Horie Tomoaki, Horie Rie, Chan Wai-Yin, Leung Ho-Yin, Schroeder Julian I
Division of Biological Sciences, Cell and Developmental Biology Section, and Center for Molecular Genetics, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0116, USA.
Plant Cell Physiol. 2006 May;47(5):622-33. doi: 10.1093/pcp/pcj029. Epub 2006 Mar 15.
T-DNA disruption mutations in the AtHKT1 gene have previously been shown to suppress the salt sensitivity of the sos3 mutant. However, both sos3 and athkt1 single mutants show sodium (Na+) hypersensitivity. In the present study we further analyzed the underlying mechanisms for these non-additive and counteracting Na+ sensitivities by characterizing athkt1-1 sos3 and athkt1-2 sos3 double mutant plants. Unexpectedly, mature double mutant plants grown in soil clearly showed an increased Na+ hypersensitivity compared with wild-type plants when plants were subjected to salinity stress. The salt sensitive phenotype of athkt1 sos3 double mutant plants was similar to that of athkt1 plants, which showed chlorosis in leaves and stems. The Na+ content in xylem sap samples of soil-grown athkt1 sos3 double and athkt1 single mutant plants showed dramatic Na+ overaccumulation in response to salinity stress. Salinity stress analyses using basic minimal nutrient medium and Murashige-Skoog (MS) medium revealed that athkt1 sos3 double mutant plants show a more athkt1 single mutant-like phenotype in the presence of 3 mM external Ca2+, but show a more sos3 single mutant-like phenotype in the presence of 1 mM external Ca2+. Taken together multiple analyses demonstrate that the external Ca2+ concentration strongly impacts the Na+ stress response of athkt1 sos3 double mutants. Furthermore, the presented findings show that SOS3 and AtHKT1 are physiologically distinct major determinants of salinity resistance such that sos3 more strongly causes Na+ overaccumulation in roots, whereas athkt1 causes an increase in Na+ levels in the xylem sap and shoots and a concomitant Na+ reduction in roots.
先前的研究表明，AtHKT1基因中的T-DNA破坏突变可抑制sos3突变体的盐敏感性。然而，sos3和athkt1单突变体均表现出对钠（Na+）的超敏感性。在本研究中，我们通过对athkt1-1 sos3和athkt1-2 sos3双突变体植株进行表征，进一步分析了这些非累加性和相互抵消的Na+敏感性的潜在机制。出乎意料的是，当植株受到盐胁迫时，在土壤中生长的成熟双突变体植株与野生型植株相比，明显表现出更高的Na+超敏感性。athkt1 sos3双突变体植株的盐敏感表型与athkt1植株相似，叶片和茎部出现黄化。土壤种植的athkt1 sos3双突变体和athkt1单突变体植株木质部汁液样本中的Na+含量显示，在盐胁迫下Na+大量积累。使用基本最低营养培养基和Murashige-Skoog（MS）培养基进行的盐胁迫分析表明，在存在3 mM外部Ca2+的情况下，athkt1 sos3双突变体植株表现出更类似athkt1单突变体的表型，但在存在1 mM外部Ca2+的情况下，表现出更类似sos3单突变体的表型。综合多项分析表明，外部Ca2+浓度强烈影响athkt1 sos3双突变体的Na+胁迫反应。此外，研究结果表明，SOS3和AtHKT1是生理上不同的耐盐性主要决定因素，因此sos3更强烈地导致根部Na+过度积累，而athkt1导致木质部汁液和地上部Na+水平升高，同时根部Na+减少。
