The CCCH-type zinc finger protein SZF12 negatively regulates salt stress tolerance in rice by suppressing...

Soil salinity represents one of the most damaging abiotic stresses constraining rice (Oryza sativa L.) production globally. Although CCCH-type zinc finger proteins have emerged as important regulators of stress responses in plants, the molecular mechanisms by which individual members modulate salt tolerance are not yet fully elucidated. Here, we characterize SZF12, a rice CCCH-type zinc finger protein containing two C2HC motifs and one canonical CCCH motif, as a negative regulator of salt stress tolerance. SZF12 is localized to the nucleus, possesses transcriptional activation activity, and is induced by salt stress. CRISPR/Cas9-derived loss-of-function mutants (szf12-c1 and szf12-c2) displayed significantly enhanced salt tolerance at both seedling stage and reproductive stages, with higher survival rates, lower Na⁺ accumulation and Na⁺/K⁺ ratio under salt stress, and increased grain yield compared to wild-type Zhonghua 11 (ZH11), whereas SZF12-overexpressing lines (OE1 and OE2) exhibited reduced salt tolerance, retarded growth, and increased grain length. Transcriptomic analysis revealed that loss of SZF12 enables a more targeted stress-responsive transcriptional reprogramming, specifically activating ion transport genes and suppressing carbon metabolism genes under salt stress. Taken together, our findings identify SZF12 as a negative regulator of salt stress tolerance in rice that modulates the amplitude of stress-responsive gene expression, and underscore its value as a gene-editing target for breeding salt-tolerant varieties.