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Senescence is modulated by ORESARA1 (ORE1), a NAC transcription factor that interacts with hormones to fully induce senescence. The <i>At-ore1</i> gene acts as a suppressor of leaf senescence; however, its exact role in this respect has not been clearly defined. In this study, the function of <i>At-ore1</i> during leaf senescence was analyzed in soybeans. The precocious leaf senescence of the <i>ore1</i>-1 line was associated with greater chlorophyll loss, leaf necrosis, and redox imbalance in the early vegetative stage during the hyper-accumulation of endogenous abscisic acid (ABA) by enhancing the expression of GmNECD3-related ABA synthesis. <i>At-ore1</i> induced ABA regulation of the H₂O₂-GmARF2-GmNAC081 signaling circuit, which relays the <i>At-ore1</i>-induced cell death signal mediation to the caspase-1-like vacuolar processing enzyme (VPE) expression, triggering programmed cell death. In contrast, it was found that <i>At-ore1</i> functions in IAA to delay leaf-senescence-mediated suppression of the expression of ABA, ROS, and senescence-associated gene 39 (<i>GmSAG39</i>). The IAA-induced <i>GmNAC065</i> expression controls soybean leaves’ longevity, as discovered by screening <i>At-ore1</i> expression in <i>ore1</i>-6 for a more stay-green leaf phenotype by helping to increase seed yields. These results uncover a mechanism that modulates <i>ore1</i> plants’ amplitude expression involved in the ABA/IAA balance in the activation of <i>GmNAC081</i>- or <i>GmNAC065</i>-dependent H₂O₂ levels, which are crucial in the senescence or delayed leaf senescence of soybeans.