Affiliation:
1. Department of Biological Sciences, University of Idaho, Moscow, Idaho, USA
2. Paul G. Allen School for Global Animal Health, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA
Abstract
Chlamydia trachomatis
is an obligate intracellular bacterium that can cause trachoma, cervicitis, urethritis, salpingitis, and pelvic inflammatory disease. To establish infection in host cells,
Chlamydia
must complete a multiple-cell-type developmental cycle. The developmental cycle consists of specialized cells, the EB cell, which mediates infection of new host cells, and the RB cell, which replicates and eventually produces more EB cells to mediate the next round of infection. By developing and testing mathematical models to discriminate between two competing hypotheses for the nature of the signal controlling RB-to-EB cell type switching, we demonstrate that RB-to-EB development follows a cell-autonomous program that does not respond to environmental cues. Additionally, we show that RB-to-EB development is a function of chlamydial growth and division. This study serves to further our understanding of the chlamydial developmental cycle that is central to the bacterium’s pathogenesis.
Funder
Division of Intramural Research, National Institute of Allergy and Infectious Diseases
Publisher
American Society for Microbiology
Subject
Computer Science Applications,Genetics,Molecular Biology,Modelling and Simulation,Ecology, Evolution, Behavior and Systematics,Biochemistry,Physiology,Microbiology
Cited by
15 articles.
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