Skip to main content
ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #338622

Title: Silencing of OsGRX17 in rice improves drought stress tolerance by modulating ROS accumulation and stomatal closure

item HU, YING - Kansas State University
item WU, QINGYU - Kansas State University
item PENG, ZHAO - Kansas State University
item SPRAGUE, STUART - Kansas State University
item WANG, WEI - Kansas State University
item PARK, JUNGEUN - Kansas State University
item AKHUNOV, EDUARD - Kansas State University
item JAGADISH, KRISHNA - Kansas State University
item Nakata, Paul
item CHENG, NINGHUI - Children'S Nutrition Research Center (CNRC)
item HIRSCHI, KENDAL - Children'S Nutrition Research Center (CNRC)
item WHITE, FRANK - Kansas State University
item PARK, SUNGHUN - Kansas State University

Submitted to: Scientific Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/9/2017
Publication Date: 11/21/2017
Citation: Hu, Y., Wu, Q., Peng, Z., Sprague, S.A., Wang, W., Park, J., Akhunov, E., Jagadish, K.S., Nakata, P.A., Cheng, N., Hirschi, K.D., White, F.F., Park, S. 2017. Silencing of OsGRX17in rice improves drought stress tolerance by modulating ROS accumulation and stomatal closure. Scientific Reports. 7(1):15950.

Interpretive Summary: Drought is a major environmental factor limiting the production of various crop plants including rice. An important drought tolerant factor in plants is the ability to reduce the size of small pore like structures, called stomata, which are distributed over the surface of the underside of leaves. By closing these small pores, the plant can conserve water during drought conditions. In this study, we report the identification of a gene called OsGRXS17 which encodes an enzyme that plays a role in the regulation of events leading to the closure of these small pores. Gene expression studies revealed that OsGRXS17 is up-regulated under water deficit conditions. Localization studies showed that this enzyme resides within both the cytoplasm and nucleus of the cell. Plants that have been engineered to have a reduction in OxGRXS17 expression displayed reduced pore openings, lower rates of water loss, and enhanced survival rates compared to controls under drought conditions. By understanding how this enzyme fits into the pathways controlling the opening and closing of these small plant pores it may be possible, in the future, to develop strategies to increase drought tolerance in plants.

Technical Abstract: Glutaredoxins (GRXs) have emerged as key mediators in plant responses to environmental stimuli by modulating redox-dependent signaling pathways. Here, we report that RNAi-mediated suppression of the rice gene OsGRXS17, encoding a monothiol GRX with a CGFS-type active site motif, elevates H2O2 production in the guard cells, promotes sensitivity to abscisic acid (ABA), and enhances stomatal closure. OsGRXS17 was expressed in all rice tissues and up-regulated under water deficit conditions, and GFP-OsGRXS17 fusion proteins were localized to both the cytoplasm and the nuclear envelope. OsGRXS17 silenced rice plants displayed reduced stomatal apertures, lower rates of water loss and stomatal conductance, higher relative water content, and enhanced survival compared to wild-type control plants under water deficit stress. The silenced lines also accumulated H2O2 in the root tips and exhibited hypersensitivity to ABA during the seed germination and post-germination stages. This ABA-mediated inhibition of seed germination and postembryonic growth of OsGRXS17 silenced rice plants was ameliorated by addition of reduced glutathione (GSH). Global metabolite profiling of OsGRXS17 silenced plants revealed reduced peptides, amino acids, and amino acid derivatives as well as an increase in phospholipids compared to the wild-type counterparts under water deficit stress. The results indicate that OsGRXS17 plays an important role in controlling the level of H2O2 during H2O2-mediated ABA signaling under water stress.