OsPLT1 negatively regulates salt tolerance by modulating ion homeostasis and oxidative stress responses in rice.

Soil salinity represents a major abiotic constraint that limits rice development and grain production. To investigate the role of OsPLT1 in rice salt tolerance, we analyzed mutants with disrupted gene function and overexpression lines under salt stress. Under non-stress conditions, seedling growth was largely comparable among the examined genotypes. Under salt treatment, however, the osplt1 mutants exhibited significantly enhanced tolerance, whereas OsPLT1-overexpressing lines showed increased sensitivity. Compared with wild-type Nipponbare (Nip), the mutants maintained better growth vigor, accumulated markedly less Na+, and effectively retained K+, resulting in lower Na+/K+ ratios in both root and shoot tissues. Furthermore, the osplt1 mutants displayed mitigated oxidative damage, as evidenced by weaker 3,3'-diaminobenzidine (DAB) staining, lower hydrogen peroxide (H2O2) and malondialdehyde (MDA) contents, and enhanced superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT) activities. In contrast, the overexpression lines showed exacerbated growth inhibition, reduced chlorophyll retention, and profound ionic imbalance. The stronger induction of a broader set of salt-responsive genes involved in Na+ transport, SOS signaling, vacuolar ion compartmentalization, K+ retention and osmotic adjustment further suggests that the absence of OsPLT1 enhances salt-responsive transcriptional responses. Collectively, our data support a role for OsPLT1 as a suppressor of salt tolerance in rice, with its effects associated with altered ion homeostasis and antioxidant defense capacity.