Saline-alkaline stress is a worldwide problem that threatens the growth and yield of crops. However, how crops adapt to saline-alkaline stress remains less studied. Here we show that the saline-alkaline tolerance was compromised during tomato domestication and improvement, and a natural variation in promoter of SlSCaBP8, an EF-hand Ca2+ binding protein, contributes to the loss of saline-alkaline tolerance during tomato improvement. The biochemical and genetic data showed that SlSCaBP8 is a positive regulator of saline-alkaline tolerance in tomato. The introgression-line Pi-75, derived from a cross between wild Solanum pimpinellifolium LA1589 and cultivar E6203, containing the SlSCaBP8LA1589 locus, showed stronger saline-alkaline tolerance than E6203. Pi-75 and LA1589 also showed enhanced saline-alkaline-induced SlSCaBP8 expression than that of E6203. By sequence analysis, a natural variation was found in promoter of SlSCaBP8 and the accessions with the wild haplotype showed enhanced saline-alkaline tolerance, compared with the cultivar haplotype. Our studies clarify the mechanism of saline-alkaline tolerance conferred by SlSCaBP8 and provide an important natural variation in promoter of SlSCaBP8 for tomato breeding.

中文翻译：

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SlSCaBP8启动子的自然变异导致番茄改良过程中盐碱耐受性的丧失

盐碱胁迫是威胁农作物生长和产量的世界性问题。然而，作物如何适应盐碱胁迫的研究还较少。在这里，我们发现，在番茄驯化和改良过程中，盐碱耐受性受到损害，而 EF-hand Ca2+ 结合蛋白 SlSCaBP8 启动子的自然变异导致了番茄改良过程中盐碱耐受性的丧失。生化和遗传数据表明，SlSCaBP8是番茄耐盐碱性的正调节因子。基因渗入系 Pi-75 源自野生 Solanum pimpinellifolium LA1589 和含有 SlSCaBP8LA1589 位点的栽培品种 E6203 之间的杂交，显示出比 E6203 更强的盐碱耐受性。Pi-75和LA1589还显示出比E6203增强的盐碱诱导的SlSCaBP8表达。通过序列分析，发现SlSCaBP8启动子存在天然变异，与栽培品种单倍型相比，具有野生单倍型的材料表现出增强的耐盐碱能力。我们的研究阐明了SlSCaBP8赋予的耐盐碱机制，并为SlSCaBP8启动子的番茄育种提供了重要的自然变异。