PRC2-Mediated H3K27me3 Contributes to Transcriptional Regulation of FIT-Dependent Iron Deficiency Response
PRC2-Mediated H3K27me3 Contributes to Transcriptional Regulation of FIT-Dependent Iron Deficiency Response
复制标题
DOI：
10.3389/fpls.2019.00627
复制
发表时间：
2019-05-16
影响因子：
5.6
通讯作者：
Jeong, Jeeyon
中科院分区：
文献类型：
--
作者：
Park, Emily Y.;Tsuyuki, Kaitlyn M.;Jeong, Jeeyon
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物种的形成。因此，铁的获取和动态平衡必须受到严格的调控。植物进化出了复杂的机制来优化它们对铁的利用，铁是土壤中最具限制性的养分之一。特别是，转录调控对于调节植物中的铁是至关重要的，许多工作已经揭示了转录因子在这方面的作用。我们的研究为植物铁稳态的转录调控提供了新的见解，表明组蛋白3赖氨酸27三甲基化(H3K27me3)通过染色质重塑调节缺铁条件下FIT依赖基因的表达。我们提供的证据表明，FIT依赖的铁获取基因IRT1和FRO2以及FIT本身是PRC2介导的H3K27me3的直接靶标。在缺乏优势H3K27三甲基转移酶的clf突变体中，缺铁条件下根中FIT、FRO2、IRT1等FIT调控基因的诱导显著高于野生型。此外，我们观察到clf突变体比野生型对缺铁的耐受性更强，这表明基因表达水平似乎限制了植物获得铁的能力。我们认为，H3K27me3减弱了缺铁条件下FIT靶基因的诱导，并假设这可能是一种限制铁获取基因诱导的最大水平以防止铁超载的机制。
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, IRT1 and FRO2, as well as FIT itself are direct targets of PRC2-mediated H3K27me3. In the clf mutant, which lacks the predominant H3K27 tri-methyltransferase, induction of FIT, FRO2, IRT1, and other FIT-regulated genes in roots is significantly higher under iron deficient conditions than in wild type. Furthermore, we observe that clf 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.