FRD3 (FERRIC REDUCTASE DEFECTIVE 3) plays a major role in iron (Fe) and zinc (Zn) homeostasis in Arabidopsis. It transports citrate, which enables metal distribution in the plant. An frd3 mutant is dwarf and chlorotic and displays a constitutive Fe-deficiency response and strongly altered metal distribution in tissues. Here, we have examined the interaction between Fe and Zn homeostasis in an frd3 mutant exposed to varying Zn supply. Detailed phenotyping using transcriptomic, ionomic, histochemical and spectroscopic approaches revealed the full complexity of the frd3 mutant phenotype, which resulted from altered transition metal homeostasis, manganese toxicity, and oxidative and biotic stress responses. The cell wall played a key role in these processes, as a site for Fe and hydrogen peroxide accumulation, and displayed modified structure in the mutant. Finally, we showed that Zn excess interfered with these mechanisms and partially restored root growth of the mutant, without reverting the Fe-deficiency response. In conclusion, the frd3 mutant molecular phenotype is more complex than previously described and illustrates how the response to metal imbalance depends on multiple signaling pathways.

中文翻译：

---

拟南芥frd3突变体中的金属稳态，氧化和生物应激反应交织在一起。

FRD3（铁还原酶缺陷3）在拟南芥中的铁（Fe）和锌（Zn）体内稳态中起主要作用。它运输柠檬酸盐，使金属在工厂中分布。frd3突变体是矮化和褪绿的，显示出组成型铁缺乏反应和组织中金属分布的强烈变化。在这里，我们检查了暴露于不同锌供应的frd3突变体中Fe和Zn稳态之间的相互作用。使用转录组学，基因组学，组织化学和光谱学方法进行的详细表型分析揭示了frd3突变体表型的全部复杂性，这是由于过渡金属稳态，锰毒性以及氧化和生物应激反应的改变所致。细胞壁在这些过程中起着关键作用，因为它是铁和过氧化氢积聚的部位，并在突变体中显示出修饰的结构。最后，我们证明了过量的锌干扰了这些机制并部分恢复了突变体的根生长，而没有还原铁缺乏反应。总之，frd3突变分子的表型比以前描述的更为复杂，并说明了对金属不平衡的反应如何取决于多种信号通路。