ArticleBMC plant biology2026
Loss of function of OsWRKY53-OsARF18-OsRR22 significantly enhances rice salt tolerance.
Article in BMC plant biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundSalt stress is a key abiotic stress factor limiting rice growth and development. Previous studies have shown that OsWRKY53, OsARF18, and OsRR22 not only serve as important negative regulators of salt tolerance in rice but are also crucial for growth and development. However, the relative strengths of salt tolerance among these three genes and their combined effects within the same rice variety have not yet been reported.
resultsIn this study, we employed CRISPR/Cas9-mediated genome editing to simultaneously disrupt OsWRKY53, OsARF18, and OsRR22 in the rice cultivar Shuanghui 459. Salt tolerance increases sequentially in single-gene, double-gene, and triple-gene mutants. Under 1.0% NaCl stress, the triple mutant exhibited approximately 80% survival versus complete lethality in the wild type (WT). Physiologically, ROS accumulation progressively declined, while key antioxidant enzyme activities (CAT, SOD, POD) significantly increased. This suggests that the enhanced salt tolerance of the mutants may be associated with increased antioxidant enzyme activity. More importantly, molecular analysis revealed that the WRKY domain of OsWRKY53 binds to the W-box elements in the promoters of OsARF18 and OsRR22, thereby downregulating their expression. Reciprocally, OsARF18 and OsRR22 knockout downregulated OsWRKY53. Furthermore, OsWRKY53 and OsRR22 directly interact at the protein level.
conclusionsTaken together, our results reveal that OsWRKY53, OsARF18, and OsRR22 constitute a reciprocal negative-feedback loop, wherein these three transcriptional regulators mutually antagonize each other. The significant enhancement of salt tolerance in the triple mutant may be related to the relief of this antagonistic interaction. Importantly, the polygenic aggregation of OsWRKY53-OsARF18-OsRR22 not only significantly enhances rice salt tolerance but also does not affect normal plant growth and development. These findings provide new strategies for polygenic aggregation-based genetic improvement of salt-tolerant rice varieties.
Indexed as
Identifiers
42458265What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.