Iron- and Ferritin-Dependent Reactive Oxygen Species Distribution: Impact on Arabidopsis Root System Architecture
Iron- and Ferritin-Dependent Reactive Oxygen Species Distribution: Impact on Arabidopsis Root System Architecture
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DOI：
10.1016/j.molp.2014.11.014
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发表时间：
2015-03-02
期刊：
影响因子：
27.5
通讯作者：
Briat, Jean-Francois
中科院分区：
文献类型：
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作者：
Reyt, Guilhem;Boudouf, Soukaina;Briat, Jean-Francois
铁（Fe）稳态与活性氧（ROS）的产生相结合，根尖的分布参与根生长的控制。过量的铁会增加铁蛋白的丰度，从而能够储存铁，从而有助于保护植物免受铁引起的氧化应激。 AtFer1和AtFer3是在拟南芥根的分生组织区、中柱鞘和内皮层中表达的两个铁蛋白基因，我们正是在这些区域中观察到Fe染色点。这种染色在三重 fer1-3-4 铁蛋白突变体中消失。在野生型和 fer1-3-4 突变体中，铁过量会以相同的方式降低初生根长度。相反，由于 LR 出苗缺陷，Fe 介导的侧根 (LR) 长度和密度减少在 fer1-3-4 植物中增强。我们观察到，过量的铁、铁蛋白和根系结构（RSA）之间的这种相互作用部分是由 H2O2/O-2.(-) 介导的，根细胞增殖和分化区域之间的平衡受 UPB1 转录因子的调节。在铁蛋白突变植物中，分生组织大小也会因铁蛋白过量而减小，这表明在铁蛋白和 RSA 之间的相互作用中，ROS 激活的 SMR5/SMR7 细胞周期蛋白依赖性激酶抑制剂途径介导的细胞周期停滞。
Iron (Fe) homeostasis is integrated with the production of reactive oxygen species (ROS), and distribution at the root tip participates in the control of root growth. Excess Fe increases ferritin abundance, enabling the storage of Fe, which contributes to protection of plants against Fe-induced oxidative stress. AtFer1 and AtFer3 are the two ferritin genes expressed in the meristematic zone, pericycle and endodermis of the Arabidopsis thaliana root, and it is in these regions that we observe Fe stained dots. This staining disappears in the triple fer1-3-4 ferritin mutant. Fe excess decreases primary root length in the same way in wild-type and in fer1-3-4 mutant. In contrast, the Fe-mediated decrease of lateral root (LR) length and density is enhanced in fer1-3-4 plants due to a defect in LR emergence. We observe that this interaction between excess Fe, ferritin, and root system architecture (RSA) is in part mediated by the H2O2/O-2.(-) balance between the root cell proliferation and differentiation zones regulated by the UPB1 transcription factor. Meristem size is also decreased in response to Fe excess in ferritin mutant plants, implicating cell cycle arrest mediated by the ROS-activated SMR5/SMR7 cyclin-dependent kinase inhibitors pathway in the interaction between Fe and RSA.