Although increasing intracellular proline under stressed condition could help the plants survive, treating plant with high level of proline under normal condition could be inhibitory to plant growth. Among other possible mechanisms, proline-induced mitochondrial reactive oxygen species (ROS) production due to electron overflow in mitochondria electron transport chain (mETC) caused by elevated proline degradation may contribute to the proline toxicity. However, direct evidences are still elusive. Here, we reported a functional characterization of SSR1, encoding a protein localized in mitochondria matrix, in maintaining the function of mETC through analyzing the proline hypersensitive phenotype of an Arabidopsis mutant ssr1-1 with a truncated SSR1 protein. Our analysis demonstrated that upon proline treatment, there were higher mitochondrial ROS, lower ATP content, reduced activity of mETC complex I and II, and reduced iron content in ssr1-1, in comparison to the wild type. Therefore, SSR1 is involved in maintaining normal capacity of mETC in transporting electrons in a way that related to iron homeostasis. Our results also supported that normal mETC activity is required for alleviating the proline toxicity.

中文翻译：

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SSR1 参与维持拟南芥中脯氨酸处理后线粒体电子传递链和铁稳态的功能

虽然在胁迫条件下增加细胞内脯氨酸可以帮助植物存活，但在正常条件下用高水平脯氨酸处理植物可能会抑制植物生长。在其他可能的机制中，由于脯氨酸降解升高引起的线粒体电子传递链 (mETC) 中的电子溢出，脯氨酸诱导的线粒体活性氧 (ROS) 产生可能导致脯氨酸毒性。然而，直接证据仍然难以捉摸。在这里，我们报告了 SSR1 的功能表征，编码定位于线粒体基质中的蛋白质，通过分析具有截短的 SSR1 蛋白的拟南芥突变体 ssr1-1 的脯氨酸过敏表型来维持 mETC 的功能。我们的分析表明，脯氨酸处理后，线粒体 ROS 较高，与野生型相比，降低 ATP 含量，降低 mETC 复合物 I 和 II 的活性，并降低 ssr1-1 中的铁含量。因此，SSR1 参与维持 mETC 以与铁稳态相关的方式传输电子的正常能力。我们的结果还支持正常的 mETC 活性是减轻脯氨酸毒性所必需的。