A key feature of innate immunity is the ability to recognize and respond to potential pathogens in a highly sensitive and specific manner. In plants, the first layer of defense is induced after recognition by pattern recognition receptors of microbe-associated molecular patterns. This recognition elicits a defense program known as pattern-triggered immunity. Pathogen entry into host tissue is a critical early step in causing infection. For foliar bacterial pathogens, natural surface openings such as stomata, are important entry sites. Stomata in contact with bacteria rapidly close and can thus restrict bacterial entry into leaves. The molecular mechanisms regulating stomatal closure upon pathogen perception are not yet well-understood. Plant lectin receptor kinases are thought to play crucial roles during development and in the adaptive response to various stresses. Although the function of most plant lectin receptor kinases is still not clear, a role for this kinase family in plant innate immunity is emerging. Here, we summarize recent progresses in the identification of lectin receptor kinases involved in plant innate immunity. We also discuss the role of lectin receptor kinases in stomatal innate immunity signaling.

SIF2 is critical for Arabidopsis (Arabidopsis thaliana) resistance to bacteria by regulating stomatal immunity, belongs to the FLS2/BAK1 immunity receptor compl

Epigenetic modifications involve complex and sophisticated control over chromatin states and DNA methylation patterns, which are important for stress tolerance in plants. While the identification of epigenetic modulating enzymes keeps growing, such as MET1, for CG methylation; CMT3, DRM2, DRM3 for CHH methylation; and IBM1, SUVH4 for CHG methylation; the molecular roles of these regulators in specific physiological functions remain obscure. In a mutant screen, we identified IBM1 as a new player in plant immunity. The ibm1 mutants were hyper-susceptible to hemi-biotrophic bacteria Pseudomonas syringae. Accordingly, bacteria-induced up-regulation of PR1, PR2, and FRK1 defense markers was abolished in ibm1 mutants. Consistently, at the chromatin level, these defense marker genes showed enrichment of the inactivation mark, H3K9me2; while the activation mark H3K4me3 was reduced in ibm1 mutants. Immunoprecipitation of associated chromatin further demonstrated that IBM1 binds directly to the gene body of PR1, PR2, and FRK1. Taken together, these data suggest that IBM1 plays a critical role in modulating Arabidopsis immunity through direct regulation of defense gene expression. Notably, IBM1 maintains a permissive chromatin environment to ensure proper induction of defense genes under some biotic stress.