Reyt Guilhem, Boudouf Soukaina, Boucherez Jossia, Gaymard Frédéric, Briat Jean-Franois
Biochimie et Physiologie Moléculaire des Plantes. Centre National de la Recherche Scientifique, Institut National de la Recherche Agronomique, Université Montpellier 2, SupAgro. Bat 7, 2 place Viala, 34060 Montpellier cedex 1, France Present address : University of Aberdeen. Institute of Biological and Environmental Sciences. Cruickshank Building, St Machar Drive, Aberdeen, Scotland AB24 3UU, United Kingdom.
Biochimie et Physiologie Moléculaire des Plantes. Centre National de la Recherche Scientifique, Institut National de la Recherche Agronomique, Université Montpellier 2, SupAgro. Bat 7, 2 place Viala, 34060 Montpellier cedex 1, France.
Mol Plant. 2014 Nov 9. doi: 10.1093/mp/ssu133.
Iron (Fe) homeostasis is integrated with the production of Reactive Oxygen Species (ROS) whose 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 (Arabidopsis) 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 RSA is in part mediated by the HO/O balance between the root cell proliferation and differentiation zones regulated by the UPB1 transcription factor. Further, 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.
铁（Fe）稳态与活性氧（ROS）的产生相互关联，ROS在根尖的分布参与了对根生长的调控。过量的铁会增加铁蛋白的丰度，从而实现铁的储存，这有助于保护植物免受铁诱导的氧化应激。AtFer1和AtFer3是在拟南芥根的分生区、中柱鞘和内皮层中表达的两个铁蛋白基因，正是在这些区域我们观察到了铁染色点。这种染色在fer1-3-4铁蛋白三突变体中消失。过量的铁以相同的方式缩短野生型和fer1-3-4突变体的主根长度。相反，由于侧根发生缺陷，fer1-3-4植株中铁介导的侧根长度和密度的降低更为明显。我们观察到，过量的铁、铁蛋白和根系结构之间的这种相互作用部分是由UPB1转录因子调控的根细胞增殖和分化区之间的HO/O平衡介导的。此外，在铁蛋白突变体植株中，分生组织大小也会因过量铁而减小，这表明在铁与根系结构的相互作用中，ROS激活的SMR5/SMR7细胞周期蛋白依赖性激酶抑制剂途径介导了细胞周期停滞。
