Seminars

Environmental challenges to plants typically entail retardation of vegetative growth and delay or cessation of flowering. We have uncovered a link between flowering time regulator, GIGANTEA (GI) and adaptation to salt stress that is mechanistically related with GI degradation under saline conditions and the consequential retardation of flowering. GI, an important switch in the photoperiod pathway and circadian clock control, and the SNF1-related protein kinase SOS2 in the SOS (Salt-Overly-Sensitive) pathway functionally interact. In the absence of stress the inhibition of SOS2 kinase activity due to its partition in a complex with GI precludes activation of SOS1, the major plant Na+/H+-antiporter that mediates adaptation to salinity. GI over-expressing, rapidly flowering plants show enhanced salt sensitivity, whereas gi mutants exhibit enhanced salinity 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 adaptative environmental stress tolerance in Arabidopsis.

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