The State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China.
The State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
Mol Plant. 2018 Sep 10;11(9):1166-1183. doi: 10.1016/j.molp.2018.06.005. Epub 2018 Jun 28.
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.
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。已经表明，包括茉莉酸（JA）在内的几类植物激素参与调节植物中铁吸收和/或缺铁响应基因的表达。然而，JA 调节铁吸收的分子机制尚不清楚。在这项研究中，我们发现 JA 通过下调铁摄取关键调控因子 FIT（bHLH29）、bHLH38、bHLH39、bHLH100 和 bHLH101 的表达，以及促进 FIT 蛋白的降解来负调控铁摄取。我们进一步证明，亚组 IVa bHLH 蛋白 bHLH18、bHLH19、bHLH20 和 bHLH25 是 FIT 的新型互作蛋白，它们促进 JA 诱导的 FIT 蛋白降解。这四个 IVa bHLHs 功能冗余，在缺铁条件下拮抗 Ib bHLHs（如 bHLH38）对 FIT 蛋白稳定性的调节。这四个 IVa bHLH 基因主要在根中表达，并可被 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 基因表达中起着关键作用，而它们差异地调节 bHLH18、bHLH19、bHLH20 和 bHLH25 的表达，以调节 FIT 在缺铁条件下的积累。综上所述，这些结果表明，JA 信号通过转录调控不同的 bHLH 基因表达谱，促进 FIT 降解，导致铁摄取基因 IRT1 和 FRO2 的表达降低，以及对缺铁的敏感性增加。我们的数据表明，在存在 JA 的情况下，拟南芥中存在铁缺乏响应的多层次抑制。
