Iron (Fe)-shortage is a serious limitation in Strategy I dicot crops including soybean (Glycine max L.). Fe-deficiency causes chlorosis, growth retardation, low photosynthetic performance, and productivity. Nitric oxide (NO) is known to serve as a signalling molecule in plants, but its role in mitigating Fe-deficiency in soybeans is still vague. Therefore, the study aims to explore physiological and molecular mechanisms associated with Fe-acquisition and homeostasis is highly demandable. In this study, we found Fe-deficiency occurred leaf chlorosis, inhibiting photosynthetic performance and biomass yield in soybean. However, the exogenous supplementation of sodium nitroprusside, a donor of nitric oxide (NO) significantly restored these physiological attributes. The fluorescence intensity of NO indicates that NO-singling induced in response to Fe-deficiency, along with NO induces conversion of Fe3+ to Fe2+, which leads to Fe acquisition and homeostasis mechanism in Strategy I soybean plants. This study further suggests that NO up-regulates the expression candidate genes ZmIRT1, ZmFRO2, and ZmSultr1;3 related to Fe-acquisition and homeostasis in soybean plants. These findings might be useful to soybean breeders and farmers for coping with Fe-deficiency in Strategy I soybean and other grains crops.
Key words: Glycine max, Fe-shortage, Strategy-I, nitric-oxide signaling, chlorosis
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