Title: Genetic analysis of salt tolerance in Arabidopsis: Evidence for the role of Ca(2+)/H(+) transporter CAX1 Authors
|Yang, Jian -|
|Hirschi, Kendal -|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: February 28, 2012
Publication Date: May 16, 2012
Citation: Yang, J., Hirschi, K.D. 2012. Genetic analysis of salt tolerance in Arabidopsis: Evidence for the role of Ca(2+)/H(+) transporter CAX1 [abstract]. Proceedings of the 4th Pan American Plant Membrane Biology Workshop, May 16-20, 2012, Asilomar, California. p. 45. Technical Abstract: Coordinate regulation of transporters at both the plasma membrane and vacuole contribute to plant cell's ability to adapt to a changing environment and play a key role in the maintenance of the chemiosmotic circuits required for cellular growth. The plasma membrane (PM) Na+/H+ antiporter SOS1 is involved in salt tolerance, presumably in sodium extrusion; the vacuolar Ca2+/H+ antiporter CAX1 is involved in vacuolar calcium sequestration. Here we investigate the relationship between these transporters utilizing loss-of-function mutants of SOS1 (sos1-1) and AtCAX1 (cax1-1). There is a complex interplay among various ions within plants, particularly Na+ and Ca2+. For example, supplemental Ca2+ is known to mitigate the adverse effects of salinity on plant growth. Interestingly, CAX1 appears to be upregulated during Na+ stress, and signaling molecules such as SOS2 that regulate PM Na+/H+ transport may also regulate CAX1. Moreover, in planta, the high level of expression of a deregulated version of CAX1 caused salt sensitivity. However, functional redundancy and compensatory mechanisms have hindered our ability to directly access the role of CAX transporters in Na+ tolerance. In this study, we use genetic approaches to examine the interplay between CAX1 and SOS1. cax1-1 and sos1-1 single mutants were crossed to generate cax1-1/sos1-1 double mutants. To test whether CAX1 is epistatic to SOS1, we will perform Na+ tolerance assays using the double mutants. To test whether SOS1 is epistatic to CAX1, we will examine several phenotypes that are characteristic of cax1-1 such as the ionome (decreased Mn2+ and Zn2+), altered P-ATPase and V-ATPase activities and Mg2+ tolerance. Considering the potential interplay between the transport of Na+, Ca2+ and other metals ions, we will also measure the double mutant's tolerance to metals such as Mn, Zn, and Cd. In summary, this study will examine one of the potential mechanims of interplay between Na+ and Ca2+ transport and whether AtCAX1 plays a role in SOS1 mediated salt tolerance using genetic analysis.