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Infection and Immunity, August 2007, p. 3925-3934, Vol. 75, No. 8
0019-9567/07/$08.00+0 doi:10.1128/IAI.00106-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Division of Infectious Diseases, School of Public Health, University of California—Berkeley, Berkeley, California 94720
Received 19 January 2007/ Returned for modification 23 February 2007/ Accepted 25 April 2007
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 used to disrupt proteins with established roles in clathrin-mediated endocytosis (clathrin heavy chain, dynamin-2, heat shock 70-kDa protein 8, Arp2, cortactin, and calmodulin), caveola-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 small interfering RNA-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 caveola-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.
Published ahead of print on 14 May 2007.
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