背景回顾：Despite serving as a major inorganic nitrogen source for plants, ammonium causes toxicity at elevated concentrations, inhibiting root elongation early on. 

提出问题：While previous studies have shown that ammonium-inhibited root development relates to ammonium uptake and formation of reactive oxygen species (ROS) in roots, it remained open which mechanisms are underlying the repression of root growth and how plants cope with this inhibitory effect of ammonium. 

主要发现：Here, we demonstrate that ammonium-induced apoplastic acidification co-localizes with Fe precipitation and hydrogen peroxide (H2O2) accumulation along the stele of the elongation and differentiation zone in root tips, indicating Fe-dependent ROS formation. 

结果1-突变体库筛选：By screening ammonium sensitivity in T-DNA insertion lines of ammonium-responsive genes, we identified PDX1.1, which is upregulated by ammonium in the root stele and catalyzes biosynthesis de novo of vitamin B₆. 

结果2-pdx1.1突变及拯救：Root growth of pdx1.1 mutants is hypersensitive to ammonium, while chemical complementation or overexpression of PDX1.1 restores root elongation. 

结果3-非磷酸化维生素B6：This salvage strategy requires non-phosphorylated forms of vitamin B6 that are able to quench reactive molecular oxygen species and rescue root growth from ammonium inhibition. 

结论：We propose PDX1.1-mediated synthesis of non-phosphorylated B6 vitamers as a primary strategy to protect roots from ammonium-dependent ROS formation.

 摘 要 

尽管铵是植物一个主要的无机氮源，但是高浓度的铵会到植物产生毒性，在早期抑制根的伸长。先前的研究表明，受到铵抑制的根发育与根系对铵的吸收以及活性氧物质（ROS）的形成有关，但关于根生长抑制以及植物如何应对这种铵抑制作用的分子机制仍未有定论。本文中，作者发现铵诱导的质外体酸化与铁沉淀和过氧化氢积累共定位于沿根尖伸长区和分化区的中柱，表明存在铁依赖性的ROS形成。通过对铵响应基因T-DNA插入突变体株系筛选其对铵的敏感性，作者成功鉴定到了 PDX1.1基因，根中柱中的铵会诱导该基因的上调表达，从而催化维生素B6的从头生物合成。pdx1.1突变体的根系生长对铵较为敏感，而通过化学互补或者PDX1.1的过表达，能够恢复根的伸长。这种拯救策略需要维生素B6的非磷酸化形式，这种形式的维生素B6能够抑制活性分子氧物种，并且从铵抑制中拯救根的生长。因此，作者提出利用PDX1.1介导的非磷酸化B6维生素体的合成是保护根免受铵依赖性ROS形成的主要策略。