Magnesium deficiency damages the youngest mature leaf in rice through tissue-specific iron toxicity
Magnesium deficiency damages the youngest mature leaf in rice through tissue-specific iron toxicity
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DOI：
10.1007/s11104-018-3658-x
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发表时间：
2018-07-01
期刊：
影响因子：
4.9
通讯作者：
Tanoi, Keitaro
中科院分区：
文献类型：
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作者：
Kobayashi, Natsuko I.;Ogura, Takaaki;Tanoi, Keitaro
缺镁可引起淀粉积累、光合作用抑制和叶片衰老，尤其是在幼龄叶片中。本研究采用基因芯片技术分析了缺镁胁迫2、4、5 d时小麦幼叶中的基因表达，并筛选出了几个铁响应基因，以确定缺镁胁迫下小麦幼叶衰老的起始过程。转录组分析显示，在30个上调最多的基因中，有7个是铁敏感基因，在30个下调最多的基因中，有11个是铁敏感基因。特别地，OsFER2的上调和OsMIR和OsIRO2的下调暗示在Mg缺乏下过量Fe胁迫的诱导。降低无镁溶液中的铁浓度和在第4天不改变铁浓度的情况下再供应镁通过抑制氧化应激和使铁响应基因的表达正常化来挽救叶片免于衰老。缺镁可诱导过量的铁胁迫，而过量的铁胁迫又会在光合作用受到抑制之前引起氧化胁迫。有人建议，镁缺乏破坏了机制存储有毒的铁离子进入液泡中的扩大年轻的叶细胞。
Magnesium deficiency can cause starch accumulation, photosynthesis inhibition and senescence particularly in young mature leaves. This study was performed to identify the initial process leading to leaf senescence under Mg deficiency.Gene expression in the young leaf was analyzed at days 2, 4, 5 of Mg deficiency using microarray analysis, and several Fe responsive genes were identified. Therefore, the effect of lowering Fe supply on gene expression and oxidative stress under Mg deficiency was evaluated.Transcriptome analysis revealed that 7 of the 30 most upregulated genes and 11 of the 30 most downregulated genes were Fe-responsive. Particularly, the upregulation of OsFER2 and downregulation of OsMIR and OsIRO2 hinted at the induction of excess Fe stress under Mg deficiency. Both lowering of Fe concentration in Mg-free solutions and resupply of Mg without modifying Fe concentrations at day 4 rescued leaves from senescence by inhibiting oxidative stress and normalising the expression of Fe-responsive genes. Meanwhile, Fe content was equal between control, Mg-deficient and Mg-resupplied plants.Mg shortage can induce excess Fe stress, which in turn causes oxidative stress before inhibition of photosynthesis. It is proposed that Mg deficiency disrupts a mechanism for storing toxic Fe ions into the vacuole in the expanding young leaf cells.