Myoinositol enhances heat tolerance in Chenopodium quinoa through integrated physiological, biochemical, and molecular responses

As global temperatures continue to rise, heat stress poses a serious threat to crop productivity and food security. Developing effective strategies to enhance thermotolerance is therefore critical. This study investigates the physiological, biochemical, and molecular mechanisms underlying the protective role of myo-inositol (MyIs) in enhancing heat tolerance in Chenopodium quinoa exposed to varying thermal stress conditions (30°C, 35°C, and 40°C), with or without MyIs application. Heat stress markedly reduced biomass accumulation, relative water content (RWC), photosynthetic efficiency, and membrane stability, while increasing oxidative damage, as evidenced by elevated malondialdehyde (MDA), hydrogen peroxide (H2O2), superoxide radicals (O2•-), and electrolyte leakage (EL). MyIs significantly mitigated these adverse effects by enhancing shoot and root growth, maintaining higher RWC and photosynthetic performance, and reducing oxidative stress markers. Biochemical profiling revealed restoration of total soluble sugars, protein, and free amino acids, alongside elevated glycine betaine (GB) and abscisic acid (ABA), contributing to improved osmotic adjustment and stress signaling. Gene expression analysis showed upregulation of key heat-responsive genes (sHSP18.1, HSP20, HSP70, HSP83, and NSY), indicating a transcriptional basis for MyIs-induced heat tolerance. Collectively, these findings demonstrate that MyIs functions as a potent bio-regulator, conferring thermoprotection through integrated physiological and molecular responses, and offers promising potential for improving heat resilience in crops.