Genetic Dissection of Fe-Dependent Signaling in Root Developmental Responses to Phosphate Deficiency
Genetic Dissection of Fe-Dependent Signaling in Root Developmental Responses to Phosphate Deficiency
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根系发育对磷酸盐缺乏反应中铁依赖性信号传导的遗传解析
DOI：
10.1104/pp.18.00907
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发表时间：
2019
期刊：
影响因子：
7.4
通讯作者：
Liu Dong
中科院分区：
文献类型：
--
作者：
Wang Xiaoyue;Wang Zhen;Zheng Zai;Dong Jinsong;Song Li;Sui Liqian;Nussaume Laurent;Desnos Thierry;Liu Dong
拟南芥（Arabidopsis thaliana）对缺磷胁迫的一个主要反应是主根生长受到抑制。先前的研究已经独立地揭示了低磷酸盐反应1（LPR 1）铁氧化酶、液泡膜定位的铝敏感3（ALS 3）/对铝根毒敏感1（STAR 1）转运蛋白复合体和对质子根毒敏感1（STAR 1）转运蛋白复合体的关键作用。（STOP 1;一种转录因子）-铝激活的苹果酸转运蛋白1（ALMT 1;苹果酸转运蛋白）调节模块通过控制根中的铁（Fe）稳态来介导这种反应，但这三种组分如何相互作用以调节Pi缺乏下的PR生长仍然未知。在此，我们剖析了这三个关键组分之间的遗传关系，发现（1）STOP 1、ALMT 1和LPR 1在磷缺乏下控制PR生长的过程中起着下游作用：（2）ALS 3/STAR 1通过抑制STOP 1蛋白在细胞核中的积累来抑制STOP 1-ALMT 1通路;（3）STOP 1-ALMT 1和LPR 1以相互依赖的方式调控缺磷条件下PR的生长，促进苹果酸依赖的Fe在根中的积累。此外，这种苹果酸介导的铁积累取决于外部的Pi的可用性。我们还进行了详细的分析的动态变化的组织特异性铁积累模式暴露于磷缺乏植物的根尖。结果表明，缺磷对PR生长的抑制程度与根尖分生组织或伸长区的铁积累水平无关。我们的工作提供了深入了解的分子机制，调节根发育反应，磷缺乏。
The inhibition of primary root (PR) growth is a major developmental response of Arabidopsis (Arabidopsis thaliana) to phosphate (Pi) deficiency. Previous studies have independently uncovered key roles of the LOW PHOSPHATE RESPONSE1 (LPR1) ferroxidase, the tonoplast-localized ALUMINUM SENSITIVE3 (ALS3)/SENSITIVE TO ALUMINUM RHIZOTOXICITY1 (STAR1) transporter complex, and the SENSITIVE TO PROTON RHIZOTOXICITY1 (STOP1; a transcription factor)-ALUMINUM-ACTIVATED MALATE TRANSPORTER1 (ALMT1; a malate transporter) regulatory module in mediating this response by controlling iron (Fe) homeostasis in roots, but how these three components interact to regulate PR growth under Pi deficiency remains unknown. Here, we dissected genetic relationships among these three key components and found that (1) STOP1, ALMT1, and LPR1 act downstream of ALS3/STAR1 in controlling PR growth under Pi deficiency; (2) ALS3/STAR1 inhibits the STOP1-ALMT1 pathway by repressing STOP1 protein accumulation in the nucleus; and (3) STOP1-ALMT1 and LPR1 control PR growth under Pi deficiency in an interdependent manner involving the promotion of malate-dependent Fe accumulation in roots. Furthermore, this malate-mediated Fe accumulation depends on external Pi availability. We also performed a detailed analysis of the dynamic changes in the tissue-specific Fe accumulation patterns in the root tips of plants exposed to Pi deficiency. The results indicate that the degree of inhibition of PR growth induced by Pi deficiency is not linked to the level of Fe accumulated in the root apical meristem or the elongation zone. Our work provides insights into the molecular mechanism that regulates the root developmental response to Pi deficiency.