Release of SOS2 kinase from sequestration with GIGANTEA determines salt tolerance in Arabidopsisopen access
- Authors
- Kim, Woe-Yeon; Ali, Zahir; Park, Hee Jin; Park, Su Jung; Cha, Joon-Yung; Perez-Hormaeche, Javier; Javier Quintero, Francisco; Shin, Gilok; Kim, Mi Ri; Qiang, Zhang; Ning, Li; Park, Hyeong Cheol; Lee, Sang Yeol; Bressan, Ray A.; Pardo, Jose M.; Bohnert, Hans J.; Yun, Dae-Jin
- Issue Date
- Jan-2013
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.4
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 4
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/20882
- DOI
- 10.1038/ncomms2357
- ISSN
- 2041-1723
- Abstract
- Environmental challenges to plants typically entail retardation of vegetative growth and delay or cessation of flowering. Here we report a link 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, a switch in photoperiodicity and circadian clock control, and the SNF1-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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