背景回顾：Iron (Fe) deficiency is common in agricultural crops and affects millions of people worldwide. Translocation of Fe in the xylem is a key step for Fe distribution in plants. The mechanism controlling this process remains largely unknown. 

主要发现：Here, we report that two Arabidopsis ferroxidases, LPR1 and LPR2, play a crucial and redundant role in controlling Fe translocation in the xylem. 

结果1-表达模式：LPR1 and LPR2 are mainly localized in the cell walls of xylem vessels and the surrounding cells in roots, leaves and stems. 

结果2-双突表型：Knockout of both LPR1 and LPR2 increased the proportion of Fe(II) in the xylem sap, and caused Fe deposition along the vascular bundles especially in the petioles and main veins of leaves, which was alleviated by blocking blue light. The double mutant displayed constitutive expression of Fe-deficiency response genes and overaccumulation of Fe in the roots and mature leaves under Fe-sufficient supply, but Fe-deficiency chlorosis in the new leaves and inflorescences under low Fe supply. The double mutant showed lower Fe concentrations in the xylem and phloem saps and impaired 57Fe translocation along the xylem. 

结果3-体外试验：In vitro assays showed that Fe(III)-citrate, the main form of Fe in xylem sap, is easily photoreduced to Fe(II)-citrate, which is unstable and prone to adsorption by cell walls. 

结论：Taken together, these results indicate that LPR1 and LPR2 are required to oxidize Fe(II) and maintain Fe(III)-citrate stability and mobility during xylem translocation against photoreduction. This study not only uncovers an essential physiological role of LPR1 and LPR2 but also reveals a new mechanism by which plants maintain Fe mobility during long-distance translocation in the xylem.

缺铁是农作物普遍面临的问题，影响着全球数百万人的粮食安全。木质部中的铁转运是决定植物中铁分布的关键步骤。然而，控制这一过程的分子机制并不明晰。本文中，作者报道了两个拟南芥亚铁氧化酶LPR1和LPR2在控制木质部铁转运方面发挥重要且冗余的功能。LPR1和LPR2主要定位于根、叶和茎的木质部导管及其周边细胞的细胞壁中。同时敲除LPR1和LPR2基因会增加木质部汁液中的Fe(II)占比，并且导致叶柄和叶主脉中铁沿着维管束的沉积，而这一表型可以通过阻断蓝光加以缓解。在铁充分条件下，lpr1 lpr2双突变体仍表现出缺铁响应基因的组成型表达，以及根和成熟叶中铁的过量积累；但在铁不充分条件下，lpr1 lpr2双突变体的新叶和花序表现出由缺铁所导致的褪绿。lpr1 lpr2双突变体的木质部和韧皮部汁液含铁浓度较低，并且沿着木质部的铁转运出现缺陷。体外试验表明，木质部汁液中的铁主要形式，即Fe(III)-柠檬酸盐很容易就发生光还原反应，转化成Fe(II)-柠檬酸盐，而后者是不稳定的且易于被细胞壁吸附。综上，本文的研究结果揭示了LPR1和LPR2作用于Fe(II)的氧化，从而帮助Fe(III)-柠檬酸盐在木质部运输过程中对抗光还原并维持其稳定性和移动性。本文的研究不仅揭示了LPR1和LPR2的重要生理作用，同时还解析了植物在木质部中进行长距离转运时维持铁移动性的新机制。