Background <p>Eggplant (<i>Solanum melongena</i> L.), a nutritionally valuable solanaceous crop, exhibits pronounced sensitivity to cold stress, which limits its growth and development. Cytochrome P450 (CYP450) enzymes are widely implicated in plant developmental regulation and abiotic stress responses; however, their functional roles in eggplant remain unexplored.</p> Results <p>In this study, we systematically identified 176 <i>SmCYP450</i> homologs in the eggplant genome, which were phylogenetically classified into 24 distinct subfamilies. Evolutionary analysis revealed that segmental duplication events predominantly drove the expansion of the SmCYP450 family, and codon usage bias within these genes was primarily shaped by natural selection pressures. Notably, transcriptomic profiling identified <i>SmCYP82C1</i> as a cold–responsive candidate, displaying significant upregulation under cold stress. Heterologous overexpression of <i>SmCYP82C1</i> in <i>Arabidopsis thaliana</i> enhanced plant cold tolerance, as evidenced by significantly reduced malondialdehyde (MDA) accumulation and elevated activities of key antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), and peroxidase (POD), under cold stress relative to wild–type controls. Furthermore, transgenic lines exhibited upregulated expression of cold-signaling regulators (<i>CBF1</i>/2/3, <i>ICE1</i>) and the stress–responsive marker <i>COR47</i>, suggesting activation of conserved cold-adaptation pathways. Yeast one–hybrid and dual–luciferase reporter assays demonstrated that the zinc–finger transcription factor SmZIP1 directly binds to the <i>SmCYP82C1</i> promoter to transcriptionally activate its expression.</p> Conclusion <p>This study therefore offers a new gene target to improve cold stress tolerance in eggplant and reveals that <i>SmCYP82C1</i> enhances cold tolerance through dual mechanisms: mitigating oxidative damage via antioxidant system potentiation and modulating stress–associated gene networks.</p>

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Genome-wide characterization of the cytochrome P450 gene family in Solanum melongena and functional analysis of SmCYP82C1 under cold stress

  • Yanhong Lan,
  • Fangyi Gong,
  • Xiaojun Liu,
  • Duchen Liu,
  • Genyun Liang,
  • Chun Li,
  • Feng Xia,
  • Yifan Li,
  • Chao Fang,
  • Peng cai

摘要

Background

Eggplant (Solanum melongena L.), a nutritionally valuable solanaceous crop, exhibits pronounced sensitivity to cold stress, which limits its growth and development. Cytochrome P450 (CYP450) enzymes are widely implicated in plant developmental regulation and abiotic stress responses; however, their functional roles in eggplant remain unexplored.

Results

In this study, we systematically identified 176 SmCYP450 homologs in the eggplant genome, which were phylogenetically classified into 24 distinct subfamilies. Evolutionary analysis revealed that segmental duplication events predominantly drove the expansion of the SmCYP450 family, and codon usage bias within these genes was primarily shaped by natural selection pressures. Notably, transcriptomic profiling identified SmCYP82C1 as a cold–responsive candidate, displaying significant upregulation under cold stress. Heterologous overexpression of SmCYP82C1 in Arabidopsis thaliana enhanced plant cold tolerance, as evidenced by significantly reduced malondialdehyde (MDA) accumulation and elevated activities of key antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), and peroxidase (POD), under cold stress relative to wild–type controls. Furthermore, transgenic lines exhibited upregulated expression of cold-signaling regulators (CBF1/2/3, ICE1) and the stress–responsive marker COR47, suggesting activation of conserved cold-adaptation pathways. Yeast one–hybrid and dual–luciferase reporter assays demonstrated that the zinc–finger transcription factor SmZIP1 directly binds to the SmCYP82C1 promoter to transcriptionally activate its expression.

Conclusion

This study therefore offers a new gene target to improve cold stress tolerance in eggplant and reveals that SmCYP82C1 enhances cold tolerance through dual mechanisms: mitigating oxidative damage via antioxidant system potentiation and modulating stress–associated gene networks.