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内质网驻留蛋白PDR2和LPR1介导根分生组织对磷有效性的发育响应。

ER-resident proteins PDR2 and LPR1 mediate the developmental response of root meristems to phosphate availability.

作者信息

Ticconi Carla A, Lucero Rocco D, Sakhonwasee Siriwat, Adamson Aaron W, Creff Audrey, Nussaume Laurent, Desnos Thierry, Abel Steffen

机构信息

Department of Plant Sciences, University of California, One Shields Avenue, Davis, CA 95616, USA.

出版信息

Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):14174-9. doi: 10.1073/pnas.0901778106. Epub 2009 Aug 7.

DOI:10.1073/pnas.0901778106
PMID:19666499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2723163/
Abstract

Inadequate availability of inorganic phosphate (Pi) in the rhizosphere is a common challenge to plants, which activate metabolic and developmental responses to maximize Pi acquisition. The sensory mechanisms that monitor environmental Pi status and regulate root growth via altered meristem activity are unknown. Here, we show that PHOSPHATE DEFICIENCY RESPONSE 2 (PDR2) encodes the single P(5)-type ATPase of Arabidopsis thaliana. PDR2 functions in the endoplasmic reticulum (ER) and is required for proper expression of SCARECROW (SCR), a key regulator of root patterning, and for stem-cell maintenance in Pi-deprived roots. We further show that the multicopper oxidase encoded by LOW PHOSPHATE ROOT 1 (LPR1) is targeted to the ER and that LPR1 and PDR2 interact genetically. Because the expression domains of both genes overlap in the stem-cell niche and distal root meristem, we propose that PDR2 and LPR1 function together in an ER-resident pathway that adjusts root meristem activity to external Pi. Our data indicate that the Pi-conditional root phenotype of pdr2 is not caused by increased Fe availability in low Pi; however, Fe homeostasis modifies the developmental response of root meristems to Pi availability.

摘要

根际无机磷酸盐(Pi)供应不足是植物面临的一个常见挑战,植物会激活代谢和发育反应以最大限度地获取Pi。监测环境Pi状态并通过改变分生组织活性来调节根生长的感知机制尚不清楚。在这里,我们表明磷酸盐缺乏反应2(PDR2)编码拟南芥中的单一P(5)型ATP酶。PDR2在内质网(ER)中发挥作用,是根模式关键调节因子稻草人(SCR)正确表达以及Pi缺乏根中干细胞维持所必需的。我们进一步表明,低磷根1(LPR1)编码的多铜氧化酶定位于内质网,并且LPR1和PDR2在遗传上相互作用。由于这两个基因的表达域在干细胞龛和远端根分生组织中重叠,我们提出PDR2和LPR1在内质网驻留途径中共同发挥作用,该途径将根分生组织活性调整到外部Pi。我们的数据表明,pdr2的Pi条件性根表型不是由低Pi中增加的铁可用性引起的;然而,铁稳态会改变根分生组织对Pi可用性的发育反应。

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本文引用的文献

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