Submitted to: Planta
Publication Type: Peer reviewed journal
Publication Acceptance Date: 10/8/2007
Publication Date: 10/30/2007
Publication URL: springerlink.com/content/w82v64344t772q80/
Citation: Zhao, J., Barkla, B.J., Marshall, J., Pittman, J.K., Hirschi, K.D. 2008. The "Arabidopsis cax3" mutants display altered salt tolerance, pH sensitivity and reduced plasma membrane H(+)-ATPase activity. Planta. 227(3):659-669. Interpretive Summary: Plant transporters move nutrients and toxins and distribute these compounds throughout the plant. We are interested in helping plants deal with sodium toxicity. Soils throughout the world are contaminated because too much salt is hindering plant growth. To engineer transporters to impact plant productivity, we must first identify their biological functions. This work identifies a transporter that moves the nutrient calcium when salt levels are high. This finding suggest that plants use similar strategies to control calcium and sodium tranpsort activities. Our findings provide a platform to manipulate calcium transporters to impact salt tolerance in plants. In the future, this work could provide insights into engineering agriculturally important crops to thrive in marginal soils.
Technical Abstract: Perturbing CAX1, an "Arabidopsis" vacuolar H(+)/Ca(2+) antiporter, and the related vacuolar transporter CAX3, has been previously shown to cause severe growth defects; however, the specific function of CAX3 has remained elusive. Here, we describe plant phenotypes that are shared among "cax1" and "cax3" including an increased sensitivity to both abscisic acid (ABA) and sugar during germination, and an increased tolerance to ethylene during early seedling development. We have also identified phenotypes unique to "cax3", namely salt, lithium, and low pH sensitivity. We used biochemical measurements to ascribe these "cax3" sensitivities to a reduction in vacuolar H(+)/Ca(2+) transport during salt stress and decreased plasma membrane H(+)-ATPase activity. These findings catalog an array of CAX phenotypes and assign a specific role for CAX3 in response to salt tolerance.