Alberdi Lucrecia, Vergnes Alexandra, Manneville Jean-Baptiste, Tembo Dumizulu L, Fang Ziyan, Zhao Yaya, Schroeder Nina, Dumont Audrey, Lagier Margaux, Bassereau Patricia, Redondo-Morata Lorena, Gorvel Jean-Pierre, Méresse Stéphane
Aix-Marseille Université, CNRS, INSERM, CIML, Marseille, France.
Institut Curie, PSL Research University, CNRS, UMR 144, 26 rue d'Ulm, F-75005, Paris, France.
J Cell Sci. 2020 May 14;133(9):jcs239863. doi: 10.1242/jcs.239863.
is an intracellular bacterial pathogen. The formation of its replication niche, which is composed of a vacuole associated with a network of membrane tubules, depends on the secretion of a set of bacterial effector proteins whose activities deeply modify the functions of the eukaryotic host cell. By recruiting and regulating the activity of the kinesin-1 molecular motor, effectors PipB2 and SifA play an essential role in the formation of the bacterial compartments. In particular, they allow the formation of tubules from the vacuole and their extension along the microtubule cytoskeleton, and thus promote membrane exchanges and nutrient supply. We have developed and assays to better understand the specific role played by these two effectors in the recruitment and regulation of kinesin-1. Our results reveal a specific interaction between the two effectors and indicate that, contrary to what studies on infected cells suggested, interaction with PipB2 is sufficient to relieve the autoinhibition of kinesin-1. Finally, they suggest the involvement of other effectors in the control of the activity of this molecular motor.This article has an associated First Person interview with the first author of the paper.
是一种细胞内细菌病原体。其复制龛由与膜小管网络相关的液泡组成，其形成依赖于一组细菌效应蛋白的分泌，这些效应蛋白的活性深刻改变了真核宿主细胞的功能。效应蛋白PipB2和SifA通过招募和调节驱动蛋白-1分子马达的活性，在细菌区室的形成中发挥重要作用。特别是，它们允许从液泡形成小管并使其沿着微管细胞骨架延伸，从而促进膜交换和营养供应。我们开发了[具体实验名称1]和[具体实验名称2]分析方法，以更好地了解这两种效应蛋白在招募和调节驱动蛋白-1中所起的特定作用。我们的结果揭示了这两种效应蛋白之间的特定相互作用，并表明，与对感染细胞的研究结果相反，与PipB2的相互作用足以解除驱动蛋白-1的自身抑制。最后，结果表明其他效应蛋白参与了对这种分子马达活性的控制。本文配有对该论文第一作者的第一人称访谈。
