Abstract
Zinc-finger transcription factors essentially mediate plant responses to abiotic stress. In this study, a salt-inducible and nucleus-localized C2H2-type zinc-finger transcription factor designated as PdbZAT11 was screened and identified. Overexpression and mutant lines of PdbZAT11 were generated via genetic transformation. Phenotypic and physiological analyses demonstrated that PdbZAT11 overexpression enhanced salt tolerance by increasing antioxidant enzyme activities and proline accumulation, thereby alleviating reactive oxygen species (ROS)-induced cellular damage, whereas disruption of PdbZAT11 resulted in the opposite effect. As a transcriptional activator, PdbZAT11 specifically bound to the IBOX element in the promoter region and directly activated expression of its target gene PdbTLP3. Generation of PdbTLP3 overexpression and pdbtlp3 mutant lines further revealed that PdbTLP3 conferred salt tolerance by strengthening ROS scavenging capacity. Collectively, these findings establish that PdbZAT11 enhances salt tolerance through direct transcriptional activation of PdbTLP3, accompanied by improved osmotic regulation and ROS scavenging capacity.