Nuclear‐localized AtHSPR links abscisic acid‐dependent salt tolerance and antioxidant defense in Arabidopsis

Abstract

These two authors contributed equally to this work. SUMMARYSalt stress from soil or irrigation water limits plant growth. A T-DNA insertion mutant in C24, named athspr (Arabidopsis thaliana heat shock protein-related), showed several phenotypes, including reduced organ size and enhanced sensitivity to environmental cues. The athspr mutant is severely impaired under salinity levels at which wild-type (WT) plants grow normally. AtHSPR encodes a nuclear-localized protein with ATPase activity, and its expression was enhanced by high salinity and abscisic acid (ABA). Overexpression (OE) of AtHSPR significantly enhanced tolerance to salt stress by increasing the activities of the antioxidant system and by maintaining K + /Na + homeostasis. Quantitative RT-PCR analyses showed that OE of AtHSPR increased the expression of ABA/stress-responsive, salt overly sensitive (SOS)-related and antioxidantrelated genes. In addition, ABA content was reduced in athspr plants with or without salt stress, and exogenous ABA restored WT-like salt tolerance to athspr plants. athspr exhibited increased leaf stomatal density and stomatal index, slower ABA-induced stomatal closure and reduced drought tolerance relative to the WT. AtHSPR OE enhanced drought tolerance by reducing leaf water loss and stomatal aperture. Transcript profiling in athspr showed a differential salt-stress response for genes involved in accumulation of reactive oxygen species (ROS), ABA signaling, cell death, stress response and photosynthesis. Taken together, our results suggested that AtHSPR is involved in salt tolerance in Arabidopsis through modulation of ROS levels, ABA-dependent stomatal closure, photosynthesis and K + /Na + homeostasis.

AtHSPR may function in salt-induced cell death and ER stress in Arabidopsis

“…More recently, we report that AtHSPR/ SMXL4 as a positive regulator enhanced salt tolerance and drought resistance in transgenic Arabidopsis through modulation of ROS levels, ABA-dependent stomatal closure, photosynthesis and K C /Na C homeostasis. 12 In this study, we further show a potential role of AtHSPR in salt-induced cell death and ER stress signaling in Arabidopsis.…”

“…These results were consistent with the evidence that cell death was dramatically higher in the athspr mutant after salt treatment compared with the salt-treated WT plants. 12 Also upregulated genes that respond to unfolded / misfolded proteins or to ER stress were found in comparison of salttreated athspr plants with salt-treated WT(athspr-s/WT-s, Fig. 1C).…”

“…T-DNA-inserted athspr mutant not only exhibit reduced organs in size, darker green rosette leaves and delayed flowering time, 12 but also show slight cell death in leaf apex under normal soil growth condition compared with WT (Fig. 1A).…”

“…1A). Meanwhile, the transcriptome data from our recent publication 12 indicated several genes involved in both regulations of cell death and aging were highly expressed in the athspr mutant under both normal and salt conditions (Fig. 1B).…”

“…[8][9][10][11] AtHSPR (Arabidopsis thaliana Heat Shock Protein Related) is a member of a new SMXL(SUPPRESSOR OF MORE AXILLARY GROWTH2-LIKE) family consisting of eight 8 genes that are closely related to HSP101, also called SMXL4 in the Arabidopsis Columbia background. 12,13 Recently, SMAX1 [SUPPRESSOR OF MORE AXILLARY GROWTH2(MAX2) 1] 13 has been demonstrated to suppress the seed germination and seedling growth phenotypes of max2. MAX2 has been reported to play a role in Strigolactone (SL) responses.…”