Send to:

Choose Destination
See comment in PubMed Commons below
Nat Commun. 2013;4:1352. doi: 10.1038/ncomms2357.

Release of SOS2 kinase from sequestration with GIGANTEA determines salt tolerance in Arabidopsis.

Author information

  • 1Division of Applied Life Science (BK21 Program), Plant Molecular Biology and Biotechnology Research Center, Graduate School of Gyeongsang National University, Jinju 660-701, South Korea.

Erratum in

  • Nat Commun. 2013;4:1820.


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.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Write to the Help Desk