Chlamydia causes fragmentation of the Golgi compartment to ensure reproduction

Dagmar Heuer et al. Nature 2009; 457:731-737

Speaker: Chih-Yu Huang (黃智郁)                                       Time: 15:00-16:00, May 27, 2009

Commentator: Dr. Jiunn-Jong Wu (吳俊忠老師)         Place: Room 601

Abstract:

Chlamydia trachomatis, an obligate intracellular pathogen, can infect many types of cells and replicate within a membrane-bound vacuole called inclusion body. It has long been recognized that the inability to produce high-energy compounds, such as ATP and GTP, makes chlamydia undergo a special parasitic lifestyle¹. Recent studies have shown that the host cell-derived sphingolipids from Golgi apparatus are also required for the intracellular growth of C. trachomatis². However, the mechanisms by which this intracellular pathogen acquire host cell lipids for growth are not well understood. In this study, the authors demonstrated that during chlamydia infection the Golgi apparatus of infected cells were fragmented into small ministacks surrounding the bacterial inclusion body. Fragmentation of Golgi apparatus was due to processing of golgin-84, which forms the Golgi matrix, by an intracellular cysteine protease, calpain, and the inflammatory caspases. Furthermore, treatment of host cell with the inflammatory caspase inhibitor, Z-WEHD-FMK, after infection could effectively block the acquisition of sphingolipid and, consequently, bacterial reproduction. On the other hand, inhibition of fragmentation of Golgi apparatus by RNAi knockdown of some Golgi matrix proteins, including golgin-84 before infection could result in an increase of bacteria load. Collectively, the authors revealed a novel infection mechanism in which a pathogen utilizes the host cell organelle for its own propagation.

References:

1.          Moulder, J.W. (1962) The Biochemistry of Intracellular Parasitism. Moulder, J.W. (ed.). Chicago: The university of Chicago Press, pp. 122-124

2.          Christiaan van Ooij, et al. Host cell-derived sphinolipids are required for the intracellular growth of Chlamydia trachomatis. Cellular Microbiology, 2000; 2:627-637