Carotenoid Metabolism in Plant Stress Adaptation: Pathway Regulation, Flux Distribution, and Stress-Adaptive Functions

Carotenoids are plastid-localized isoprenoid metabolites essential for photosynthesis, photoprotection, and plant development. Their metabolism also provides precursors for abscisic acid (ABA), strigolactones (SLs), and diverse apocarotenoids involved in environmental adaptation. Both abiotic and biotic stresses can alter carotenoid biosynthesis, composition, and turnover, although the underlying regulatory mechanisms and physiological consequences vary with stress type. This review examines how carotenoid pathway regulation influences metabolite allocation and stress-adaptive functions, with particular emphasis on the control of precursor supply and metabolic branch points. We discuss the contributions of carotenoid metabolism to ABA-mediated stress responses, photoprotection and redox homeostasis, and signaling by carotenoid-derived metabolites, including zaxinone, β-ionone, β-cyclocitral, and SLs. The distinct and overlapping roles of these processes in abiotic stress adaptation and biotic defense are evaluated, while senescence is considered as a developmental process associated with changes in carotenoid turnover and downstream signaling. We further examine how functional specialization among pathway genes, transcriptional and chromatin regulation, RNA-mediated control, protein stability, and enzyme interactions influence pathway activity. Metabolite feedback and competition for shared precursors, particularly at the methylerythritol 4-phosphate (MEP) and geranylgeranyl diphosphate (GGPP) nodes, provide additional mechanisms for regulating metabolic branch allocation. The reversible interconversion between ABA and ABA glucose ester (ABA-GE) is also discussed as a mechanism of ABA homeostasis distinct from de novo carotenoid-dependent biosynthesis. Importantly, the extent to which changes in metabolite abundance reflect actual flux redistribution remains insufficiently resolved. Future research should therefore prioritize quantitative flux analysis, the mechanisms underlying tissue- and stress-specific regulation, the perception of carotenoid-derived signals, and strategies to improve stress resilience while minimizing growth and yield penalties.