Attachment of Chlamydia trachomatis L2 to host cells requires sulfation
Name
Ploegh-2012-Attachment of Chlamydia trachomatis L2 to host cells requires.pdf
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Author(s)
Ploegh, Hidde
Rosmarin, David M.
Carette, Jan E.
Olive, Andrew J.
Starnbach, Michael N.
Brummelkamp, Thijn R.
Date Issued
June 2012
Journal
Proceedings of the National Academy of Sciences of the United States of America
Publisher
National Academy of Sciences (U.S.)
Citation
Rosmarin, D. M. et al. “Attachment of Chlamydia Trachomatis L2 to Host Cells Requires Sulfation.” Proceedings of the National Academy of Sciences 109.25 (2012): 10059–10064. © 2012 National Academy of Sciences
Version
Final published version
Abstract
Chlamydia trachomatis is a pathogen responsible for a prevalent sexually transmitted disease. It is also the most common cause of infectious blindness in the developing world. We performed a loss-of-function genetic screen in human haploid cells to identify host factors important in C. trachomatis L2 infection. We identified and confirmed B3GAT3, B4GALT7, and SLC35B2, which encode glucuronosyltransferase I, galactosyltransferase I, and the 3′-phosphoadenosine 5′-phosphosulfate transporter 1, respectively, as important in facilitating Chlamydia infection. Knockout of any of these three genes inhibits Chlamydia attachment. In complementation studies, we found that the introduction of functional copies of these three genes into the null clones restored full susceptibility to Chlamydia infection. The degree of attachment of Chlamydia strongly correlates with the level of sulfation of the host cell, not simply with the amount of heparan sulfate. Thus, other, as-yet unidentified sulfated macromolecules must contribute to infection. These results demonstrate the utility of screens in haploid cells to study interactions of human cells with bacteria. Furthermore, the human null clones generated can be used to investigate the role of heparan sulfate and sulfation in other settings not limited to infectious disease.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Whitehead Institute for Biomedical Research
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DOI of Published Version
https://doi.org/10.1073/pnas.1120244109
