Centro de Estudios Fotosintéticos y Bioquímicos (CEFOBI), CONICET-Universidad Nacional de Rosario, Suipacha 531, 2000, Rosario, Argentina.
Departamento de Microbiologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Prof. Lineu Prestes 1374, São Paulo, 05508-900, Brazil.
Plant Mol Biol. 2016 Nov;92(4-5):613-628. doi: 10.1007/s11103-016-0537-9. Epub 2016 Sep 21.
Plants overexpressing AtHSCB and hscb knockdown mutants showed altered iron homeostasis. The overexpression of AtHSCB led to activation of the iron uptake system and iron accumulation in roots without concomitant transport to shoots, resulting in reduced iron content in the aerial parts of plants. By contrast, hscb knockdown mutants presented the opposite phenotype, with iron accumulation in shoots despite the reduced levels of iron uptake in roots. AtHSCB play a key role in iron metabolism, probably taking part in the control of iron translocation from roots to shoots. Many aspects of plant iron metabolism remain obscure. The most known and studied homeostatic mechanism is the control of iron uptake in the roots by shoots. Nevertheless, this mechanism likely involves various unknown sensors and unidentified signals sent from one tissue to another which need to be identified. Here, we characterized Arabidopsis thaliana plants overexpressing AtHSCB, encoding a mitochondrial cochaperone involved in [Fe-S] cluster biosynthesis, and hscb knockdown mutants, which exhibit altered shoot/root Fe partitioning. Overexpression of AtHSCB induced an increase in root iron uptake and content along with iron deficiency in shoots. Conversely, hscb knockdown mutants exhibited increased iron accumulation in shoots and reduced iron uptake in roots. Different experiments, including foliar iron application, citrate supplementation and iron deficiency treatment, indicate that the shoot-directed control of iron uptake in roots functions properly in these lines, implying that [Fe-S] clusters are not involved in this regulatory mechanism. The most likely explanation is that both lines have altered Fe transport from roots to shoots. This could be consistent with a defect in a homeostatic mechanism operating at the root-to-shoot translocation level, which would be independent of the shoot control over root iron deficiency responses. In summary, the phenotypes of these plants indicate that AtHSCB plays a role in iron metabolism.
过表达 AtHSCB 的植物和 hscb 敲低突变体表现出改变的铁稳态。AtHSCB 的过表达导致铁摄取系统的激活和根中的铁积累,而没有伴随向地上部分的运输,导致植物地上部分的铁含量降低。相比之下,hscb 敲低突变体表现出相反的表型,尽管根中的铁摄取水平降低,但铁在地上部分积累。AtHSCB 在铁代谢中起关键作用,可能参与控制铁从根到地上部分的转运。植物铁代谢的许多方面仍然不清楚。最著名和研究最多的稳态机制是地上部分对根中铁摄取的控制。然而,这种机制可能涉及到各种未知的传感器和从一个组织到另一个组织发送的未识别信号,这些信号需要被识别。在这里,我们对过表达 AtHSCB 的拟南芥植物进行了表征,AtHSCB 编码一种参与 [Fe-S] 簇生物合成的线粒体伴侣蛋白,以及 hscb 敲低突变体,它们表现出改变的地上/地下铁分配。AtHSCB 的过表达诱导根中铁摄取和含量的增加,同时地上部分缺铁。相反,hscb 敲低突变体表现出地上部分铁积累增加和根中铁摄取减少。包括叶面铁应用、柠檬酸盐补充和缺铁处理在内的不同实验表明,这些系中根中铁摄取的地上部分导向控制正常运作,这意味着 [Fe-S] 簇不参与这种调节机制。最可能的解释是,这两条线都改变了铁从根到地上部分的运输。这可能与在根到地上部分转运水平上起作用的稳态机制的缺陷一致,该机制独立于地上部分对根缺铁反应的控制。总之,这些植物的表型表明 AtHSCB 在铁代谢中起作用。