SnRK2.5-mediated phosphorylation of PIN2 links osmotic stress signaling to auxin-dependent root adaptive growth in Arabidopsis

Zhang, S.; Cui, Z.; Gao, Y.; Liao, Q.; Li, W.; Yuan, S.; Li, Z.; Zhang, X.; Ding, K.; Zhang, W.; Shen, L.; Kudla, J.; Zhang, W.; Zhang, J.; Zhang, Q.

Abstract

The spatiotemporal regulation of polar auxin transport by PIN-FORMED (PIN) efflux carriers is essential for coordinating plant development with environmental cues. However, whether and how osmotic stress signaling affects auxin transport to regulate plant stress adaptation remain largely unclear. In this study, we identify SnRK2.5, an abscisic acid–independent member of the SNF1-related protein kinase family, as a key molecular link between osmotic stress signaling and auxin transport regulation in Arabidopsis. Osmotic stress activates SnRK2.5, which directly phosphorylates PIN2 at Ser237 and Ser259. Genetic and cell biological analyses demonstrate that these phosphorylation events govern PIN2 vesicular trafficking, vacuolar targeting, and auxin transport activity. Disruption of these phosphorylation sites impairs PIN2-dependent auxin redistribution, thereby compromising root tropic responses and reducing osmotic stress tolerance. Our findings uncover a regulatory mechanism by which SnRK2.5-mediated phosphorylation of PIN2 dynamically adjusts auxin flux in response to water availability, representing a critical adaptive strategy that optimizes plant growth under osmotic stress.