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Summary The plant stress response mechanism is activated by biotic and abiotic stresses, but its continuous activation typically affects growth. The role of ferritin in regulating biomass accumulation has been extensively characterized in diverse plant species; however, the underlying mechanisms through which it contributes to salt stress tolerance and Fusarium resistance remain poorly understood. Here, we confirm that overexpression of ferritin leads to iron accumulation and Fe 3+ sequestration in both aboveground and roots, activating the iron uptake and transport system. More importantly, GmFER1 enhances salt stress tolerance and Fusarium resistance. First, GmFER1 is localized in chloroplasts and significantly induced by salt stress and Fusarium infection. Overexpression of GmFER1 increases soybean yield per plant by enhancing net photosynthetic rate and Rubisco enzyme activity, without activating the reactive oxygen scavenging mechanism. Under salt stress, GmFER1 enhances resistance by improving the activities of SOD and CAT enzymes, as well as Na + efflux capacity. Under Fusarium infection, GmFER1 enhances resistance to the pathogen by boosting antioxidant capacity. Moreover, iron‐deficiency tests revealed that increased CAT and SOD activities under salt stress are linked to iron ions accumulation. Lastly, we analysed the effects of GmFER1 gene variation on salt tolerance, disease resistance and 23 agronomic traits related to yield and quality. Further analysis of GmFER1 gene variation revealed that the Hap2 haplotypes could potentially enhance salt resistance, disease resistance, pod number and oil content in soybean. Our research offers a new way to reduce growth penalties while boosting plant resistance to salt stress and Fusarium infection.
Zhang et al. (Wed,) studied this question.