Graduate School of Bioresources, Mie University, Kurimamachiya-cho 1577, Tsu, Mie, 514-8507 Japan.
Plant Cell Physiol. 2011 Aug;52(8):1433-42. doi: 10.1093/pcp/pcr089. Epub 2011 Jul 8.
Nickel (Ni) is an essential nutrient for plants, but excessive amounts can be toxic. Ni competes with iron (Fe) in vivo, raising the possibility that Ni is competitively taken up via the Fe uptake system in plants. Here, we show evidence that AtIRT1, the primary Fe(2+) uptake transporter in the root, mediates Ni accumulation in Arabidopsis thaliana. In hydroponic cultures, excess Ni exposure increased Fe accumulation and the relative transcription level of AtIRT1 in roots, indicating that excess Ni induces AtIRT1 expression in roots. An Fe-deficient treatment increased Ni accumulation in plants, suggesting that excess Ni was absorbed via the Fe uptake system, which was induced by Fe starvation. Moreover, Ni accumulation under Fe-deficient conditions was markedly lower in AtIRT1-defective mutants than in the wild-type, Col-0. Furthermore, AtIRT1 showed Ni(2+) uptake activity in a yeast expression system. These data demonstrate that AtIRT1 transports Ni(2+) in roots, and strongly suggest that Ni accumulation is further accelerated by AtIRT1 that is expressed in response to excess Ni.
镍（Ni）是植物必需的营养元素，但过量会有毒性。Ni 在体内与铁（Fe）竞争，这增加了 Ni 通过植物中的 Fe 摄取系统进行竞争摄取的可能性。在这里，我们提供的证据表明，AtIRT1 是根中主要的 Fe（2+）摄取转运蛋白，介导拟南芥中 Ni 的积累。在水培培养中，过量 Ni 暴露增加了 Fe 积累和根中 AtIRT1 的相对转录水平，表明过量 Ni 诱导根中 AtIRT1 的表达。Fe 缺乏处理增加了植物中的 Ni 积累，表明过量的 Ni 通过 Fe 摄取系统吸收，该系统是由 Fe 饥饿诱导的。此外，在 Fe 缺乏条件下，AtIRT1 缺陷突变体中的 Ni 积累明显低于野生型 Col-0。此外，AtIRT1 在酵母表达系统中表现出 Ni（2+）摄取活性。这些数据表明 AtIRT1 在根中转运 Ni（2+），并强烈表明，响应过量 Ni 表达的 AtIRT1 进一步加速了 Ni 的积累。
