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Soil salinity is a major constraint that affects plant growth and development. Rice is a staple food for more than half of the human population but is extremely sensitive to salinity. Among the several known mechanisms, the ability of the plant to exclude cytosolic Na+ is strongly correlated with salinity stress tolerance in different plant species. This exclusion is mediated by the plasma membrane (PM) Na+/H+ antiporter encoded by Salt Overly Sensitive (SOS1) gene and driven by a PM H+-ATPase generated proton gradient. However, it is not clear to what extent this mechanism is operational in wild and cultivated rice species, given the unique rice root anatomy and the existence of the bypass flow for Na+. As wild rice species provide a rich source of genetic diversity for possible introgression of abiotic stress tolerance, we investigated physiological and molecular basis of salinity stress tolerance in Oryza species by using two contrasting pairs of cultivated (Oryza sativa) and wild rice species (Oryza alta and Oryza punctata). Accordingly, dose- and age-dependent Na+ and H+ fluxes were measured using a non-invasive ion selective vibrating microelectrode (the MIFE technique) to measure potential activity of SOS1-encoded Na+/H+ antiporter genes. Consistent with GUS staining data reported in the literature, rice accessions had (~4–6-fold) greater net Na+ efflux in the root elongation zone (EZ) compared to the mature root zone (MZ). Pharmacological experiments showed that Na+ efflux in root EZ is suppressed by more than 90% by amiloride, indicating the possible involvement of Na+/H+ exchanger activity in root EZ. Within each group (cultivated vs. wild) the magnitude of amiloride-sensitive Na+ efflux was higher in tolerant genotypes; however, the activity of Na+/H+ exchanger was 2–3-fold higher in the cultivated rice compared with their wild counterparts. Gene expression levels of SOS1, SOS2 and SOS3 were upregulated under 24 h salinity treatment in all the tested genotypes, with the highest level of SOS1 transcript detected in salt-tolerant wild rice genotype O. alta (~5–6-fold increased transcript level) followed by another wild rice, O. punctata. There was no significant difference in SOS1 expression observed for cultivated rice (IR1-tolerant and IR29-sensitive) under both 0 and 24 h salinity exposure. Our findings suggest that salt-tolerant cultivated rice relies on the cytosolic Na+ exclusion mechanism to deal with salt stress to a greater extent than wild rice, but its operation seems to be regulated at a post-translational rather than transcriptional level. [ABSTRACT FROM AUTHOR]

Abstract: Abiotic stresses such as cold, salinity, drought, wounding, and heavy metal contamination adversely affect crop productivity throughout the world. Prosopis juliflora is a phreatophyte that can tolerate severe adverse [...]

Oryza coarctata is the only wild rice species with significant salinity tolerance. The present work examines the role of the substantial rhizomatous tissues of O. coarctata in conferring salinity tolerance. Transition to an erect phenotype (shoot emergence) from prostrate growth of rhizome tissues is characterized by marked lignification and suberization of supporting sclerenchymatous tissue, epidermis, and bundle sheath cells in aerial shoot-proximal nodes and internodes in O. coarctata. With salinity, however, aerial shoot-proximal internodal tissues show reductions in lignification and suberization, most probably related to re-direction of carbon flux towards synthesis of the osmporotectant proline. Concurrent with hypolignification and reduced suberization, the aerial rhizomatous biomass of O. coarctata appears to have evolved mechanisms to store Na+ in these specific tissues under salinity. This was confirmed by histochemical staining, quantitative real-time reverse transcription–PCR expression patterns of genes involved in lignification/suberization, Na+ and K+ contents of internodal tissues, as well as non-invasive microelectrode ion flux measurements of NaCl-induced net Na+, K+, and H+ flux profiles of aerial nodes were determined. In O. coarctata , aerial proximal internodes appear to act as 'traffic controllers', sending required amounts of Na+ and K+ into developing leaves for osmotic adjustment and turgor-driven growth, while more deeply positioned internodes assume a Na+ buffering/storage role. [ABSTRACT FROM AUTHOR]

This study aimed to reveal the mechanistic basis of the melatonin‐mediated amelioration of salinity stress in plants. Electrophysiological experiments revealed that melatonin decreased salt‐induced K+ efflux (a critical determinant of plant salt tolerance) in a dose‐ and time‐dependent manner and reduced sensitivity of the plasma membrane K+‐permeable channels to hydroxyl radicals. These beneficial effects of melatonin were abolished by NADPH oxidase blocker DPI. Transcriptome analyses revealed that melatonin induced 585 (448 up‐ and 137 down‐regulated) and 59 (54 up‐ and 5 down‐regulated) differentially expressed genes (DEGs) in the root tip and mature zone, respectively. The most noticeable changes in the root tip were melatonin‐induced increase in the expression of several DEGs encoding respiratory burst NADPH oxidases (OsRBOHA and OsRBOHF), calcineurin B‐like/calcineurin B‐like‐interacting protein kinase (OsCBL/OsCIPK), and calcium‐dependent protein kinase (OsCDPK) under salt stress. Melatonin also enhanced the expression of potassium transporter genes (OsAKT1, OsHAK1, and OsHAK5). Taken together, these results indicate that melatonin improves salt tolerance in rice by enabling K+ retention in roots, and that the latter process is conferred by melatonin scavenging of hydroxyl radicals and a concurrent OsRBOHF‐dependent ROS signalling required to activate stress‐responsive genes and increase the expression of K+ uptake transporters in the root tip. Melatonin improves salt tolerance in rice by enabling K+ retention in roots; this process is conferred by melatonin scavenging of hydroxyl radicals and a concurrent OsRBOHF‐dependent ROS signalling required to activate stress‐responsive genes and increasing the expression of K+ uptake transporters, particularly OsHAK5, in the root tip. [ABSTRACT FROM AUTHOR]