The Electrophysiological Analysis Of Salt-resistance Regulated By SOS3 In Arabidopsis Thaliana

Soil salinity is one of the most significant abiotic stress for plant agriculture. More recently, the SOS salt stress signaling pathway in Arabidopsis thaliana was determined to have a pivotal regulatory function in salt tolerance, fundamental of which is the control factor of ion homeostasis. The protein SOSl, SOS2, and SOS3 are components of SOS salt stress signaling pathway that controls ion homeostasis and salt tolerance. The elicitor of this pathway is Ca2+, Ca2+ binds to SOS3, which leads to interaction with SOS2, a Ser/Thr protein kinase of 446 amino acids, and activated the kinase. The transcription and post-transcription of SOSl, an putative Na+/H+ antiporter on the membrane is controlled by the SOS3-SOS2 complex. Inaddition to regulating SOSl exchange acitivity, SOS3-SOS2 may regulate other salt tolerance effectors. One such effector might be the Na+ transporter AtHKTl. Recently, research on the sos3/athktl double mutants in Arabidopsis showed functional disruption of AtHKTl was shown to suppress the salt sensitive phenotype of sos3 mutant indicating that wild-type SOS3 may inhibit the activity of AtHKTl as a Na+ influx transporter.But hitherto there is no evidences in electrophysiology about regulation of K+ and Na+ influx by SOS3 protein. Here we analysized the changes of whole cell inward K+ current by using patch-clamp techniques in WT, sos3 and sos3/athktl plants.The data showed that the inward whole cell K+ current in the root protoplasts of both wild-type (SOS3/ATHKT1, ecotype Columbia) and the double mutant (sos3/athkt1) decreased 5 minutes after added 50 mmol / L Na+ to the bath solution. But the inward whole cell K+ current of single mutant (sos3/AtHKTl) increased after the same treatment. It suggest that in the single mutant (sos3/AtHKT1) the increased current most possibly is the Na+ influx, and that the protein AtHKTl is a Na+ influx thransporter which induced the overly salt sensitivity in sos3/AtHKTl. Furthermore, the wild-type protein SOS3 maybe down regulated the protein AtHKTl. Because when both the gene SOS3 and the gene AtHKTl are mutanted in the double mutant (sos3/athkt1) the inward whole cell K+ current decreased.The pharmacology analysis on the increased current in the single mutant (sos3/AtHKT1) indicated that the increased current, possibly contributed by AtHKTl activity, could be inhibited by TTX and Ca2+. It is insensitive to TEA* and have the same selectivity to Li+. The data suggest that the protein AtHKTl perhaps is a Na+-permeable channel. The protein SOS3 down regulated it...