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

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.