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Alkaline stress and iron deficiency regulate iron uptake and riboflavin synthesis gene expression differently in root and leaf tissue: implications for iron deficiency chlorosis

机译:碱性压力和铁缺乏调节铁的摄取和摄取 核黄素合成基因在根和根中的表达不同 叶组织:对缺铁性萎黄病的影响

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摘要

Iron (Fe) is an essential mineral that has low solubility in alkaline soils, where its deficiency results in chlorosis. Whether low Fe supply and alkaline pH stress are equivalent is unclear, as they have not been treated as separate variables in molecular physiological studies. Additionally, molecular responses to these stresses have not been studied in leaf and root tissues simultaneously. We tested how plants with the Strategy I Fe uptake system respond to Fe deficiency at mildly acidic and alkaline pH by measuring root ferric chelate reductase (FCR) activity and expression of selected Fe uptake genes and riboflavin synthesis genes. Alkaline pH increased cucumber (Cucumis sativus L.) root FCR activity at full Fe supply, but alkaline stress abolished FCR response to low Fe supply. Alkaline pH or low Fe supply resulted in increased expression of Fe uptake genes, but riboflavin synthesis genes responded to Fe deficiency but not alkalinity. Iron deficiency increased expression of some common genes in roots and leaves, but alkaline stress blocked up-regulation of these genes in Fe-deficient leaves. In roots of the melon (Cucumis melo L.) fefe mutant, in which Fe uptake responses are blocked upstream of Fe uptake genes, alkaline stress or Fe deficiency up-regulation of certain Fe uptake and riboflavin synthesis genes was inhibited, indicating a central role for the FeFe protein. These results suggest a model implicating shoot-to-root signaling of Fe status to induce Fe uptake gene expression in roots.
机译:铁(Fe)是在碱性土壤中溶解度低的必需矿物质,其缺乏会导致绿化。低铁供应量和碱性pH应力是否相等尚不清楚,因为在分子生理学研究中尚未将它们视为单独的变量。此外,尚未同时在叶和根组织中研究对这些压力的分子反应。我们通过测量根系铁螯合物还原酶(FCR)活性以及选定的Fe摄取基因和核黄素合成基因的表达,测试了具有I型Fe摄取系统的植物如何应对中度酸性和碱性pH下的Fe缺乏。在完全供应铁的情况下,碱性pH值会增加黄瓜(Cucumis sativus L.)根FCR的活性,但是碱性胁迫消除了对低铁供应的FCR的响应。碱性pH或低Fe供应导致Fe摄取基因表达增加,但核黄素合成基因对Fe缺乏但对碱度无反应。缺铁会增加根和叶中某些常见基因的表达,但是碱性胁迫会阻止缺铁叶中这些基因的上调。在甜菜(Cucumis melo L.)fefe突变体的根中,Fe吸收反应在Fe吸收基因的上游被阻断,碱性胁迫或某些Fe吸收和核黄素合成基因的Fe缺乏上调被抑制,这表明了核心作用为FeFe蛋白。这些结果表明牵涉根系铁状态信号以诱导根中铁吸收基因表达的模型。

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