ArticleScience China. Life sciences2023
Type-B response regulator OsRR22 forms a transcriptional activation complex with OsSLR1 to modulate OsHKT2;1 expression in rice.
Article in Science China. Life sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Loss of function of OsWRKY53-OsARF18-OsRR22 significantly enhances rice salt tolerance.BMC plant biology · 2026Article
- Crops exposed to extreme conditions: perspectives of gene editing to improve stress tolerance.Plant cell reports · 2026Review
- Cytokinin derivatives as tools to enhance plant stress resilience.Frontiers in plant science · 2026Review
- Article
- Integrated QTL mapping and candidate gene analysis for yield-related traits and salt tolerance in a rice RIL population.Frontiers in plant science · 2025Article
- A spatially resolved multiomic single-cell atlas of soybean development.bioRxiv : the preprint server for biology · 2024Article
- Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
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Abstract
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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