SOBIR1 integrates pathogen recognition and hormonal metabolism in Nicotiana tabacum.

The receptor-like kinase SOBIR1 (SUPPRESSOR OF BIR1) is a core component of immune receptor complexes mediating plant responses to extracellular immunogenic signals. While its role in pattern-triggered immunity is well defined in model species, its broader physiological functions remain largely unexplored. Here, we generated CRISPR-Cas9-derived double knockouts of 2 homeologous SOBIR1 genes in allotetraploid Nicotiana tabacum. The resulting Nt sobir1 double mutants failed to trigger elicitor-induced cell death in response to elicitins from Phytophthora and Pythium spp. but retained an attenuated early reactive oxygen species (ROS) response while lacking sustained ROS accumulation, showing that the transient and sustained ROS outputs differ in their dependence on SOBIR1. Functionally, the mutants showed compromised resistance to Phytophthora parasitica but unaltered responses to Botrytis cinerea and Pseudomonas syringae, pointing to pathogen-specific SOBIR1 roles. Beyond immunity, SOBIR1 appears to interface with developmental signaling modules involving CLAVATA2 and ERECTA-YODA, implicating it in phytohormone signaling, meristem regulation, and cell proliferation. Notably, Nt sobir1 mutants displayed increased hypocotyl cell wall stiffness despite transcriptional upregulation of wall-loosening genes, suggesting compensatory cell wall remodeling and perturbed integrity signaling. Transcriptome and phytohormone profiling revealed tissue-specific expression changes and altered levels of cytokinins, salicylic acid, jasmonic acid, and their conjugates. These findings position SOBIR1 as a multifunctional regulatory hub that links immune perception with phytohormone dynamics and cell wall mechanics in N. tabacum, expanding our understanding of co-receptor signaling plasticity across plant lineages.