Arbuscular mycorrhizal symbiosis enhances salt tolerance in Eucalyptus grandis by coordinating antioxidant defense, hormone accumulation and ion homeostasis

Eucalyptus is a globally important timber species, yet its productivity is markedly constrained by salt stress. Although arbuscular mycorrhizal (AM) fungi play crucial roles under environmental stress, the integrated physiological and molecular mechanisms by which they confer salinity tolerance in E. grandis remain incompletely understood. In this study, we explored the impact of inoculation with the AM fungus Rhizophagus irregularis on the physiological, biochemical, and transcriptional responses of E. grandis seedlings across a NaCl gradient (0-200 mM). The results indicated that AM symbiosis significantly alleviated salt-induced growth inhibition, membrane damage and water deficit. Relative to non-mycorrhizal plants, AM-colonized seedlings exhibited lower accumulations of osmolytes and oxidative stress markers, while maintaining higher activities of key antioxidant enzymes. Hormonal profiling revealed a coordinated downregulation of stress-related phytohormones in mycorrhizal plants under salinity. Additionally, AM plants accumulated less sodium (Na + ) and more potassium (K + ) concentration than non-mycorrhizal controls, suggesting enhanced Na + efflux and K + uptake under salt stress. Genome-wide analysis identified 23 candidate SOS pathway genes in E. grandis , and qPCR expression profiling revealed that all of these responded to AM symbiosis under salt stress, suggesting that AM symbiosis may regulate SOS pathway gene expression as part of its salt tolerance mechanism. Redundancy analysis suggested strong correlations among enhanced antioxidant enzyme activity, hormonal adjustments, ion homeostasis and the expression of specific EgSOS genes. Collectively, these findings provide integrated physiological and molecular evidence that AM symbiosis improves salt tolerance in a woody species through modulation of antioxidant defenses, hormonal balance, ion homeostasis and SOS pathway gene expression.