Aims <p>Concurrent salt and drought stresses frequently challenge cultivated plants, significantly restricting the distribution and yield of major crops. However, the underlying mechanisms of plant responses to combined stresses remain poorly understood. Previously, we identified sweetpotato <i>IbERF7</i> as a candidate gene for regulating abiotic stress response, while its functional role in combined stress tolerance remained elusive.</p> Methods <p><i>IbERF7</i>-transgenic Arabidopsis plants were subjected to single and combined salt and osmotic stresses. Phenotypic differences, physiological and biochemical responses, and gene expression changes were investigated. IbERF7 interaction partners and target genes were screened and functionally validated.</p> Results <p><i>IbERF7</i> expression was more strongly induced by combined salt and osmotic stresses than by either stress alone. IbERF7 was a nuclear-localized DREB-type transcription factor lacking transactivation activity. Ectopic expression of <i>IbERF7</i> reduced Arabidopsis tolerance to single and combined salt and osmotic stresses and downregulated transcription of various stress-responsive genes. IbERF7 indirectly interacted with the intrinsically disordered protein STRP. Mutation of <i>STRP</i> dramatically impaired tolerance to both single and combined stresses. Furthermore, IbERF7 repressed the expression of the CCHC-type <i>zinc finger protein 1</i> (<i>ZFP1</i>) gene by directly binding to DRE/CRT elements. Consistently, <i>ZFP1</i> mutation remarkably reduced tolerance to single and combined stresses. Additionally, <i>IbERF7</i>-transgenic plants exhibited ABA hypersensitivity accompanied by upregulated expression of ABA signaling-related genes.</p> Conclusions <p>These data provide the molecular evidence that the IbERF7-STRP-<i>ZFP1</i> transcriptional cascade regulates the combined salt and osmotic stress tolerance through the ABA signaling pathway.</p>

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The sweetpotato AP2/ERF transcription factor, IbERF7, negatively modulates single and combined salt and osmotic stress tolerance

  • Xiaoqing Meng,
  • Haiting Hong,
  • Jing Yu,
  • Siyuan Liu,
  • Yumeng Lv,
  • Weiwei Liu,
  • Yifei Wang,
  • Tingting Dong,
  • Zongyun Li,
  • Mingku Zhu

摘要

Aims

Concurrent salt and drought stresses frequently challenge cultivated plants, significantly restricting the distribution and yield of major crops. However, the underlying mechanisms of plant responses to combined stresses remain poorly understood. Previously, we identified sweetpotato IbERF7 as a candidate gene for regulating abiotic stress response, while its functional role in combined stress tolerance remained elusive.

Methods

IbERF7-transgenic Arabidopsis plants were subjected to single and combined salt and osmotic stresses. Phenotypic differences, physiological and biochemical responses, and gene expression changes were investigated. IbERF7 interaction partners and target genes were screened and functionally validated.

Results

IbERF7 expression was more strongly induced by combined salt and osmotic stresses than by either stress alone. IbERF7 was a nuclear-localized DREB-type transcription factor lacking transactivation activity. Ectopic expression of IbERF7 reduced Arabidopsis tolerance to single and combined salt and osmotic stresses and downregulated transcription of various stress-responsive genes. IbERF7 indirectly interacted with the intrinsically disordered protein STRP. Mutation of STRP dramatically impaired tolerance to both single and combined stresses. Furthermore, IbERF7 repressed the expression of the CCHC-type zinc finger protein 1 (ZFP1) gene by directly binding to DRE/CRT elements. Consistently, ZFP1 mutation remarkably reduced tolerance to single and combined stresses. Additionally, IbERF7-transgenic plants exhibited ABA hypersensitivity accompanied by upregulated expression of ABA signaling-related genes.

Conclusions

These data provide the molecular evidence that the IbERF7-STRP-ZFP1 transcriptional cascade regulates the combined salt and osmotic stress tolerance through the ABA signaling pathway.