首页> 美国卫生研究院文献>Plant Physiology >CESA TRAFFICKING INHIBITOR Inhibits Cellulose Deposition and Interferes with the Trafficking of Cellulose Synthase Complexes and Their Associated Proteins KORRIGAN1 and POM2/CELLULOSE SYNTHASE INTERACTIVE PROTEIN1
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CESA TRAFFICKING INHIBITOR Inhibits Cellulose Deposition and Interferes with the Trafficking of Cellulose Synthase Complexes and Their Associated Proteins KORRIGAN1 and POM2/CELLULOSE SYNTHASE INTERACTIVE PROTEIN1

机译:CESA交通抑制剂抑制纤维素沉积并干扰纤维素合成酶复合物及其相关蛋白KORRIGAN1和POM2 /纤维素合成酶相互作用蛋白1的运输。

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摘要

Cellulose synthase complexes (s) at the plasma membrane () are aligned with cortical microtubules (s) and direct the biosynthesis of cellulose. The mechanism of the interaction between s and s, and the cellular determinants that control the delivery of s at the , are not yet well understood. We identified a unique small molecule, CESA TRAFFICKING INHIBITOR (CESTRIN), which reduces cellulose content and alters the anisotropic growth of Arabidopsis (Arabidopsis thaliana) hypocotyls. We monitored the distribution and mobility of fluorescently labeled cellulose synthases (s) in live Arabidopsis cells under chemical exposure to characterize their subcellular effects. CESTRIN reduces the velocity of s and causes their accumulation in the cell cortex. The -associated proteins KORRIGAN1 (KOR1) and POM2/CELLULOSE SYNTHASE INTERACTIVE PROTEIN1 (CSI1) were differentially affected by CESTRIN treatment, indicating different forms of association with the s. KOR1 accumulated in bodies similar to ; however, POM2/CSI1 dissociated into the cytoplasm. In addition, stability was altered without direct inhibition of polymerization, suggesting a feedback mechanism caused by cellulose interference. The selectivity of CESTRIN was assessed using a variety of subcellular markers for which no morphological effect was observed. The association of href="#def3" rid="def3" class=" def">CESAs with vesicles decorated by the trans-Golgi network-localized protein SYNTAXIN OF PLANTS61 (SYP61) was increased under CESTRIN treatment, implicating SYP61 compartments in href="#def3" rid="def3" class=" def">CESA trafficking. The properties of CESTRIN compared with known href="#def3" rid="def3" class=" def">CESA inhibitors afford unique avenues to study and understand the mechanism under which href="#def1" rid="def1" class=" def">PM-associated href="#def2" rid="def2" class=" def">CSCs are maintained and interact with href="#def4" rid="def4" class=" def">MTs and to dissect their trafficking routes in etiolated hypocotyls.
机译:将质膜上的纤维素合酶复合物与皮层微管对准,并指导纤维素的生物合成。 s和s之间相互作用的机制,以及控制s在s处传递的细胞决定因子,目前尚不十分清楚。我们确定了一种独特的小分子,CESA流量抑制剂(CESTRIN),可降低纤维素含量并改变拟南芥(Arabidopsis thaliana)下胚轴的各向异性生长。我们在化学暴露下监测了活的拟南芥细胞中荧光标记的纤维素合酶的分布和迁移,以表征其亚细胞效应。 CESTRIN降低了s的速度,并导致它们在细胞皮质中积累。关联蛋白KORRIGAN1(KOR1)和POM2 /纤维素合成酶相互作用蛋白1(CSI1)受CESTRIN处理的差异影响,表明与s的缔合形式不同。 KOR1积累在类似的体内;但是,POM2 / CSI1分离到细胞质中。另外,在不直接抑制聚合的情况下改变了稳定性,表明由纤维素干扰引起的反馈机制。使用多种未观察到形态学作用的亚细胞标记物评估CESTRIN的选择性。在CESTRIN下,href="#def3" rid="def3" class=" def"> CESA 与反式高尔基网络定位蛋白SYNTAXIN OF PLANTS61(SYP61)装饰的囊泡的关联增加处理,这意味着href="#def3" rid="def3" class=" def"> CESA 交易中的SYP61隔离专区。与已知的href="#def3" rid="def3" class=" def"> CESA 抑制剂相比,CESTRIN的性质提供了独特的途径来研究和理解href =“#def1维护与CSC 关联的与href="#def2" rid="def2" class=" def"> CSC 关联的 a href =“#def4” rid =“ def4” class =“ def”> MT 并在黄化的下胚轴中解剖其贩运路线。

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