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

Year: 2025
Type: article
Abstract: Aluminum (Al) toxicity posed a severe threat to sweetpotato production, significantly reducing crop yield. The mechanisms underlying Al tolerance in sweetpotato remained unclear. This study employed a gradient stress treatment, integrated with physiological parameter measurements and transcriptome profiling, to elucidate the response mechanisms of sweetpotato roots to Al stress. Al stress inhibited root growth and development while inducing increases in oxidative and antioxidant parameters, including malondialdehyde (MDA), superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT). Comparative transcriptome analysis identified 2268 common differentially expressed genes (DEGs), among which 1893 genes showed significant correlations with Al stress-related traits. qRT-PCR validation of 11 selected DEGs confirmed the reliability and accuracy of the transcriptome data. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of DEGs demonstrated significant alterations in biological processes or pathways such as phenylpropanoid biosynthesis, photosynthesis and plant secondary metabolism after Al treatment. Further analysis revealed that these DEGs were significantly involved in lignin biosynthesis, organic acid efflux and cell wall modification, collectively conferring Al tolerance to sweetpotato roots. Additionally, transcription factor families including ERF, WRKY and MYB were implicated as key regulators in the Al stress response of sweetpotato. In summary, Al toxicity activated core stress-responsive pathways and triggered specific genes to effectively mitigate Al stress effects in sweetpotato. The candidate genes anchored in this study provide novel insights for subsequent functional characterization and mechanistic dissection of Al stress responses in sweetpotato.
Language: English
Subfield: Plant Science
Open Access status: gold
Estimated APC paid: $3,000
OpenAlex ID: W4416688564
FWCI: 1.005
Cites: 60
Cited by: 2
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