Institut Pasteur, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, Paris, France.
Institut Pasteur, Plateforme Protéomique, Unité de Spectrométrie de Masse pour la Biologie, C2RT, USR 2000 CNRS, Paris, France.
Cell Rep. 2019 Dec 17;29(12):3958-3973.e7. doi: 10.1016/j.celrep.2019.11.049.
Salmonella is a human and animal pathogen that causes gastro-enteric diseases. The key to Salmonella infection is its entry into intestinal epithelial cells, where the bacterium resides within a Salmonella-containing vacuole (SCV). Salmonella entry also induces the formation of empty macropinosomes, distinct from the SCV, in the vicinity of the entering bacteria. A few minutes after its formation, the SCV increases in size through fusions with the surrounding macropinosomes. Salmonella also induces membrane tubules that emanate from the SCV and lead to SCV shrinkage. Here, we show that these antipodal events are utilized by Salmonella to either establish a vacuolar niche or to be released into the cytosol by SCV rupture. We identify the molecular machinery underlying dynamic SCV growth and shrinkage. In particular, the SNARE proteins SNAP25 and STX4 participate in SCV inflation by fusion with macropinosomes. Thus, host compartment size control emerges as a pathogen strategy for intracellular niche regulation.
沙门氏菌是一种人类和动物病原体,可引起肠胃疾病。沙门氏菌感染的关键是其进入肠道上皮细胞,在那里细菌存在于沙门氏菌包含的空泡(SCV)中。沙门氏菌进入还会诱导在进入细菌附近形成与 SCV 不同的空的巨胞饮泡。形成后几分钟,SCV 通过与周围巨胞饮泡融合而增大。沙门氏菌还诱导从 SCV 发出的膜小管,导致 SCV 收缩。在这里,我们表明,这些对映事件被沙门氏菌利用,要么在液泡中建立一个小生境,要么通过 SCV 破裂将其释放到细胞质中。我们确定了动态 SCV 生长和收缩的分子机制。特别是,SNARE 蛋白 SNAP25 和 STX4 通过与巨胞饮泡融合参与 SCV 的膨胀。因此,宿主隔室大小控制成为细胞内小生境调节的病原体策略。