作者: Shawna C.O. Reed , Rebecca L. Lamason , Viviana I. Risca , Emma Abernathy , Matthew D. Welch
DOI: 10.1016/J.CUB.2013.11.025
关键词:
摘要: Many intracellular bacterial pathogens undergo actin-based motility to promote cell-cell spread during infection [1]. For each pathogen, was assumed be driven by a single actin polymerization pathway. Curiously, spotted fever group Rickettsia differ from other in possessing two actin-polymerizing proteins. RickA, an activator of the host Arp2/3 complex, initially proposed drive [2, 3]. Sca2, mimic formins [4, 5], later shown required for [6]. Whether and how their activities are coordinated has remained unclear. Here, we show that protein directs independent mode parkeri at different times infection. Early after invasion, is slow meandering, generating short, curved tails enriched with complex cofilin. requires RickA correlated transient localization pole. Later infection, faster directionally persistent, resulting long, straight tails. Late which accumulates Both pathways facilitate cell-to-cell spread. The ability exploit assembly may allow establish niche between diverse cells throughout prolonged