Abstract
Mitochondria are the source of reactive oxygen species (ROS) in plant cells and play a central role in the mitochondrial electron transport chain (ETC) and tricarboxylic acid cycle (TCA) cycles; however, ROS production and regulation for seed germination, seedling growth, as well as mitochondrial responses to abiotic stress, are not clear. This study was conducted to obtain basic information on seed germination, embryo mitochondrial antioxidant responses, and protein profile changes in artificial aging in oat seeds (Avena sativa L.) exposed to exogenous nitric oxide (NO) treatment. The results showed that the accumulation of H2O2 in mitochondria increased significantly in aged seeds. Artificial aging can lead to a loss of seed vigor, which was shown by a decline in seed germination and the extension of mean germination time (MGT). Seedling growth was also inhibited. Some enzymes, including catalase (CAT), glutathione reductase (GR), dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR), maintained a lower level in the ascorbate-glutathione (AsA-GSH) scavenging system. Proteomic analysis revealed that the expression of some proteins related to the TCA cycle were down-regulated and several enzymes related to mitochondrial ETC were up-regulated. With the application of 0.05 mM NO in aged oat seeds, a protective effect was observed, demonstrated by an improvement in seed vigor and increased H2O2 scavenging ability in mitochondria. There were also higher activities of CAT, GR, MDHAR, and DHAR in the AsA-GSH scavenging system, enhanced TCA cycle-related enzymes (malate dehydrogenase, succinate-CoA ligase, fumarate hydratase), and activated alternative pathways, as the cytochrome pathway was inhibited. Therefore, our results indicated that seedling growth and seed germinability could retain a certain level in aged oat seeds, predominantly depending on the lower NO regulation of the TCA cycle and AsA-GSH. Thus, it could be concluded that the application of 0.05 mM NO in aged oat seeds improved seed vigor by enhancing the mitochondrial TCA cycle and activating alternative pathways for improvement.
Highlights
High-quality seeds are extremely important to agricultural production, productivity, and germplasm conservation
Seed aging and deterioration during storage could induce the loss of seed vigor, and seed germination, especially Mean germination time (MGT), is usually used to reflect the level of seed vigor
The differences among A1, A2, and A3 were not significant, which meant that the improvement in seed germination was sensitive to lower contents of nitric oxide (NO)
Summary
High-quality seeds are extremely important to agricultural production, productivity, and germplasm conservation. Seed deterioration occurs during storage, even under optimal storage conditions, which causes the loss of seed vigor. Various biochemical and metabolic alterations take place during seed aging, including electrolyte leakage, the loss of cell membrane integrity, DNA alteration, and damage of mitochondrial structure and function [1,2,3]. The mechanisms of seed aging are still being researched, reactive oxygen species (ROS) are considered the main factor contributing to seed aging and leading to the damage of lipids, DNA, and proteins [4,5]. It is necessary to explore the aging mechanisms of the detrimental role of ROS in deteriorated seeds
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