Physiological and molecular bases of the nickel toxicity responses in tomato.

Hao Yu, Weimin Li, Xiaoxiao Liu, Qianqian Song, Junjun Li, Jin Xu
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引用次数: 0

Abstract

Nickel (Ni), a component of urease, is a micronutrient essential for plant growth and development, but excess Ni is toxic to plants. Tomato (Solanum lycopersicum L.) is one of the important vegetables worldwide. Excessive use of fertilizers and pesticides led to Ni contamination in agricultural soils, thus reducing yield and quality of tomatoes. However, the molecular regulatory mechanisms of Ni toxicity responses in tomato plants have largely not been elucidated. Here, we investigated the molecular mechanisms underlying the Ni toxicity response in tomato plants by physio-biochemical, transcriptomic and molecular regulatory network analyses. Ni toxicity repressed photosynthesis, induced the formation of brush-like lateral roots and interfered with micronutrient accumulation in tomato seedlings. Ni toxicity also induced reactive oxygen species accumulation and oxidative stress responses in plants. Furthermore, Ni toxicity reduced the phytohormone concentrations, including auxin, cytokinin and gibberellic acid, thereby retarding plant growth. Transcriptome analysis revealed that Ni toxicity altered the expression of genes involved in carbon/nitrogen metabolism pathways. Taken together, these results provide a theoretical basis for identifying key genes that could reduce excess Ni accumulation in tomato plants and are helpful for ensuring food safety and sustainable agricultural development.

番茄镍毒性反应的生理和分子基础。
镍(Ni)是脲酶的一种成分,是植物生长和发育所必需的微量营养元素,但过量的镍对植物有毒。番茄(Solanum lycopersicum L.)是世界上重要的蔬菜之一。化肥和农药的过度使用导致农业土壤中的镍污染,从而降低了番茄的产量和质量。然而,番茄植株对镍毒性反应的分子调控机制大多尚未阐明。在此,我们通过生理生化、转录组学和分子调控网络分析,研究了番茄植物镍毒性反应的分子机制。镍毒性抑制了番茄幼苗的光合作用,诱导了刷状侧根的形成,并干扰了微量营养元素的积累。镍毒性还诱导植物体内活性氧积累和氧化应激反应。此外,镍毒性还降低了植物激素的浓度,包括辅助素、细胞分裂素和赤霉素,从而阻碍了植物的生长。转录组分析表明,镍毒性改变了参与碳/氮代谢途径的基因的表达。综上所述,这些结果为确定可减少番茄植株过量镍积累的关键基因提供了理论依据,有助于确保食品安全和农业可持续发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
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