SnRK2 kinases sense molecular crowding and form condensates to disrupt ABI1 inhibition.

Abstract

Plants sense and respond to hyperosmotic stress via quick activation of sucrose nonfermenting 1-related protein kinase 2 (SnRK2). Under unstressed conditions, the protein phosphatase type 2C (PP2C) in clade A interact with and inhibit SnRK2s in subgroup III, which are released from the PP2C inhibition via pyrabactin resistance 1-like (PYL) abscisic acid receptors. However, how SnRK2s are released under osmotic stress is unclear. Here, we outline how subgroup I SnRK2s sense molecular crowding to interrupt PP2C-mediated inhibition in plants. Severe hyperosmotic stress triggers condensate formation to activate the subgroup I SnRK2s, which requires their intrinsically disordered region. PP2Cs interact with and inhibit subgroup I SnRK2s, and this interaction is disrupted by phase separation of SnRK2s. The subgroup I SnRK2s are critical for severe osmotic stress responses. Our findings elucidate a mechanism for how macromolecular crowding is sensed in plants and demonstrate that physical separation of signaling molecules can segregate negative regulators to initiate signaling.