Molecular connections between salinity stress signaling and the regulation of flowering time in Arabidopsis

The ability to sense and respond to environmental stimuli is among the most fundamental processes that enable plants to survive. The Salt Overly Sensitive (SOS) signaling pathway that comprises the sodium transport protein SOS1, the protein kinase SOS2, and the calcium-dependent interacting proteins SOS3 and CBL10, has been shown to mediate cellular signaling under salt stress. The SOS pathway maintains cellular ion homeostasis and mediates the long distance transport of sodium ions from roots to shoots, thereby imparting salt tolerance to all plant species that have been genetically tested. Environmental challenges, including salinity, typically entail retardation of vegetative growth and delay or cessation of flowering. Recently, a molecular link has been discovered between the flowering time regulator, GIGANTEA (GI), and adaptation to salt stress that is mechanistically based on GI degradation under saline conditions, thus retarding flowering. GI and the salt tolerance-related protein kinase SOS2 functionally interact. In the absence of stress, the GI:SOS2 complex prevents SOS2-based activation of SOS1, the major plant Na/H-antiporter mediating adaptation to salinity. GI overexpressing, rapidly flowering plants show enhanced salt sensitivity, whereas gi mutants exhibit enhanced salt tolerance and delayed flowering. Salt-induced degradation of GI confers salt tolerance by the release of the SOS2 kinase. The GI–SOS2 interaction introduces a higher order regulatory circuit that can explain in molecular terms, the long observed connection between floral transition and adaptive environmental stress tolerance in Arabidopsis.

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