Robert Faris, Marlena Merling, Shelby E Andersen, Cheryl A Dooley, Ted Hackstadt, Mary M Weber
Author Information
Robert Faris: Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.
Marlena Merling: Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA; Department of Biology, University of Dayton, Dayton, OH 45469, USA.
Shelby E Andersen: Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.
Cheryl A Dooley: Host Parasite Interactions Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institutes of Allergy and Infectious Disease, NIH, Hamilton, MT 59840, USA.
Ted Hackstadt: Host Parasite Interactions Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institutes of Allergy and Infectious Disease, NIH, Hamilton, MT 59840, USA.
Mary M Weber: Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA. Electronic address: mary-weber@uiowa.edu.
Chlamydial infection requires the formation of a membrane-bound vacuole, termed the inclusion, that undergoes extensive interactions with select host organelles. The importance of the Inc protein CT229 in the formation and maintenance of the chlamydial inclusion was recently highlighted by studies demonstrating that its absence during infection results in reduced bacterial replication, premature inclusion lysis, and host cell death. Previous reports have indicated that CT229 binds Rab GTPases; however, the physiological implications of this interaction are unknown. Here, we show that CT229 regulates host multivesicular trafficking by recruiting multiple Rab GTPases and their cognate effectors to the inclusion. We demonstrate that CT229 specifically modulates clathrin-coated vesicle trafficking and regulates the trafficking of transferrin and the mannose-6-phosphate receptor, both of which are crucial for proper chlamydial development. This study highlights CT229 as a master regulator of multiple host vesicular trafficking pathways essential for chlamydial infection.
