Arsenate is a highly toxic element and excessive accumulation of arsenic in the aquatic environment easily triggers a problem threatening the ecological health. Phytoremediation has been widely explored as a method to alleviate As contamination. Here, the green algae, was investigated by profiling the accumulation of arsenate and phosphorus, which share the same uptake pathway, in response to arsenic stress. Both wild type C30 and the mutant were cultured under arsenic stress, and demonstrated a similar growth phenotype under limited phosphate supply. Sufficient phosphate obviously increased the uptake of polyphosphate and intercellular phosphate in the mutant, which increased the arsenic tolerance of the mutant under stress from 500 µmol L As(V). Upregulation of the gene in the mutant increased accumulation of phosphate in the cytoplasm under arsenate stress, which triggered a regulatory role for the differentially expressed genes that mediated improvement of the glutathione redox cycle, antioxidant activity and detoxification. While the wild type C30 showed weak arsenate tolerance because of little phosphate accumulation. These results suggest that the enhanced arsenic tolerance of the mutant is regulated by the gene mediation. This study provides insight onto the responsive mechanisms of the gene-mediated in alleviating arsenic toxicity in plants.

中文翻译：

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莱茵衣藻中磷积累与线粒体 PHT3 介导的砷酸盐耐受性增强相关


砷酸盐是一种剧毒元素，砷在水生环境中的过量积累容易引发威胁生态健康的问题。植物修复作为减轻砷污染的方法已被广泛探索。在这里，通过分析砷酸盐和磷的积累来研究绿藻，砷酸盐和磷具有相同的吸收途径，以响应砷胁迫。野生型C30和突变体均在砷胁迫下培养，并在有限的磷酸盐供应下表现出相似的生长表型。充足的磷酸盐明显增加了突变体对多磷酸盐和细胞间磷酸盐的摄取，从而提高了突变体在500 µmol·L As(V)胁迫下的砷耐受性。突变体中该基因的上调增加了砷酸盐胁迫下细胞质中磷酸盐的积累，从而引发了差异表达基因的调节作用，介导了谷胱甘肽氧化还原循环、抗氧化活性和解毒的改善。而野生型C30由于磷酸盐积累很少，表现出较弱的砷耐受性。这些结果表明突变体增强的砷耐受性是由基因介导调节的。这项研究提供了对基因介导的减轻植物砷毒性的响应机制的见解。