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 G2/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.
Balsara
Zarine R
ZR
Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Ave., Boston, MA 02115, USA.
Misaghi
Shahram
S
Lafave
James N
JN
Starnbach
Michael N
MN
D000818:Animals; D001426:Bacterial Proteins / Q000378:metabolism; D002453:Cell Cycle; D018797:Cell Cycle Proteins / Q000378:metabolism*; D002478:Cells, Cultured; D002690:Chlamydia Infections / Q000378:metabolism*; D002692:Chlamydia trachomatis; D006224:Cricetinae; D019926:Cyclin B / Q000378:metabolism*; D056744:Cyclin B1; D006801:Humans; D008938:Mitosis; D014176:Protein Biosynthesis
D001426:Bacterial Proteins; C534699:CCNB1 protein, human; D018797:Cell Cycle Proteins; D019926:Cyclin B; D056744:Cyclin B1