ABC1K (Activity of BC1 complex Kinase) is an evolutionarily primitive atypical kinase family widely distributed among prokaryotes and eukaryotes. The ABC1K protein kinases in Arabidopsis are predicted to localize either to the mitochondria or chloroplasts, in which plastid-located ABC1K proteins are involved in the response against photo-oxidative stress and cadmium-induced oxidative stress. Here, we report that the mitochondria-localized ABC1K10a functions in plant salt stress tolerance by regulating reactive oxygen species (ROS). Our results show that the ABC1K10a expression is induced by salt stress, and the mutations in this gene result in overaccumulation of ROS and hypersensitivity to salt stress. Exogenous application of the ROS-scavenger GSH significantly represses ROS accumulation and rescues the salt hypersensitive phenotype of abc1k10a. ROS overaccumulation in abc1k10a mutants under salt stress is likely due to the defect in mitochondria electron transport chain. Furthermore, defects of several other mitochondria-localized ABC1K genes also result in salt hypersensitivity. Taken together, our results reveal that the mitochondria-located ABC1K10a regulates mitochondrial ROS production and is a positive regulator of salt tolerance in Arabidopsis.

中文翻译：

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非典型激酶ABC1K10a在植物盐胁迫耐受中起作用。

ABC1K（BC1复合激酶的活性）是一个进化上原始的非典型激酶家族，广泛分布于原核生物和真核生物之间。拟南芥中的ABC1K蛋白激酶预计定位于线粒体或叶绿体，其中质体定位的ABC1K蛋白参与对光氧化应激和镉诱导的氧化应激的响应。在这里，我们报告线粒体定位的ABC1K10a通过调节活性氧（ROS）在植物盐胁迫耐受中发挥作用。我们的结果表明，ABC1K10a表达是由盐胁迫诱导的，该基因中的突变导致ROS的过度积累和对盐胁迫的超敏感性。ROS清除剂GSH的外源应用显着抑制了ROS的积累并拯救了abc1k10a的盐超敏表型。盐胁迫下，abc1k10a突变体中的ROS过度积累可能是由于线粒体电子传输链的缺陷所致。此外，其他几个线粒体定位的ABC1K基因的缺陷也导致盐超敏反应。两者合计，我们的结果表明，位于线粒体的ABC1K10a调节线粒体ROS的产生，并且是拟南芥中耐盐性的正向调节剂。