Chlamydia trachomatis infection induces cleavage of the mitotic cyclin B1

The obligate intracellular pathogen Chlamydia trachomatis interferes with a number of host cell processes, including cytoskeletal organization, vesicular trafficking, and apoptosis. In this study we report that C trachomatis-infected cells proliferate more slowly than uninfected cells, suggesting that C trachomatis may also manipulate the eukaryotic cell cycle. We further demonstrate that C trachomatis infection destabilizes specific cell cycle proteins involved in the G(2)/M transition. C trachomatis-infected cells, compared to uninfected cells, have lower levels of cyclin-dependent kinase 1. Additionally, C trachomatis infection induces an N-terminal truncation of the mitotic cyclin B1. Manipulation of the host cell cycle may represent a strategy used by C trachomatis to ensure a stable environment conducive to bacterial growth and replication.