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参与海藻糖诱导甜瓜幼苗耐冷性的CmTGA8-CmAPX1/CmGSTU25调控模型

CmTGA8-CmAPX1/CmGSTU25 regulatory model involved in trehalose induced cold tolerance in oriental melon seedlings.

作者信息

Xu Dongdong, Han Yuqing, Zhang Yujie, Khan Abid, Dong Lin, Shao Li, Liang Adan, Liu Tao, Qi Hongyan

机构信息

College of Horticulture, Shenyang Agricultural University, Shenyang, 110866, China; Key Laboratory of Protected Horticulture of Education of Ministry and Liaoning Province, China; Northern National & Local Joint Engineering Research Center of Horticultural Facilities Design and Application Technology, Shenyang, Liaoning, 110866, China.

Department of Horticulture, The University of Haripur, Haripur, Pakistan.

出版信息

Plant Physiol Biochem. 2025 Mar;220:109432. doi: 10.1016/j.plaphy.2024.109432. Epub 2024 Dec 19.

DOI:10.1016/j.plaphy.2024.109432
PMID:39884148
Abstract

Plants have developed complex regulatory networks to adapt to various stresses, including cold stress. Trehalose (Tre), known as the "sugar of life," plays a crucial role in enhancing cold tolerance by triggering antioxidation. However, the underlying regulatory mechanisms remain unclear. This study examines the transcription factor gene CmTGA8, which is induced by Tre under normal and cold conditions in melon seedlings (Cucumis melo L.), through transcriptome analysis and RT-qPCR. Reverse genetic analyses showed that silencing CmTGA8 reduced ascorbate peroxidase (APX) and glutathione S-transferase (GST) activities, suppressed CmAPX1 and CmGSTU25 expression, and increased cold susceptibility in melon seedlings. Our previous reports illustrated that Tre treatment significantly induced the expression of respiratory burst oxidase homologues (CmRBOHD) gene, encoding NADPH oxidases responsible for generating apoplastic HO. Silencing CmRBOHD markedly inhibited CmTGA8, CmAPX1, and CmGSTU25 expression and reduced cold tolerance. Moreover, HO treatment upregulated CmTGA8 expression, while the NADPH oxidase inhibitor diphenyleneiodonium (DPI) treatment downregulated it. Additionally, CmTGA8 physically interacted with CmAPX1 and CmGSTU25 to promote their expression. Silencing CmGSTU25 decreased GST activity and ferric reducing ability of plasma (FRAP), further increasing cold sensitivity. These findings identify a novel regulatory hierarchy of the HO-CmTGA8-CmAPX1/CmGSTU25 cascade in the Tre-mediated cold response pathway in melon seedlings.

摘要

植物已经发展出复杂的调控网络以适应各种胁迫,包括冷胁迫。海藻糖(Tre),即“生命之糖”,在通过触发抗氧化作用提高耐寒性方面发挥着关键作用。然而,其潜在的调控机制仍不清楚。本研究通过转录组分析和RT-qPCR,研究了甜瓜幼苗(Cucumis melo L.)在正常和寒冷条件下由Tre诱导的转录因子基因CmTGA8。反向遗传学分析表明,沉默CmTGA8会降低抗坏血酸过氧化物酶(APX)和谷胱甘肽S-转移酶(GST)的活性,抑制CmAPX1和CmGSTU25的表达,并增加甜瓜幼苗对寒冷的敏感性。我们之前的报告表明,Tre处理显著诱导了呼吸爆发氧化酶同源物(CmRBOHD)基因的表达,该基因编码负责产生质外体HO的NADPH氧化酶。沉默CmRBOHD显著抑制了CmTGA8、CmAPX1和CmGSTU25的表达,并降低了耐寒性。此外,HO处理上调了CmTGA8的表达,而NADPH氧化酶抑制剂二苯基碘鎓(DPI)处理则下调了它的表达。此外,CmTGA8与CmAPX1和CmGSTU25发生物理相互作用以促进它们的表达。沉默CmGSTU25会降低GST活性和血浆铁还原能力(FRAP),进一步增加对寒冷的敏感性。这些发现确定了甜瓜幼苗Tre介导的冷响应途径中HO-CmTGA8-CmAPX1/CmGSTU25级联的新型调控层次。

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