Mesophyll K(+) retention ability has been recently reported as an important component of salinity stress tolerance in wheat. In order to investigate the role of ROS in regulating NaCl(-)induced K(+) efflux in wheat leaf mesophyll, a series of pharmacological experiments was conducted using MV (methyl viologen, superoxide radical inducer), DPI (an inhibitor of NADPH oxidase), H2O2 (to mimic apoplastic ROS), and EGCG ((-)-Epigallocatechin gallate, ROS scavenger). Mesophyll pre-treatment with 10 μM MV resulted in a significantly higher NaCl(-)induced K(+) efflux in leaf mesophyll, while 50 μM EGCG pre-treatment alleviated K(+) leakage under salt stress. No significant change in NaCl(-)induced K(+) efflux in leaf mesophyll was found in specimens pre-treated by H2O2 and DPI, compared with the control. The highest NaCl(-)induced H(+) efflux in leaf mesophyll was also found in samples pre-treated with MV, suggesting a futile cycle between increased H(+)-ATPase activity and ROS-induced K(+) leak. Overall, it is suggested that, under saline stress, K(+) efflux from wheat mesophyll is mediated predominantly by non-selective cation channels (NSCC) regulated by ROS produced in chloroplasts, at least in bread wheat.
No takes yet. Share an insight, caveat, or question.
Wu et al. (2015) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: