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HISN3 介导莱茵衣藻对过量镍的适应性反应。

HISN3 mediates adaptive response of Chlamydomonas reinhardtii to excess nickel.

机构信息

Department of Biochemistry and Molecular Biology, College of Life Science, Nanjing Agricultural University, Nanjing, China.

出版信息

Plant Cell Physiol. 2013 Dec;54(12):1951-62. doi: 10.1093/pcp/pct130. Epub 2013 Sep 28.

DOI:10.1093/pcp/pct130
PMID:24078767
Abstract

Investigation of genes for heavy metal [e.g. nickel (Ni) and zinc (Zn)] absorption and detoxification in green algae is of great importance because some of the metals have become one of the major contaminants in the aquatic ecosystem. In plants, overload of heavy metals modifies many aspects of biological processes. However, the mechanisms by which heavy metals exert detrimental effects are not fully understood. The present study identified a biological role for HISN3 (the gene coding for phosphoribosylformimino-5-aminoimidazole carboxamide ribonucleotide isomerase) in regulating the response of Chlamydomonas reinhardtii, a unicellular green alga, to Ni toxicity. In higher plants, HISN3 encodes an enzyme catalyzing the fourth step in the histidine biosynthesis pathway, but its functional importance is yet to be identified. Transgenic algae overexpressing HISN3 in C. reinhardtii showed high tolerance to excess Ni, with a 48.3-57.4% increase in cell population and moderate histidine accumulation compared with the wild type. HISN3 overexpression improved accumulation of Chl and photosynthesis efficiency, but suppressed Ni-induced generation of reactive oxygen species and lipid peroxides. Interestingly, more Ni and other metals [Zn, iron (Fe), copper (Cu), manganese (Mn) and magnesium (Mg)] were accumulated in HISN3-overexpressing cells than in the wild type. In contrast, RNA interference of HISN3 depressed Ni accumulation but caused cellular sensitivity to Ni. The elevated metal absorption in the HISN3-overexpressing algae implies that the metals can be removed from water media. Thus, our work presents an example for algae genetically designed to improve tolerance to metal toxicity and environmental restoration of metal-contaminated aquatic ecosystems.

摘要

研究藻类对重金属(如镍(Ni)和锌(Zn))的吸收和解毒基因非常重要,因为其中一些金属已成为水生生态系统中的主要污染物之一。在植物中,重金属过载会改变许多生物过程。然而,重金属产生有害影响的机制尚未完全了解。本研究鉴定了 HISN3(编码磷酸核糖基甲酰咪唑-5-氨基咪唑甲酰胺核苷酸异构酶的基因)在调节单细胞绿藻莱茵衣藻对 Ni 毒性反应中的生物学作用。在高等植物中,HISN3 编码一种酶,可催化组氨酸生物合成途径的第四步,但它的功能重要性尚未确定。在莱茵衣藻中过表达 HISN3 的转基因藻类对过量 Ni 的耐受性较高,与野生型相比,细胞群体增加了 48.3-57.4%,组氨酸积累适中。HISN3 的过表达提高了 Chl 的积累和光合作用效率,但抑制了 Ni 诱导的活性氧和脂质过氧化物的产生。有趣的是,与野生型相比,过表达 HISN3 的细胞中积累了更多的 Ni 和其他金属(Zn、Fe、Cu、Mn 和 Mg)。相比之下,HISN3 的 RNA 干扰抑制了 Ni 的积累,但使细胞对 Ni 敏感。过表达 HISN3 的藻类对金属的吸收增加,这意味着可以将金属从水介质中去除。因此,我们的工作为通过基因工程设计藻类以提高对金属毒性的耐受性和修复金属污染的水生生态系统提供了一个范例。

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