Insights into genomics of salt stress response in rice

Abstract

Plants, as sessile organisms experience various abiotic stresses, which pose serious threat to crop production. Plants adapt to environmental stress by modulating their growth and development along with the various physiological and biochemical changes. This phenotypic plasticity is driven by the activation of specific genes encoding signal transduction, transcriptional regulation, ion transporters and metabolic pathways. Rice is an important staple food crop of nearly half of the world population and is well known to be a salt sensitive crop. The completion and enhanced annotations of rice genome sequence has provided the opportunity to study functional genomics of rice. Functional genomics aids in understanding the molecular and physiological basis to improve the salinity tolerance for sustainable rice production. Salt tolerant transgenic rice plants have been produced by incorporating various genes into rice. In this review we present the findings and investigations in the field of rice functional genomics that includes supporting genes and networks (ABA dependent and independent), osmoprotectants (proline, glycine betaine, trehalose, myo-inositol, and fructans), signaling molecules (Ca2+, abscisic acid, jasmonic acid, brassinosteroids) and transporters, regulating salt stress response in rice.

Figure 1

Diagrammatic representation of salt stress response in rice. Growth and division of the cell under salt stress depends on osmotic and ionic signaling.

Figure 2

Overall signaling pathway in rice during salt stress. Salt stress evokes both osmotic and ionic stress. Osmotic stress signaling is transduced via ABA-dependent or ABA-independent pathway. ABA dependent pathway includes mitogen activated protein kinase (MAP Kinase) cascades, calcium-dependent protein kinases (CDPK), receptor-like kinases (RLK), SNF1-related protein kinases (SnRK), transcription factors (OsRAB1, MYC/MYB and OsNAC/SNAC) and micro RNAs. ABA-independent pathway includes transcription factors (OsDREB1 and OsDREB2) and stress related genes (OsPSY1, OsNCEDs). Ionic stress does signaling via Ca²⁺/PLC pathway and salt overly sensitive (SOS) pathway and Calmodulin (CaM) pathway. Ca²⁺ is sensed by Ca²⁺ sensor (OsCBL4) and the sensor activates calcineurin B-like protein kinase (OsCIPK24), which in turns activates Na⁺/H⁺ antiporter (OsSOS1), H⁺/Ca⁺ antiporter (OsCAX1), vacuolar H⁺/ATPase, vacuolar Na⁺/H⁺ exchangers (OsNHX1) and suppress K⁺/Na⁺ symporter (OsHKT1) to maintain ionic homeostasis under salt stress. Ca²⁺ also activates calmodulin (OsMSR2) which also activates vacuolar Na⁺/H⁺ exchanger (OsNHX1). Blue arrow indicates ABA dependent pathway, green arrow shows ABA-independent pathway, violet arrow shows ROS pathway, red arrow shows Ca²⁺/PLC pathway and orange arrow shows SOS pathway.

Figure 3

Schematic diagram of a plant cell showing regulation of ion homeostasis by various ion transporters. The salinity stress signal is perceived by receptor(s) or salt sensor(s) probably present at the plasma membrane of the cell. The signal is responsible for activating the SOS pathway, the component of which helps in regulating some of these transporters. The transporters are K⁺ inward-rectifying channel (OsAKT1), K⁺/Na⁺ symporter (OsHKT1), nonselective cation channel (NCC), K⁺ outward-rectifying channel (OsKCO1), Na⁺/H⁺ antiporters (OsSOS1), vacuolar Na⁺/H⁺ exchangers (OsNHX1-4), endosomal Na⁺/H⁺ exchanger (OsNHX5), H⁺/Ca⁺ antiporter (OsCAX1) and vacuolar chloride channel (OsCLC1). Na⁺ extrusion from plant cells is powered by the electrochemical gradient generated by H⁺-ATPases, which permits the Na⁺/H⁺ antiporters to couple the passive movement of H⁺ inside along the electrochemical gradient and extrusion of Na⁺ out of cytosol. ER, endoplasmic reticulum; TGN/EE, trans-Golgi network/early endosome; LE/PVC/MVB, late endosome/pre-vacuolar compartment/multivesicular body; RE, recycling endosome. The stress signal sensed by SOS3 activates SOS2, which activates SOS1, details is given in the text.