A β-1,3-glucanase antagonizes a phase-separating WRKY repressor to confer saline-alkaline tolerance in rice.

Saline-alkaline stress imposes combined ionic and high-pH challenges that severely limit rice productivity, yet the molecular mechanisms linking stress perception to transcriptional reprogramming remain poorly understood. Here, we identify the WRKY transcription factor OsWRKY1 as a central negative regulator of saline-alkaline tolerance in rice. Loss of OsWRKY1 markedly enhances stress tolerance, whereas its overexpression causes hypersensitivity. Using inducible transcriptomics and DAP-seq, we show that OsWRKY1 directly represses genes involved in ion transport, nutrient uptake, osmotic adjustment, and redox homeostasis. Unexpectedly, OsWRKY1 undergoes stress-induced liquid-liquid phase separation (LLPS) in the nucleus, driven by a long intrinsically disordered region (IDR1) that is required for its full repressive activity. Saline-alkaline stress specifically induces the binding of the β-1,3-glucanase OsGH17 to OsWRKY1. OsGH17 directly interacts with IDR1, reduces OsWRKY1 DNA binding, decreases OsWRKY1 condensate formation, and relieves OsWRKY1-mediated transcriptional repression. Genetic epistasis indicates that OsWRKY1 and OsGH17 function in the same pathway in the saline-alkaline stress response, with OsWRKY1 being epistatic to OsGH17. Together, our findings reveal a previously unrecognized mechanism in which a β-1,3-glucanase with a noncanonical regulatory role modulates the behavior of a phase-separating transcriptional repressor and promotes stress-responsive gene expression, providing new insight into plant adaptation to saline-alkaline environments.