BIK1 and ATL31/6 are essential for fucoidan hydrolysate-triggered stomatal closure in Arabidopsis

Immune responses are initiated when pattern recognition receptors (PRRs) detect microbial molecular patterns. One such response is stomatal closure, which restricts the entry of bacterial pathogens into plants. We previously found that the fucoidan enzymatic hydrolysate (FEH) prepared from Sargassum hemiphyllum acts as a non-microbial elicitor, triggering various immune responses in Arabidopsis. However, the signaling mechanisms underlying FEH-triggered immunity remain unexplored. In this study, we show that the anion channel SLAC1 is essential for FEH-induced stomatal immunity in Arabidopsis. However, FEH signaling bypasses CERK1, which perceives chitin and several carbohydrate ligands, as well as BAK1, which functions as a co-receptor for multiple PRRs. Instead, the cytoplasmic kinase BIK1 and ubiquitin ligases ATL31/6 (regulators of BIK1 stability) were essential, with bik1 and atl31/6 mutants showing impaired FEH-induced stomatal closure. Additionally, FEH treatment promotes the degradation of CPK28. Together, these findings reveal a distinct FEH recognition mechanism engaging conserved signaling components (BIK1, ATL31/6) and SLAC1 to activate stomatal immunity, highlighting an unidentified recognition receptor complex for this non-microbial polysaccharide elicitor. This work advances understanding of plant immune diversification and FEH's potential as an agricultural protectant.