CRY1 ‐Dependent DELLA Accumulation via GA Signaling Compromises Salt Tolerance in Arabidopsis thaliana

ABSTRACT Advances in genome‐wide forward genetics and next‐generation sequencing have revitalized efforts to uncover novel regulators of plant stress tolerance. In this study, we identified CRY1 as a key genetic determinant of high salt tolerance in Arabidopsis through the isolation and characterization of the EMS‐derived sot1 mutant plant. Map‐based cloning combined with whole‐genome sequencing revealed that sot1 harbors a premature stop codon in CRY1 . Loss of CRY1 function significantly enhanced plant growth, chlorophyll retention, and photosynthetic capacity under salt stress, phenotypes that were confirmed using cry1 T‐DNA insertion mutants and complementation analyses. Physiological and molecular assessments demonstrated that cry1 and sot1 plants exhibit lower Na + /K + ratios, reduced osmolyte accumulation, and attenuated ROS production, accompanied by altered expression of stress‐responsive genes and ABA‐related transcription factors. Mechanistically, our findings show that CRY1 promotes salt‐induced accumulation of DELLA proteins through modulation of the GA–GID1–DELLA signaling pathway. In cry1 and sot1 plants, suppressed DELLA accumulation alleviates growth inhibition under salinity, whereas GAI overexpression in the sot1 plants reverses this tolerance. Together, these results reveal a previously unrecognized role of CRY1 in integrating light perception with GA‐dependent stress signaling to balance growth and survival under high salinity. This work establishes CRY1 as a negative regulator of salt tolerance and provides a mechanistic framework for developing crops with improved resilience through targeted manipulation of cryptochrome–GA–DELLA interactions.