- Future Students
- Current Students
- Faculty & Staff
Vesicular interactions of the Chlamydia trachomatis inclusion are determined by chlamydial early protein synthesis rather than route of entry.
|Title||Vesicular interactions of the Chlamydia trachomatis inclusion are determined by chlamydial early protein synthesis rather than route of entry.|
|Publication Type||Journal Article|
|Year of Publication||1996|
|Authors||Scidmore MA, Rockey DD, Fischer ER, Heinzen RA, Hackstadt T|
|Journal||Infection and immunity|
|Date Published||1996 Dec|
|Keywords||Bacterial Proteins, Chlamydia Infections, Chlamydia trachomatis, Hela Cells, Humans, Microscopy, Electron|
Chlamydiae replicate intracellularly within a vacuole that has recently been characterized as intersecting an exocytic pathway. One of the initial events during chlamydial infection is the expression of a chlamydial early gene product(s) that effectively isolates the inclusion from the endocytic-lysosomal pathway and makes it fusogenic with sphingomyelin-containing exocytic vesicles. Associated with this change in vesicular interaction is the delivery of the vacuole to the peri-Golgi region of the host cell. Inhibition of chlamydial early transcription or translation causes Chlamydia trachomatis-containing vesicles to remain dispersed throughout the cytoplasm, where they eventually fuse with lysosomes. Chlamydiae that have been internalized by Fc-mediated endocytosis also avoid lysosomal digestion by a mechanism that requires chlamydial protein synthesis. These results suggest that the vesicular interactions of the chlamydial inclusion are defined by parasite-directed modification of the endocytic vesicle rather than by the route of internalization.
|Alternate Journal||Infect. Immun.|