高浓度的氟毒害植物细胞，影响植物正常生长。为研究氟毒害植物的机理，我们以NaF为筛选试剂，从拟南芥EMS诱变库中筛选出4株耐氟突变体（ftol1-4）。遗传分析显示所筛4株突变体为等位基因隐性突变的突变体。利用图位克隆、高通量测序及回补试验，证明突变基因为LPR2，该基因编码一种多铜氧化酶。初步实验表明，高浓度Fe2+可以显著提高该突变体对氟的耐受性，推测LPR2可能将根系细胞中Fe2+氧化成Fe3+，而氟促进了该酶的活性，加剧了细胞内Fe3+毒害效应和氧化应激反应。因此，LPR2突变减缓了由氟诱导的铁毒害。本项目拟在此基础上进一步围绕上述工作假说开展相关研究，阐明LPR2基因在调控植物响应氟胁迫中的作用机制。该研究不仅有助于揭示高浓度氟对植物细胞的毒害的新机制，而且为农作物耐氟分子育种提供理论依据和技术支持。

High concentration of fluoride (F-) is toxic to plant cells, therefore inhibiting plant growth and development. In order to study the mechanisms of fluoride toxicity in plants, we obtained four F- tolerant mutants (ftol1-4) in an ethyl methane sulfonate (EMS) mutagenized population of Arabidopsis thaliana. Genetic analysis shows the mutations were recessive and allelic to each other. Map-based cloning and high throughput sequencing showed FTOL encodes a multicopper oxidase that is identical to LPR2. Preliminary studies showed ftol1 mutant grown under high concentration of Fe2+ were more tolerant to F- stress. We postulate LPR2 might catalyze the oxidation of Fe2+ to Fe3+ whereas F- aggravates this reaction with unknown mechanism, leading to Fe3+ toxicity and oxidative stress, and possibly mutations at LPR2 locus may alleviate Fe3+ toxicity induced by F-. Here, we plan to employ cutting-edge approaches to elucidate the molecular mechanism of LPR2/ FTOL in regulating plant response to F- stress. We believe the research would provide an important scientific basis for our understanding of new mechanism of F- toxicity in higher plants, and exploit novel strategies in crop molecular breeding to enhance F- resistance.