IAI Accepts, published online ahead of print on 14 May 2007
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Infect. Immun. doi:10.1128/IAI.00106-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Entry mechanisms of Chlamydia trachomatis into non-phagocytic cells

Kevin Hybiske and Richard S. Stephens*

Division of Infectious Diseases, School of Public Health, University of California, Berkeley, CA 94720

* To whom correspondence should be addressed. Email: rss{at}berkeley.edu.


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Abstract

The mechanisms of entry for the obligate intracellular bacterium C. trachomatis were examined by functional disruption of proteins essential for various modes of entry. RNA interference was employed to disrupt proteins with established roles in: clathrin-mediated endocytosis (clathrin heavy chain, dynamin-2, heat shock 70kDa protein 8, Arp2, cortactin and calmodulin), caveolae-mediated endocytosis (caveolin-1, dynamin-2, Arp2, NSF and annexin II), phagocytosis (RhoA, dynamin-2, Rac1 and Arp2) and macropinocytosis (Pak1, Rac1 and Arp2). Comparative quantitative PCR analysis was performed on siRNA-transfected HeLa cells to accurately determine the extent of C. trachomatis entry after these treatments. Key structural and regulatory factors associated with clathrin-mediated endocytosis were found to be involved in Chlamydia entry, whereas those for caveolae-mediated endocytosis, phagocytosis and macropinocytosis were not. Thus, clathrin and its coordinate accessory factors were required for entry of C. trachomatis, although additional, uncharacterized mechanisms are also utilized.




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