TargeTron Inactivation of Chlamydia trachomatis gseA Results in a Lipopolysaccharide 3-Deoxy- d -Manno-Oct-2-Ulosonic Acid-Deficient Strain That Is Cytotoxic for Cells

Author:

DeBoer Addison G.1,Lei Lei1,Yang Chunfu1,Martens Craig A.2,Anzick Sarah L.2,Antonioli-Schmit Sophia2,Suchland Robert J.3,McClarty Grant4,Caldwell Harlan D.1ORCID,Rockey Daniel D.5ORCID

Affiliation:

1. Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA

2. National Institute of Allergy and Infectious Disease, Rocky Mountain Laboratory, Hamilton, Montana, USA

3. Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington

4. Department of Medical Microbiology and Infectious Diseases, University of Manitoba Winnipeg, Winnipeg, Manitoba, Canada

5. Department of Biomedical Sciences, Oregon State University, Corvallis, Oregon, USA

Abstract

All members of the family Chlamydiaceae have lipopolysaccharides (LPS) that possess a shared carbohydrate trisaccharide antigen, 3-deoxy- d -manno-oct-2-ulosonic acid (Kdo) that is functionally uncharacterized. A single gene, genus-specific epitope ( gseA ), is responsible for attaching the tri-Kdo to lipid IVA. To investigate the function of Kdo in chlamydial host cell interactions, we made a gseA -null strain (L2Δ gseA ) by using TargeTron mutagenesis.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

Reference38 articles.

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