HISN3 mediates adaptive response of Chlamydomonas reinhardtii to excess nickel.

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.