Affiliation:
1. Division of Infectious Diseases, School of Public Health, University of California—Berkeley, Berkeley, California 94720
Abstract
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 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.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology