that involve only a few siRNAs. Furthermore, our data reveal a repressive role for the 5-leader in regulating BIR1 translation, potentially mediated by upstream open reading frames (uORFs) and a long non-coding RNA (lncRNA) derived from the natural antisense At4g39838 locus. This lncRNA is complementary to a TCA-rich repeat region encompassing cleavage site A, which may serve as a putative binding site. Together, these findings reveal a multilayered regulatory mechanism that integrates sRNA-mediated cleavage with translational control, with broader implications for the fine-tuning of stress-responsive gene expression during infection.

plant biology↗

bioRxiv2025

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

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.

plant biology↗