Department of Molecular Biology and Microbiology, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, United States; Program in Molecular Microbiology, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, United States.
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, United States.
Curr Opin Microbiol. 2020 Apr;54:51-58. doi: 10.1016/j.mib.2020.01.008. Epub 2020 Feb 7.
Intravacuolar bacterial pathogens establish intracellular niches by constructing membrane-encompassed compartments. The vacuoles surrounding the bacteria are remarkably stable, facilitating microbial replication and preventing exposure to host cytoplasmically localized innate immune sensing mechanisms. To maintain integrity of the membrane compartment, the pathogen is armed with defensive weapons that prevent loss of vacuole integrity and potential exposure to host innate signaling. In some cases, the microbial components that maintain vacuolar integrity have been identified, but the basis for why the compartment degrades in their absence is unclear. In this review, we point out that lessons from the microbial-programmed degradation of the vacuole by the cytoplasmically localized Shigella flexneri provide crucial insights into how degradation of pathogen vacuoles occurs. We propose that in the absence of bacterial-encoded guard proteins, aberrant trafficking of host membrane-associated components results in a dysfunctional pathogen compartment. As a consequence, the vacuole is poisoned and replication is terminated.
胞内细菌病原体通过构建膜包裹的隔室在细胞内建立小生境。包围细菌的液泡非常稳定，有利于微生物的复制，并防止暴露于宿主细胞质固有免疫感应机制。为了维持膜隔室的完整性，病原体配备了防御武器，以防止液泡完整性的丧失和潜在暴露于宿主固有信号。在某些情况下，已经确定了维持液泡完整性的微生物成分，但不清楚为什么在没有这些成分的情况下隔室会降解。在这篇综述中，我们指出，由细胞质定位的福氏志贺菌对液泡进行微生物程序性降解所提供的教训，为了解病原体液泡的降解方式提供了至关重要的见解。我们提出，在缺乏细菌编码的保护蛋白的情况下，宿主膜相关成分的异常运输导致功能失调的病原体隔室。结果，液泡中毒，复制终止。
