Soil salinity severely limits crop yields and quality. Plants have evolved several strategies to mitigate the adverse effects of salinity, including redistribution and compartmentalization of toxic ions using ion-specific transporters. However, the mechanisms underlying the regulation of these ion transporters have not been fully elucidated. Loss-of-function mutants of OsHKT2;1, which is involved in sodium uptake, exhibit strong salt stress-resistant phenotypes. In this study, OsHKT2;1 was identified as a transcriptional target of the type-B response regulator OsRR22. Loss-of-function osrr22 mutants showed resilience to salt stress, and OsRR22-overexpression plants were sensitive to salt stress. OsRR22 was found to activate the expression of OsHKT2;1 by directly binding to the promoter region of OsHKT2;1 via a consensus cis-element of type-B response regulators.Moreover, rice DELLA protein OsSLR1 directly interacted with OsRR22 and functioned as a transcriptional co-activator. This study has uncovered a novel transcriptional regulatory mechanism by which a type-B response regulator controls sodium transport under salinity stress.
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