Abstract

Senescence is modulated by ORESARA1 (ORE1), a NAC transcription factor that interacts with hormones to fully induce senescence. The At-ore1 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 At-ore1 during leaf senescence was analyzed in soybeans. The precocious leaf senescence of the ore1-1 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. At-ore1 induced ABA regulation of the H2O2-GmARF2-GmNAC081 signaling circuit, which relays the At-ore1-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 At-ore1 functions in IAA to delay leaf-senescence-mediated suppression of the expression of ABA, ROS, and senescence-associated gene 39 (GmSAG39). The IAA-induced GmNAC065 expression controls soybean leaves’ longevity, as discovered by screening At-ore1 expression in ore1-6 for a more stay-green leaf phenotype by helping to increase seed yields. These results uncover a mechanism that modulates ore1 plants’ amplitude expression involved in the ABA/IAA balance in the activation of GmNAC081- or GmNAC065-dependent H2O2 levels, which are crucial in the senescence or delayed leaf senescence of soybeans.

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