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  Section: Molecular Biology of Plant Pathways » Genetic Engineering for Salinity Stress Tolerance
 
 
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The SOS Signal Pathway Controls Adaptation to Hypersalinity

 
     
 

In Arabidopsis, the Ca2+ -dependent sos signaling pathway transduces salt stress to activate the plasma membrane Na+ /H+ antiporter (sos1), which mediates Na+ efflux and homeostasis necessary for salt adaptation (Guo et al., 2001; Shi et al., 2003; Zhu, 2002). Current evidence indicates that the myristoylated Ca2+ - binding protein sos3 activates the sos2 serine/threonine kinase and recruits it to the plasma membrane (Quintero et al., 2002; Talke et al., 2003; Zhu, 2003). An NaClinduced Ca2+ transient is transduced by sos3 leading to the activation of sos2 (Verslues and Bray, 2004; Zhu, 2003). The sos3–sos2 protein kinase complex phosphorylates sos1 resulting in Na +/H+ antiport activity (Quintero et al., 2002; Talke et al., 2003). The sos3–sos2 complex also activates sos1 expression, perhaps through processes that affect sos1 mRNA stability (Shi et al., 2003; Su et al., 2001; Zhu, 2003). The Ca2+ sensor SCaBP5 (sos3 family) and its interacting kinase PKS3 (sos2 family) are components of a negative regulatory circuit that controls ABA signaling through ABI1/2. This regulatory circuit presumably is a negative controller of ABA-induced Ca2+ channel gating and is necessary for Ca2+ oscillations that activate the sos pathway and other signaling required for salt adaptation (Gaxiola et al., 2001). The sensor and remaining Ca2+ perturbation components of the sos pathway, and few downstream targets of the sos pathway, are yet to be identified. sos1 has been implicated to be the Na+ sensor (Zhu, 2003). Besides sos1, only the VSP2 gene has been implicated as a sos pathway target for transcriptional control. Importantly, the affect of the sos pathway on transcription of sos1 and VSP2 indicates that an unknown TF that interacts with a promoter element(s) on sos1 and VSP2 is also activated by the sos pathway.
 
     
 
 
     



     
 
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