Nishida Sho, Kato Aki, Tsuzuki Chisato, Yoshida Junko, Mizuno Takafumi
Graduate School of Bioresources, Mie University, Kurimamachiya-cho 1577, Tsu, Mie 514-8507, Japan.
Faculty of Bioresources, Mie University, Kurimamachiya-cho 1577, Tsu, Mie 514-8507, Japan.
Int J Mol Sci. 2015 Apr 27;16(5):9420-30. doi: 10.3390/ijms16059420.
Excessive accumulation of nickel (Ni) can be toxic to plants. In Arabidopsis thaliana, the Fe²⁺ transporter, iron (Fe)-regulated transporter1 (IRT1), mediates Fe uptake and also implicates in Ni²⁺ uptake at roots; however, the underlying mechanism of Ni²⁺ uptake and accumulation remains unelucidated. In the present study, we found that zinc (Zn) deficient conditions resulted in increased accumulation of Ni in plants, particularly in roots, in A. thaliana. In order to elucidate the underlying mechanisms of Ni uptake correlating zinc condition, we traced 63Ni isotope in response to Zn and found that (i) Zn deficiency induces short-term Ni²⁺ absorption and (ii) Zn²⁺ inhibits Ni²⁺ uptake, suggesting competitive uptake between Ni and Zn. Furthermore, the Zrt/Irt-like protein 3 (ZIP3)-defective mutant with an elevated Zn-deficient response exhibited higher Ni accumulation than the wild type, further supporting that the response to Zn deficiency induces Ni accumulation. Previously, expression profile study demonstrated that IRT1 expression is not inducible by Zn deficiency. In the present study, we found increased Ni accumulation in IRT1-null mutant under Zn deficiency in agar culture. These suggest that Zn deficiency induces Ni accumulation in an IRT1-independen manner. The present study revealed that Ni accumulation is inducible in response to Zn deficiency, which may be attributable to a Zn uptake transporter induced by Zn deficiency.
镍(Ni)的过量积累对植物具有毒性。在拟南芥中,亚铁转运蛋白铁(Fe)调节转运蛋白1(IRT1)介导铁的吸收,也参与根部对镍离子的吸收;然而,镍离子吸收和积累的潜在机制仍未阐明。在本研究中,我们发现锌(Zn)缺乏条件会导致拟南芥中镍在植物体内尤其是根部的积累增加。为了阐明与锌状况相关的镍吸收潜在机制,我们追踪了63Ni同位素对锌的响应,发现:(i)锌缺乏诱导短期镍离子吸收,(ii)锌离子抑制镍离子吸收,表明镍和锌之间存在竞争性吸收。此外,对锌缺乏反应增强的Zrt/Irt样蛋白3(ZIP3)缺陷突变体比野生型表现出更高的镍积累,进一步支持了对锌缺乏的反应诱导镍积累。此前,表达谱研究表明IRT1的表达不受锌缺乏诱导。在本研究中,我们发现在琼脂培养中锌缺乏条件下IRT1基因敲除突变体中的镍积累增加。这些结果表明锌缺乏以IRT1非依赖的方式诱导镍积累。本研究揭示了镍积累可因锌缺乏而诱导,这可能归因于锌缺乏诱导的锌吸收转运蛋白。