拟南芥
拟南芥
生物
化学
细胞生物学
遗传学
基因
突变体
作者
Francisco M. Gámez-Arjona,Hee Jin Park,Elena Gómez García,Rashid Aman,Irène Villalta,Natalia Raddatz,Raúl Carranco,Akhtar Ali,Zahir Ali,Shah Zareen,Anna De Luca,Eduardo O. Leidi,Miguel Daniel-Mozo,Zheng‐Yi Xu,Armando Albert,Woe‐Yeon Kim,José M. Pardo,Clara Sánchez-Rodríguez,Dae‐Jin Yun,Francisco J. Quintero
标识
DOI:10.1073/pnas.2320657121
摘要
To control net sodium (Na + ) uptake, Arabidopsis plants utilize the plasma membrane (PM) Na + /H + antiporter SOS1 to achieve Na + efflux at the root and Na + loading into the xylem, and the channel-like HKT1;1 protein that mediates the reverse flux of Na + unloading off the xylem. Together, these opposing transport systems govern the partition of Na + within the plant yet they must be finely co-regulated to prevent a futile cycle of xylem loading and unloading. Here, we show that the Arabidopsis SOS3 protein acts as the molecular switch governing these Na + fluxes by favoring the recruitment of SOS1 to the PM and its subsequent activation by the SOS2/SOS3 kinase complex under salt stress, while commanding HKT1;1 protein degradation upon acute sodic stress. SOS3 achieves this role by direct and SOS2-independent binding to previously unrecognized functional domains of SOS1 and HKT1;1. These results indicate that roots first retain moderate amounts of salts to facilitate osmoregulation, yet when sodicity exceeds a set point, SOS3-dependent HKT1;1 degradation switches the balance toward Na + export out of the root. Thus, SOS3 functionally links and co-regulates the two major Na + transport systems operating in vascular plants controlling plant tolerance to salinity.
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