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缺少平面膜锚定结构的扭曲矮化因子1的表达会导致细胞伸长增加和超形态生长。

Expression of TWISTED DWARF1 lacking its in-plane membrane anchor leads to increased cell elongation and hypermorphic growth.

作者信息

Bailly Aurélien, Wang Bangjun, Zwiewka Marta, Pollmann Stephan, Schenck Daniel, Lüthen Hartwig, Schulz Alexander, Friml Jiri, Geisler Markus

机构信息

Department of Biology - Plant Biology, University of Fribourg, Fribourg, Switzerland; Institute of Plant Biology, University of Zurich, Zurich, Switzerland.

出版信息

Plant J. 2014 Jan;77(1):108-18. doi: 10.1111/tpj.12369. Epub 2013 Dec 9.

DOI:10.1111/tpj.12369
PMID:24313847
Abstract

Plant growth is achieved predominantly by cellular elongation, which is thought to be controlled on several levels by apoplastic auxin. Auxin export into the apoplast is achieved by plasma membrane efflux catalysts of the PIN-FORMED (PIN) and ATP-binding cassette protein subfamily B/phosphor-glycoprotein (ABCB/PGP) classes; the latter were shown to depend on interaction with the FKBP42, TWISTED DWARF1 (TWD1). Here by using a transgenic approach in combination with phenotypical, biochemical and cell biological analyses we demonstrate the importance of a putative C-terminal in-plane membrane anchor of TWD1 in the regulation of ABCB-mediated auxin transport. In contrast with dwarfed twd1 loss-of-function alleles, TWD1 gain-of-function lines that lack a putative in-plane membrane anchor (HA-TWD1-Ct ) show hypermorphic plant architecture, characterized by enhanced stem length and leaf surface but reduced shoot branching. Greater hypocotyl length is the result of enhanced cell elongation that correlates with reduced polar auxin transport capacity for HA-TWD1-Ct . As a consequence, HA-TWD1-Ct displays higher hypocotyl auxin accumulation, which is shown to result in elevated auxin-induced cell elongation rates. Our data highlight the importance of C-terminal membrane anchoring for TWD1 action, which is required for specific regulation of ABCB-mediated auxin transport. These data support a model in which TWD1 controls lateral ABCB1-mediated export into the apoplast, which is required for auxin-mediated cell elongation.

摘要

植物生长主要通过细胞伸长来实现,而细胞伸长被认为在多个层面上受质外体生长素调控。生长素向质外体的输出是由PIN形成蛋白(PIN)和ATP结合盒蛋白亚家族B/磷酸糖蛋白(ABCB/PGP)类的质膜外排催化剂实现的;后者已被证明依赖于与FKBP42、扭曲矮化1(TWD1)相互作用。在这里,我们通过转基因方法结合表型、生化和细胞生物学分析,证明了TWD1假定的C末端平面内膜锚定在ABCB介导的生长素运输调控中的重要性。与矮化的twd1功能缺失等位基因不同,缺少假定平面内膜锚定的TWD1功能获得系(HA-TWD1-Ct)表现出超形态的植物结构,其特征是茎长度和叶面积增加,但枝条分枝减少。下胚轴长度增加是细胞伸长增强的结果,这与HA-TWD1-Ct的极性生长素运输能力降低相关。因此,HA-TWD1-Ct表现出更高的下胚轴生长素积累,这导致生长素诱导的细胞伸长率升高。我们的数据突出了C末端膜锚定对TWD1作用的重要性,这是ABCB介导的生长素运输特异性调控所必需的。这些数据支持了一个模型,即TWD1控制ABCB1介导的侧向输出到质外体,这是生长素介导的细胞伸长所必需的。

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