Induction of IRT1 by the nickel-induced iron-deficient response in Arabidopsis
Induction of IRT1 by the nickel-induced iron-deficient response in Arabidopsis
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DOI：
10.4161/psb.19263
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发表时间：
2012-01-01
影响因子：
2.9
通讯作者：
Mizuno, Takafumi
中科院分区：
文献类型：
--
作者：
Nishida, Sho;Aisu, Ayaka;Mizuno, Takafumi
过量的镍（Ni）可能对植物有毒。最近，我们报道了IRT1，根中的初级铁（Fe）摄取转运体，介导了拟南芥过量的Ni积累。我们还发现，Ni暴露增加了根中IRT1的表达，这表明Ni胁迫进一步诱导了Ni的吸收。本研究表明，Ni暴露不仅诱导了IRT1的表达，还诱导了根表皮铁还原酶FRO2和转录因子FIT的表达，FIT是一种调节铁稳态相关基因表达的转录因子，包括IRT1和FRO2。这一结果表明，Ni积累诱导了铁缺乏反应，并导致IRT1的诱导。我们的研究结果表明，过量的Ni在分子水平上导致铁缺乏，并在植物细胞中诱导铁缺乏信号。
Excessive amounts of nickel (Ni) can be toxic for plants. Recently, we reported that IRT1, the primary iron (Fe) uptake transporter in roots, meditates excess Ni accumulation in Arabidopsis thaliana. We also found that Ni exposure increases IRT1 expression in roots, suggesting that Ni uptake is further induced by Ni stress. Here, we show that Ni exposure induces expression of not only IRT1, but also FRO2, a ferric reductase in the root epidermis, and FIT, a transcription factor regulating the expression of genes involved in Fe homeostasis including IRT1 and FRO2. This result suggests that Ni accumulation induces an Fe-deficient response and leads to the induction of IRT1. Our findings suggest that excess Ni causes Fe deficiency at the molecular level and induces Fe deficiency signaling in plant cells.