Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 4/4/2006
Publication Date: 5/17/2006
Citation: Cheng, N-H., Gonzales, N., Hirschi, K.D. 2006. Functional analysis of Arabidopsis H(+)/Ca(2+) exchangers, CAX[ES] [abstract]. The 2nd Pan American Plant Membrane Biology Workshop, May 17-20, 2006, South Padre Island, Texas. P23, p. 84. Interpretive Summary:
Technical Abstract: Calcium is an essential mineral nutrient for both animals and plants, and also acts as a second messenger that is involved in many biological processes. Cytosolic Ca(2+) is tightly regulated through multiple mechanisms in response to both localized and environmental changes. Our previous studies demonstrate that Arabidopsis H(+)/Ca(2+) exchangers, CAXes, play an important role in ion homeostasis and nutrient acquisition. In the present study, we further investigate the biological function and the interplay among CAXes. In a yeast expression assay, full-length CAX1 and CAX3 can partially, but not fully, suppress the Ca(2+) hypersensitive yeast phenotype and co-expression of CAX1 and CAX3 conferred tolerance to high Ca(2+) and Li(+), suggesting an interplay between CAX1 and CAX3. Genetic analysis indicates that deletion of both "CAX1" and "CAX3" causes defects in plant growth and development including cell death. These phenotypes were not seen that double mutants of CAX1 and CAX2 or CAX2 and CAX3--implicating a specific association between "CAX1" and "CAX3". Microarrays analysis and expression analysis by semi-quantitative RT-PCR revealed that Arabidopsis "TCH2, TCH3", and "TCH4" were up-regulated in "cax1, cax3", and "cax1cax3" mutant plants, suggesting an increase in cytosolic Ca(2+) due to the lack of "CAXes". Ionomic analysis demonstrated that the "cax1cax3" lines displayed increased PO(3-), Mn(2+), and Zn(2+) and decreased Ca(2+) and Mg(2+) in shoot tissues, while "cax1" and "cax3" lines were modestly perturbed. We are in the process of delineating the nature of the physical interaction among CAXes, the transport properties that these interactions may facilitate and the mechanisms of the cell-death related "cax1cax3" phenotypes.