Four IVa bHLH Transcription Factors Are Novel Interactors of FIT and Mediate JA Inhibition of Iron Uptake in Arabidopsis
Four IVa bHLH Transcription Factors Are Novel Interactors of FIT and Mediate JA Inhibition of Iron Uptake in Arabidopsis
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四种 IVa bHLH 转录因子是拟南芥中 FIT 的新型相互作用物并介导 JA 抑制铁吸收
DOI：
10.1016/j.molp.2018.06.005
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发表时间：
2018-09-10
期刊：
影响因子：
27.5
通讯作者：
Ling, Hong-Qing
中科院分区：
文献类型：
--
作者：
Cui, Yan;Chen, Chun-Lin;Ling, Hong-Qing
植物已经进化出复杂的遗传网络来调节铁（Fe）稳态以维持其生存。包括茉莉酸 (JA) 在内的几类植物激素已被证明参与调节植物中铁吸收和/或缺铁反应基因的表达。然而，JA 调节铁吸收的分子机制仍不清楚。在这项研究中，我们发现JA通过下调FIT（bHLH29）、bHLH38、bHLH39、bHLH100和bHLH101的表达并促进FIT蛋白（拟南芥铁吸收的关键调节因子）的降解来负向调节铁吸收。我们进一步证明 IVa 亚组 bHLH 蛋白 bHLH18、bHLH19、bHLH20 和 bHLH25 是 FIT 的新型相互作用因子，可促进 JA 诱导的 FIT 蛋白降解。这四种 IVa bHLH 的功能多余，可以拮抗 Ib bHLH（例如 bHLH38）在缺铁条件下调节 FIT 蛋白稳定性的活性。四个 IVa bHLH 基因主要在根中表达，并且可以通过 JA 处理诱导。此外，我们发现JA信号通路的两个关键组成部分MYC2和JAR1在介导JA抑制FIT和Ib bHLH基因的表达中发挥关键作用，而它们差异调节bHLH18、bHLH19、bHLH20和bHLH25的表达以调节缺铁条件下FIT的积累。总而言之，这些结果表明，通过转录调节不同组 bHLH 基因的表达，JA 信号传导促进 FIT 降解，导致铁吸收基因 IRT1 和 FRO2 的表达减少，并增加对缺铁的敏感性。我们的数据表明，JA 的存在对拟南芥中的缺铁反应具有多层抑制作用。
Plants have evolved sophisticated genetic networks to regulate iron (Fe) homeostasis for their survival. Several classes of plant hormones including jasmonic acid (JA) have been shown to be involved in regulating the expression of iron uptake and/or deficiency-responsive genes in plants. However, the molecular mechanisms by which JA regulates iron uptake remain unclear. In this study, we found that JA negatively modulates iron uptake by downregulating the expression of FIT (bHLH29), bHLH38, bHLH39, bHLH100, and bHLH101 and promoting the degradation of FIT protein, a key regulator of iron uptake in Arabidopsis. We further demonstrated that the subgroup IVa bHLH proteins, bHLH18, bHLH19, bHLH20, and bHLH25, are novel interactors of FIT, which promote JA-induced FIT protein degradation. These four IVa bHLHs function redundantly to antagonize the activity of the Ib bHLHs (such as bHLH38) in regulating FIT protein stability under iron deficiency. The four IVa bHLH genes are primarily expressed in roots, and are inducible by JA treatment. Moreover, we found that MYC2 and JAR1, two critical components of the JA signaling pathway, play critical roles in mediating JA suppression of the expression of FIT and Ib bHLH genes, whereas they differentially modulate the expression of bHLH18, bHLH19, bHLH20, and bHLH25 to regulate FIT accumulation under iron deficiency. Taken together, these results indicate that by transcriptionally regulating the expression of different sets of bHLH genes JA signaling promotes FIT degradation, resulting in reduced expression of iron-uptake genes, IRT1 and FRO2, and increased sensitivity to iron deficiency. Our data suggest that there is a multilayered inhibition of iron-deficiency response in the presence JA in Arabidopsis.