The role of oxidative stress-induced ribosomal dysfunction in embryogenic decline of <i>Schisandra chinensis</i>

Abstract Schisandra chinensis is a valuable medicinal woody plant, yet its industrial propagation is constrained by the rapid decline in embryogenic competence of callus during in vitro culture. Elucidating the underlying mechanism is essential for establishing a sustainable and efficient micropropagation system. This study aimed to systematically clarify the physiological and molecular mechanisms underlying the decline in embryogenic potential across successive subculture generations in S. chinensis embryogenic callus, thereby providing a theoretical foundation for optimizing the somatic embryogenesis protocol. An integrated multi-omics approach was employed, combining phenotypic, physiological, transcriptomic, and metabolomic analyses of callus at key subculture stages (P1, P4, and P7). The results indicate that embryogenic potential is maintained under a state of balanced energy metabolism and redox homeostasis. Highly embryogenic (P4) callus exhibited active energy and amino acid metabolism, supported by up-regulated hub genes (ScACO3, ScENO1, ScHSP70-4). In contrast, prolonged culture induced severe oxidative stress, characterized by the accumulation of H₂O₂ and O₂-. This oxidative burden activated a ribosomal stress response, with significant up-regulation of ribosomal protein genes (ScRPL7B, ScRPS12, ScRPS11B, ScRPL10A, ScRPL10), ultimately leading to proteostatic collapse and loss of embryogenic capacity. We propose that an “energy–redox–ribosome axis” serves as the core regulatory cascade determining cell fate under culture stress. These findings identify novel targets for delaying embryogenic decline through antioxidant supplementation and culture regimen optimization, offering a sustainable strategy to mitigate in vitro stress in the propagation of woody perennial plants.