Integrated Transcriptomic and Metabolomic Insights into the Molecular Mechanisms of Albino Leaf Formation in Sweetpotato

Leaf color mutants are valuable resources for studying photosynthesis, pigment metabolism, and gene regulatory networks in plants. In this study, a naturally occurring sweetpotato albino mutant exhibiting a stable white-leaf phenotype across developmental stages was identified and compared with its green-leaf wild type to elucidate the molecular mechanisms underlying albinism. The mutant showed a dramatic 98.8% reduction in total chlorophyll content and a markedly decreased Fv/Fm value (0.59), indicating severe impairment of PSII efficiency. Integrated transcriptomic analysis identified 3520 differentially expressed genes (DEGs), while metabolomic profiling revealed 270 differentially accumulated metabolites (DAMs). Genes involved in chlorophyll and carotenoid biosynthesis, chloroplast development, and photosynthetic electron transport were strongly repressed, including key regulators such as GLK1, PORA, and PORB. Metabolomic alterations were mainly enriched in flavonoids, phenylpropanoids, and amino acid-derived pathways, reflecting broad reprogramming of both primary and secondary metabolism. These changes were accompanied by severely disrupted chloroplast ultrastructure, suggesting a primary defect in plastid development. Collectively, the integrated multi-omics evidence provides a comprehensive understanding of the coordinated transcriptional and metabolic alterations driving the albino phenotype in sweetpotato and establishes this mutant as a potential model for studying the interplay between chloroplast biogenesis, photosynthesis, and secondary metabolism.