The Salt Overly Sensitive (SOS) Pathway: Established and Emerging Roles

Abstract

Soil salinity is a growing problem around the world with special relevance in farmlands. The ability to sense and respond to environmental stimuli is among the most fundamental processes that enable plants to survive. At the cellular level, the Salt Overly Sensitive (SOS) signaling pathway that comprises SOS3, SOS2, and SOS1 has been proposed to mediate cellular signaling under salt stress, to maintain ion homeostasis. Less well known is how cellularly heterogenous organs couple the salt signals to homeostasis maintenance of different types of cells and to appropriate growth of the entire organ and plant. Recent evidence strongly indicates that different regulatory mechanisms are adopted by roots and shoots in response to salt stress. Several reports have stated that, in roots, the SOS proteins may have novel roles in addition to their functions in sodium homeostasis. SOS3 plays a critical role in plastic development of lateral roots through modulation of auxin gradients and maxima in roots under mild salt conditions. The SOS proteins also play a role in the dynamics of cytoskeleton under stress. These results imply a high complexity of the regulatory networks involved in plant response to salinity. This review focuses on the emerging complexity of the SOS signaling and SOS protein functions, and highlights recent understanding on how the SOS proteins contribute to different responses to salt stress besides ion homeostasis.

Cell-Type-Specific H+-ATPase Activity in Root Tissues Enables K+ Retention and Mediates Acclimation of Barley (Hordeum vulgare) to Salinity Stress

“…Physiologically, plant adaptive responses to salinity can be grouped into four major categories: (1) dealing with the osmotic component of salt stress; (2) handling toxic Na + and Cl 2 ions; (3) detoxifying reactive oxygen species (ROS) produced in plant tissues under saline conditions; and (4) mediating cytosolic K + homeostasis (Tester and Davenport, 2003;Ji et al, 2013;Shabala, 2013;Shabala and Pottosin, 2014;Flowers et al, 2015;Julkowska and Testerink, 2015;Kurusu et al, 2015). All these responses rely heavily on the regulation of transport activity across cellular membranes and, specifically, those for Na + and K + ions.…”

“…All these responses rely heavily on the regulation of transport activity across cellular membranes and, specifically, those for Na + and K + ions. High cytosolic Na + concentrations are considered to be toxic for cell metabolism and, thus, are reduced by various means (Tester and Davenport, 2003;Ji et al, 2013;Flowers et al, 2015). At the same time, superior K + retention and a cell's ability to maintain cytosolic K + homeostasis correlate with salinity tolerance in a broad range of plant species (Anschütz et al, 2014;Shabala and Pottosin, 2014) and are essential for preventing salinityinduced programmed cell death (Shabala, 2009;Demidchik et al, 2010).…”

In Vitro Selection of Local Maize (Zea mays) on NaCl Stress and Its Genetic Characterization using RAPD

“…0 ppm, B. 2500 ppm, C. 5000 ppm, D.7500 ppm that comprises SOS3, SOS2, and SOS1 has been proposed to mediate cellular signaling under salt stress, to maintain ion homeostasis (Ji et al, 2013). Dehydration-responsive element binding protein (DREB) is particularly to DRE elements and induces the stress tolerance gene expression.…”

Comparative study of salt stress-induced physiological and molecular responses in tomato (Solanum lycopersicum L.)

“…Na + -induced cytosolic Ca 2+ spike generated in the cytoplasm of root cells activates the SOS signal transduction cascade (Golldack et al, 2014). Ca 2+ , triggered by excess Na + , is perceived by a myristyolated calcium-binding protein, SOS3 (Salt OverlySensitive3) acting as a calcium-sensor (Ji et al, 2013). After binding Ca 2+ , SOS3…”

“…SOS3-SOS2 interaction leads SOS2 to the plasma membrane to activate SOS1, which is a Na + /H + antiporter via phosphorylation (Ji et al, 2013). SOS pathway has a crucial role in the maintenance and regulation of ion homeostasis under salt stress.…”