CHLAMYDIA-TRACHOMATIS INTERRUPTS AN EXOCYTIC PATHWAY TO ACQUIRE ENDOGENOUSLY SYNTHESIZED SPHINGOMYELIN IN TRANSIT FROM THE GOLGI-APPARATUS TO THE PLASMA-MEMBRANE

Chlamydia trachomatis acquires C-6-NBD-sphingomyelin endogenously synt hesized from C-6-NBD-ceramide and transported to the vesicle (inclusio n) in which they multiply. Here we explore the mechanisms of this unus ual trafficking and further characterize the association of the chlamy dial inclusion with the Golgi apparatus, Endocytosed chlamydiae are tr afficked to the Golgi region and begin to acquire sphingolipids from t he host within a few hours following infection. The transport of NBD-s phingolipid to the inclusion is energy- and temperature-dependant with the characteristics of an active, vesicle-mediated process, Photo-oxi dation of C-5-DMB-ceramide, in the presence of diaminobenzidine, ident ified DMB-lipids in vesicles in the process of fusing to the chlamydia l inclusion membrane, C-6-NBD-sphingomyelin incorporated into the plas ma membrane is not trafficked to the inclusion to a significant degree , suggesting the pathway for sphingomyelin trafficking is direct from the Golgi apparatus to the chlamydial inclusion, Lectins and antibody probes for Golgi-specific glycoproteins demonstrate the close associat ion of the chlamydial inclusion with the Golgi apparatus but do not de tect these markers in the inclusion membrane, Collectively, the data a re consistent with a model in which C.trachomatis inhabits a unique ve sicle which interrupts an exocytic pathway to intercept host sphingoli pids in transit from the Golgi apparatus to the plasma membrane.