Exogenous GABA mitigates flower senescence in Hemerocallis fulva L. by modulating biochemical and molecular aspects.

Oxidative stress mediated by reactive oxygen species and the concomitant antioxidant defenses orchestrate the senescence trajectory in ethylene-insensitive flowers. This investigation delineates the potential of γ-Aminobutyric acid (GABA) in ameliorating oxidative damage and impeding senescence in detached scapes of Hemerocallis fulva, an ethylene-insensitive flower system. The delayed senescence and enhanced scape performance were attributed to the upregulation of antioxidant enzyme activities, including superoxide dismutase, catalase and ascorbate peroxidase, which were elevated by 52.83%, 129% and 126.07%, respectively. These elevated antioxidant defenses were associated with a significant 41.88% reduction in hydrogen peroxide levels, thereby alleviating oxidative stress. Elevated oxidative stress in the control group was associated with the upregulation of SAG12 (Senescence-Associated Gene 12) and LOX1 (Lipoxygenase 1) gene expression, alongside the downregulation of DAD1 (Defender Against Death 1), indicative of accelerated senescence. Conversely, treatment with 40 µM GABA significantly modulated the expression of these genes, leading to a 1.5-fold upregulation of DAD1 and marked downregulation of SAG12 and LOX1 by 4-fold and 6.5-fold, respectively, relative to the control. GABA-treated scapes also manifested significantly higher concentrations of proline, phenols, sugars and soluble proteins in floral tissues compared to the control. Furthermore, GABA enhanced membrane integrity and curtailed bacterial proliferation in vase solutions, thereby optimizing solution uptake by the flowers. Our study concluded that GABA delayed flower scape senescence not only by mitigating oxidative stress through the enhancement of antioxidant enzyme activities but also by modulating senescence-associated gene expression.

Supplementary information: The online version contains supplementary material available at 10.1007/s12298-025-01636-9.