Cytoplasmic ATR Activation Promotes Vaccinia Virus Genome Replication.

In contrast to most DNA viruses, poxviruses replicate their genomes in the cytoplasm without host involvement. We find that vaccinia virus induces cytoplasmic activation of ATR early during infection, before genome uncoating, which is unexpected because ATR plays a fundamental nuclear role in maintaining host genome integrity. ATR, RPA, INTS7, and Chk1 are recruited to cytoplasmic DNA viral factories, suggesting canonical ATR pathway activation.

SCAMP3 is a component of the Salmonella-induced tubular network and reveals an interaction between bacterial effectors and post-Golgi trafficking.

Salmonella enterica are facultative intracellular bacterial pathogens that proliferate within host cells in a membrane-bounded compartment, the Salmonella-containing vacuole (SCV). Intracellular replication of Salmonella is mediated by bacterial effectors translocated on to the cytoplasmic face of the SCV membrane by a type III secretion system. Some of these effectors manipulate the host endocytic pathway, resulting in the formation in epithelial cells of tubules enriched in late endosomal markers, known as Salmonella-induced filaments (SIFs).

Membrane dynamics and spatial distribution of Salmonella-containing vacuoles.

Salmonella enterica are facultative intracellular bacteria that cause intestinal and systemic diseases, and replicate within host cells in a membrane-bound compartment, the Salmonella-containing vacuole. Intravacuolar bacterial replication depends on spatiotemporal regulated interactions with host cell vesicular compartments. Recent studies have shown that type III secretion effector proteins control both the vacuolar membrane dynamics and intracellular positioning of bacterial vacuoles.

The SPI-2 type III secretion system restricts motility of Salmonella-containing vacuoles.

Intracellular replication of Salmonella enterica occurs in membrane-bound compartments, called Salmonella-containing vacuoles (SCVs). Following invasion of epithelial cells, most SCVs migrate to a perinuclear region and replicate in close association with the Golgi network. The association of SCVs with the Golgi is dependent on the Salmonella-pathogenicity island-2 (SPI-2) type III secretion system (T3SS) effectors SseG, SseF and SifA.