Regulation of mRNA abundance revealed a genetic program for plant leaf acclimation to iron (Fe) limitation. The transcript for SUFB, a key component of the plastid iron–sulfur (Fe–S) assembly pathway is down-regulated early after Fe deficiency, and prior to down-regulation of mRNAs encoding abundant chloroplast Fe containing proteins, which should economize the use of Fe. What controls this system is unclear. We utilized RNA-seq. aimed to identify differentially expressed transcripts that are co-regulated with SUFB after Fe deficiency in leaves. To distinguish if lack of Fe or lack of Fe–S cofactors and associated loss of enzymatic and photosynthetic activity trigger transcriptome reprogramming, WT plants on low Fe were compared with an inducible sufb-RNAi knockdown. Fe deficiency targeted a limited set of genes and predominantly affected transcripts for chloroplast localized proteins. A set of glutaredoxin transcripts was concertedly down-regulated early after Fe deficiency, however when these same genes were down-regulated by RNAi the effect on known chloroplast Fe deficiency marker proteins was minimal. In promoters of differentially expressed genes, binding motifs for AP2/ERF transcription factors were most abundant and three AP2/ERF transcription factors were also differentially expressed early after low Fe treatment. Surprisingly, Fe deficiency in a WT on low Fe and a sufb-RNAi knockdown presented very little overlap in differentially expressed genes. sufb-RNAi produced expression patterns expected for Fe excess and up-regulation of a transcript for another Fe–S assembly component not affected by low Fe. These findings indicate that Fe scarcity, not Fe utilization, triggers reprogramming of the transcriptome in leaves.

中文翻译：

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缺铁和叶绿体铁硫簇组装的丧失引发拟南芥莲座丛中明显的转录组变化

mRNA 丰度的调节揭示了植物叶片适应铁 (Fe) 限制的遗传程序。SUFB 的转录本是质体铁硫 (Fe-S) 组装途径的关键组成部分，在 Fe 缺乏后早期下调，并且在编码大量叶绿体 Fe 的蛋白质的 mRNA 下调之前，这应该节约使用铁。什么控制这个系统尚不清楚。我们使用了 RNA-seq。旨在鉴定叶片缺铁后与SUFB共调节的差异表达转录本。为了区分缺乏 Fe 或缺乏 Fe-S 辅助因子以及相关的酶和光合活性的丧失是否会触发转录组重编程，将低 Fe 的 WT 植物与诱导型sufb进行比较-RNAi 击倒。Fe 缺乏针对一组有限的基因，主要影响叶绿体定位蛋白的转录。一组谷氧还蛋白转录本在 Fe 缺乏后早期被一致下调，但是当这些相同的基因被 RNAi 下调时，对已知叶绿体 Fe 缺乏标记蛋白的影响很小。在差异表达基因的启动子中，AP2/ERF 转录因子的结合基序最为丰富，3 个 AP2/ERF 转录因子也在低 Fe 处理后早期差异表达。令人惊讶的是，低 Fe 的 WT 中的 Fe 缺乏和sufb -RNAi 敲低在差异表达的基因中几乎没有重叠。次要-RNAi 产生了预期的 Fe 过量表达模式和另一个不受低 Fe 影响的 Fe-S 组装组件的转录本的上调。这些发现表明，Fe 的缺乏，而不是 Fe 的利用，触发了叶子中转录组的重编程。