Myo-inositol (MI) is recognized as a potential stress regulator capable of alleviating abiotic stress. The objective of this study is to analyze the role of MI in the salt stress response of Daucus carota L. and its potential mechanisms. “Hongxin Qicun” carrot seedlings were subjected to five treatments: control; salt stress (50 mM NaCl); and salt stress combined with 50, 100, or 200 μM of MI. Through an integrated approach combining physiological assays, non-invasive micro-test technology (NMT), and gene expression profiling, we found that salt stress severely inhibited seedling growth, disrupted K+/Na+ homeostasis, and triggered excessive H2O2 accumulation. Exogenous MI application mitigated these salt-induced damages, with 100 μM MI exerting the optimal effect. MI enhanced Na+ efflux and reduced K+ efflux in carrot roots under salt stress. Inhibitor experiments indicated that MI-promoted Na+ efflux relies on active transport via the plasma membrane (PM) Na+/H+ antiporter system, and qRT-PCR analysis showed that this response was accompanied by the upregulation of DcSOS1. Furthermore, MI contributes to K+ homeostasis by synergistically modulating PM H+-ATPase and high-affinity potassium transporters. The established proton gradient helps reduce salt-induced K+ loss through depolarization-activated potassium channels and non-selective cation channels. MI treatment decreased electrolyte leakage, malondialdehyde content, and H2O2 accumulation by enhancing the activities of the plant antioxidant defense system. Meanwhile, MI upregulated the expression of myo-inositol oxygenase (DcMIOXs) genes, which may contribute to osmotic balance maintenance and facilitate ROS scavenging. In conclusion, exogenous MI alleviates salt-induced physiological disorders in Daucus carota L. by coordinately regulating K+/Na+ and ROS homeostasis, with 100 μM identified as the optimal concentration for this effect.
Feng et al. (Mon,) studied this question.