Park Emily Y, Tsuyuki Kaitlyn M, Hu Fengling, Lee Joohyun, Jeong Jeeyon
Program in Biochemistry and Biophysics, Amherst College, Amherst, MA, United States.
Department of Biology, Amherst College, Amherst, MA, United States.
Front Plant Sci. 2019 May 16;10:627. doi: 10.3389/fpls.2019.00627. eCollection 2019.
Iron is an essential micronutrient for nearly all organisms, but excessive iron can lead to the formation of cytotoxic reactive oxygen species. Therefore, iron acquisition and homeostasis must be tightly regulated. Plants have evolved complex mechanisms to optimize their use of iron, which is one of the most limiting nutrients in the soil. In particular, transcriptional regulation is vital for regulating iron in plants, and much work has revealed the role of transcription factors on this front. Our study adds novel insights to the transcriptional regulation of iron homeostasis in plants by showing that chromatin remodeling via histone 3 lysine 27 trimethylation (H3K27me3) modulates the expression of FIT-dependent genes under iron deficiency. We provide evidence that FIT-dependent iron acquisition genes, and , as well as itself are direct targets of PRC2-mediated H3K27me3. In the mutant, which lacks the predominant H3K27 tri-methyltransferase, induction of , , , and other FIT-regulated genes in roots is significantly higher under iron deficient conditions than in wild type. Furthermore, we observe that mutants are more tolerant to iron deficiency than wild type, indicating that gene expression levels appear to be limiting the plants ability to access iron. We propose that H3K27me3 attenuates the induction of FIT-target genes under iron deficiency and hypothesize that this may serve as a mechanism to restrict the maximum level of induction of iron acquisition genes to prevent iron overload.
铁是几乎所有生物体必需的微量营养素，但过量的铁会导致细胞毒性活性氧的形成。因此，铁的获取和稳态必须受到严格调控。植物已经进化出复杂的机制来优化对铁的利用，铁是土壤中最具限制性的养分之一。特别是，转录调控对于植物中铁的调节至关重要，许多研究揭示了转录因子在这方面的作用。我们的研究通过表明在缺铁条件下通过组蛋白3赖氨酸27三甲基化（H3K27me3）进行的染色质重塑调节依赖FIT的基因表达，为植物中铁稳态的转录调控增添了新的见解。我们提供证据表明，依赖FIT的铁获取基因以及 本身是PRC2介导的H3K27me3的直接靶标。在缺乏主要H3K27三甲基转移酶的 突变体中，在缺铁条件下，根中 、 、 以及其他FIT调节基因的诱导明显高于野生型。此外，我们观察到 突变体比野生型更耐缺铁，这表明基因表达水平似乎限制了植物获取铁的能力。我们提出，H3K27me3在缺铁条件下减弱了FIT靶基因的诱导，并推测这可能作为一种机制来限制铁获取基因的最大诱导水平，以防止铁过载。
