Suppr超能文献

丝状肌动蛋白调节蛋白调控顶端肌动蛋白聚合以控制极性花粉管生长。

Profilin Regulates Apical Actin Polymerization to Control Polarized Pollen Tube Growth.

机构信息

State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China; Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.

Center for Plant Biology, School of Life Sciences, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Joint Center for Life Sciences, Beijing 100084, China.

出版信息

Mol Plant. 2015 Dec 7;8(12):1694-709. doi: 10.1016/j.molp.2015.09.013. Epub 2015 Oct 1.

Abstract

Pollen tube growth is an essential step during flowering plant reproduction, whose growth depends on a population of dynamic apical actin filaments. Apical actin filaments were thought to be involved in the regulation of vesicle fusion and targeting in the pollen tube. However, the molecular mechanisms that regulate the construction of apical actin structures in the pollen tube remain largely unclear. Here, we identify profilin as an important player in the regulation of actin polymerization at the apical membrane in the pollen tube. Downregulation of profilin decreased the amount of filamentous actin and induced disorganization of apical actin filaments, and reduced tip-directed vesicle transport and accumulation in the pollen tube. Direct visualization of actin dynamics revealed that the elongation of actin filaments originating at the apical membrane decreased in profilin mutant pollen tubes. Mutant profilin that is defective in binding poly-L-proline only partially rescues the actin polymerization defect in profilin mutant pollen tubes, although it fully rescues the actin turnover phenotype. We propose that profilin controls the construction of actin structures at the pollen tube tip, presumably by favoring formin-mediated actin polymerization at the apical membrane.

摘要

花粉管生长是开花植物繁殖过程中的一个重要步骤,其生长依赖于一群动态的顶端肌动蛋白丝。人们认为顶端肌动蛋白丝参与了囊泡融合和靶向在花粉管中的作用。然而,调节花粉管中顶端肌动蛋白结构构建的分子机制在很大程度上仍不清楚。在这里,我们鉴定出丝状肌动蛋白结合蛋白(profilin)是调节花粉管顶端膜肌动蛋白聚合的重要参与者。下调丝状肌动蛋白结合蛋白减少了丝状肌动蛋白的含量,并诱导顶端肌动蛋白丝的紊乱,从而减少了花粉管中向顶端运输和积累的囊泡。肌动蛋白动态的直接可视化显示,起源于顶端膜的肌动蛋白丝的延伸在丝状肌动蛋白结合蛋白突变体花粉管中减少。尽管丝状肌动蛋白结合蛋白缺陷型突变体中肌动蛋白周转率表型完全得到恢复,但只能部分挽救丝状肌动蛋白结合蛋白突变体花粉管中肌动蛋白聚合缺陷。我们提出丝状肌动蛋白结合蛋白控制花粉管顶端肌动蛋白结构的构建,可能通过有利于顶端膜处的formin 介导的肌动蛋白聚合。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验