Abstract

Cytosolic K+ retention is an important determinant of salinity tolerance in many crops. However, it remains unclear whether this trait is also crucial for wild rice species. In this work, contrasting pairs of cultivated (Oryza sativa L.) and wild (Oryza alta; Oryza punctata) rice species were used to understand the mechanistic basis of salinity stress tolerance in rice and the role of K+ retention in this process. Non-invasive Microelectrode Ion Flux Measuring (MIFE) measurements showed that NaCl and ROS-induced K+ efflux from the elongation root zone were significantly (2–3-fold) higher in the wild rice species compared with their cultivated counterparts. Cultivated rice group showed relatively lower K+ efflux but greater H+ efflux in response to NaCl and ROS treatments. Pharmacological experiments revealed that tetraethylammonium chloride (TEA) and gadolinium chloride (GdCl3) markedly suppressed NaCl and ROS-induced K+ efflux (>80 % inhibition), suggesting the involvement of GORK and NSCC channels in stress-induced K+ efflux. Sodium orthovanadate suppressed H+ efflux (>90 % inhibition), suggesting the role of H+-ATPase as a major source in salt-induced H+ efflux in salt tolerant cultivars. Collectively, our results indicate that, while possessing high root K+ retention ability in the mature zone, wild rice species show higher sensitivity to NaCl and ROS in the elongation zone. It is suggested that stress-induced K+ efflux in this zone may operate as a "metabolic switch" by inhibiting energy consuming anabolic reactions and allowing energy to be saved for adaptations and repairs, which may provide an advantage to wild rice in conditions with high salinity.

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