Lilay Grmay H, Castro Pedro Humberto, Campilho Ana, Assunção Ana G L
Department of Plant and Environmental Sciences, Copenhagen Plant Science Centre, University of Copenhagen, Frederiksberg, Denmark.
CIBIO/InBIO - Research Centre in Biodiversity and Genetic Resources, University of Porto, Vairão, Portugal.
Front Plant Sci. 2019 Jan 22;9:1955. doi: 10.3389/fpls.2018.01955. eCollection 2018.
All living organisms require zinc as an essential micronutrient. Maintaining appropriate intracellular zinc supply, and avoiding deficiency or toxic excess, requires a tight regulation of zinc homeostasis. In Arabidopsis, bZIP19 and bZIP23 (basic-leucine zipper) transcription factors are the central regulators of the zinc deficiency response. Their targets include members of the ZIP (Zrt/Irt-like Protein) transporter family, involved in cellular zinc uptake, which are up-regulated at zinc deficiency. However, the mechanisms by which these transcription factors are regulated by cellular zinc status are not yet known. Here, to further our insight, we took advantage of the zinc deficiency hypersensitive phenotype of the double mutant, and used it as background to produce complementation lines of each Arabidopsis F-bZIP transcription factor, including bZIP24. On these lines, we performed complementation and localization studies, analyzed the transcript level of a subset of putative target genes, and performed elemental tissue profiling. We find evidence supporting that the zinc-dependent activity of bZIP19 and bZIP23 is modulated by zinc at protein level, in the nucleus, where cellular zinc sufficiency represses their activity and zinc deficiency is required. In addition, we show that these two transcription factors are functionally redundant to a large extent, and that differential tissue-specific expression patterns might, at least partly, explain distinct regulatory activities. Finally, we show that bZIP24 does not play a central role in the Zn deficiency response. Overall, we provide novel information that advances our understanding of the regulatory activity of bZIP19 and bZIP23.
所有生物都需要锌作为必需的微量营养素。维持适当的细胞内锌供应,避免锌缺乏或过量中毒,需要对锌稳态进行严格调控。在拟南芥中,bZIP19和bZIP23(碱性亮氨酸拉链)转录因子是锌缺乏反应的核心调节因子。它们的靶标包括ZIP(Zrt/Irt样蛋白)转运蛋白家族的成员,这些成员参与细胞对锌的摄取,在锌缺乏时会上调。然而,这些转录因子受细胞锌状态调控的机制尚不清楚。在这里,为了深入了解,我们利用双突变体的锌缺乏超敏表型,并以其为背景构建了每个拟南芥F-bZIP转录因子(包括bZIP24)的互补系。在这些互补系上,我们进行了互补和定位研究,分析了一组假定靶基因的转录水平,并进行了元素组织分析。我们发现有证据支持bZIP19和bZIP23的锌依赖性活性在细胞核中的蛋白质水平上受到锌的调节,细胞锌充足时会抑制它们的活性,而锌缺乏时则需要它们的活性。此外,我们表明这两个转录因子在很大程度上功能冗余,不同的组织特异性表达模式可能至少部分解释了它们不同的调节活性。最后,我们表明bZIP24在锌缺乏反应中不发挥核心作用。总体而言,我们提供了新的信息,增进了我们对bZIP19和bZIP23调节活性的理解。