|Cheng, Ning-Hui - BAYLOR COLL MEDICINE|
|Pittman, Jon - BAYLOR COLL MEDICINE|
|Zhu, Jian-Kang - UNIV OF ARIZONA, TUCSON|
Submitted to: Journal of Biological Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 27, 2003
Publication Date: January 23, 2004
Citation: Cheng, N., Pittman, J.K., Zhu, J., Hirschi, K. 2004. The protein kinase SOS2 activates the Arabidopsis H2/Ca2+ antiporter CAX1 to integrate calcium transport and salt tolerance. Journal of Biological Chemistry. 279(4):2922-2926. Interpretive Summary: Plants respond to environmental challenges by altering their growth. When plants are grown in high salt conditions, they tend to not grow well. Here we document how plant alter their physiology to adapt to salt conditions. Potentially, we can manipulate plant growth during salt stress to increase yield.
Technical Abstract: The regulation of ions within cells is an indispensable component of growth and adaptation. The plant SOS2 protein kinase and its associated Ca2+ sensor, SOS3, have been demonstrated to modulate the plasma membrane H+/Na+ antiporter SOS1; however, how these regulators modulate Ca2+ levels within cells is poorly understood. Here we demonstrate that SOS2 regulates the vacuolar H+/Ca2+ antiporter CAX1. Using a yeast growth assay, co-expression of SOS2 specifically activated CAX1, whereas SOS3 did not. CAX1-like chimeric transporters were activated by SOS2 if the chimeric proteins contained the N terminus of CAX1. Vacuolar membranes from CAX1-expressing cells were made to be H+/CA2+-competent by the addition of SOS2 protein in a dose-dependent manner. Using a yeast two-hybrid assay, SOS2 interacted with the N terminus of CAX1. In each of these yeast assays, the activation of CAX1 by SOS2 was SOS3-independent. In planta, the high level of expression of a deregulated version of CAX1 caused salt sensitivity. These findings suggest multiple functions for SOS2 and provide a mechanistic link between Ca2+ and Na+ homeostasis in plants.