Physiological and transcriptomic analyses reveal the mechanisms underlying the aluminum tolerance of sweetpotato

• Synergistic alleviation of ROS damage by SOD, POD and proline under aluminum stress in sweetpotato. • Aluminum stress strongly induced alterations in transcriptome profiles. • Aluminum stress significantly affected the expression of genes in phenylpropanoid pathway. • Genes associated with organic acid efflux and cell wall properties functioned in aluminum tolerance. Aluminum (Al) toxicity is a major constraint on sweetpotato productivity. To elucidate the mechanisms of Al tolerance, we integrated physiological and transcriptomic analyses of sweetpotato roots under Al stress. The stress markedly inhibited root growth and disrupted oxidative homeostasis, as evidenced by altered levels of hydrogen peroxide (H₂O₂), oxide ion (O₂⁻), superoxide dismutase (SOD), peroxidase (POD), malondialdehyde (MDA) and proline. Transcriptome profiling identified 2268 differentially expressed genes (DEGs), with 1893 significantly correlated with Al stress traits. These DEGs were profoundly enriched in critical pathways including phenylpropanoid biosynthesis, photosynthesis and secondary metabolism. Further analysis pinpointed key processes in Al tolerance, encompassing lignin biosynthesis, organic acid efflux, and cell wall modification. Additionally, transcription factors such as ERF, WRKY, and MYB were identified as potential regulators in the transcriptional network responsive to Al stress. In conclusion, our study reveals that sweetpotato coordinates a multifaceted adaptive response to mitigate Al toxicity. The candidate genes and pathways uncovered herein provide valuable resources for future functional studies and breeding efforts aimed at enhancing Al tolerance in sweetpotato.