Actin-based confinement of calcium responses during Shigella invasion

Shigella , the agent of bacillary dysentery, invades epithelial cells by locally inducing actin reorganization. Upon cell invasion, Shigella induces calcium (Ca 2+ ) signalling, but its role in invasion has remained unclear. Here we show that components involved in inositol 1, 4, 5- trisphosphate (InsP 3 ) signalling are implicated in Shigella invasion. Although global Ca 2+ responses are dispensable for bacterial invasion, local Ca 2+ responses of unprecedented long duration are associated with invasion sites. Fluorescence recovery after photo-bleaching experiments indicate that diffusion of small solutes is hindered at Shigella -invasion sites and that diffusion hindrance is dependent on bacterially induced actin reorganization. Computational simulations and experimental challenge of the model support the notion that local accumulation of InsP 3 permitted by restricted diffusion and enrichment of InsP 3 receptors account for sustained local Ca 2+ increases at entry sites. Thus, cytoskeletal reorganization through diffusion hindrance shapes the duration of local Ca 2+ signals. Shigella triggers an increase in intracellular calcium during invasion of host cells. Here the authors show that increased actin polymerization at the invasion site slows the diffusion of signalling mediators, thus sustaining localized calcium influx at invasion sites.