Katiyar-Agarwal Surekha, Zhu Jianhua, Kim Kangmin, Agarwal Manu, Fu Xinmiao, Huang Alex, Zhu Jian-Kang
Institute for Integrative Genome Biology and Department of Botany and Plant Sciences, University of California, Riverside, CA 92521, USA.
Proc Natl Acad Sci U S A. 2006 Dec 5;103(49):18816-21. doi: 10.1073/pnas.0604711103. Epub 2006 Oct 5.
The adverse effects of high salt on plants include Na(+) toxicity and hyperosmotic and oxidative stresses. The plasma membrane-localized Na(+)/H(+) antiporter SOS1 functions in the extrusion of toxic Na(+) from cells and is essential for plant salt tolerance. We report here that, under salt or oxidative stress, SOS1 interacts through its predicted cytoplasmic tail with RCD1, a regulator of oxidative-stress responses. Without stress treatment, RCD1 is localized in the nucleus. Under high salt or oxidative stress, RCD1 is found not only in the nucleus but also in the cytoplasm. Like rcd1 mutants, sos1 mutant plants show an altered sensitivity to oxidative stresses. The rcd1mutation causes a decrease in salt tolerance and enhances the salt-stress sensitivity of sos1 mutant plants. Several genes related to oxidative-stress tolerance were found to be regulated by both RCD1 and SOS1. These results reveal a previously uncharacterized function of a plasma membrane Na(+)/H(+) antiporter in oxidative-stress tolerance and shed light on the cross-talk between the ion-homeostasis and oxidative-stress detoxification pathways involved in plant salt tolerance.
高盐对植物的不利影响包括钠离子毒性、高渗胁迫和氧化胁迫。定位于质膜的钠离子/氢离子反向转运蛋白SOS1在将有毒的钠离子排出细胞的过程中发挥作用，是植物耐盐性所必需的。我们在此报告，在盐胁迫或氧化胁迫下，SOS1通过其预测的胞质尾部与氧化应激反应调节因子RCD1相互作用。在没有胁迫处理的情况下，RCD1定位于细胞核。在高盐或氧化胁迫下，不仅在细胞核中发现了RCD1，在细胞质中也发现了它。与rcd1突变体一样，sos1突变体植株对氧化胁迫的敏感性也发生了改变。rcd1突变导致耐盐性降低，并增强了sos1突变体植株对盐胁迫的敏感性。发现几个与氧化胁迫耐受性相关的基因受RCD1和SOS1共同调控。这些结果揭示了质膜钠离子/氢离子反向转运蛋白在氧化胁迫耐受性方面以前未被描述的功能，并阐明了参与植物耐盐性的离子稳态和氧化胁迫解毒途径之间的相互作用。
