SSR1 is involved in maintaining the function of mitochondria electron transport chain and iron homeostasis upon proline treatment in Arabidopsis.

ABSTRACT

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.