Chlamydia trachomatis inclusions induce asymmetric cleavage furrow formation and ingression failure in host cells.

ABSTRACT: Chlamydia trachomatis infection has been suggested to induce host genome duplication and is linked to increased risks of cervical cancer. We describe here the mechanism by which Chlamydia causes a cleavage furrow defect that consistently results in the formation of multinucleated host cells, a phenomenon linked to tumorigenesis. Host signaling proteins essential for cleavage furrow initiation, ingression, and stabilization are displaced from one of the prospective furrowing cortices after Chlamydia infection. This protein displacement leads to the formation of a unique asymmetrical, unilateral cleavage furrow in infected human cells. The asymmetrical distribution of signaling proteins is caused by the physical presence of the Chlamydia inclusion at the cell equator. By using ingested latex

SUBMITTER: Sun HS 

PROVIDER: S-EPMC3233033 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature