title: Motor rotation is essential for the formation of the periplasmic flagellar ribbon, cellular morphology, and Borrelia burgdorferi persistence within Ixodes scapularis tick and murine hosts.
abstract: Borrelia burgdorferi must migrate within and between its arthropod and mammalian hosts in order to complete its natural enzootic cycle. During tick feeding, the spirochete transmits from the tick to the host dermis, eventually colonizing and persisting within multiple, distant tissues. This dissemination modality suggests that flagellar motor rotation and, by extension, motility are crucial for infection. We recently reported that a nonmotile flaB mutant that lacks periplasmic flagella is rod shaped and unable to infect mice by needle or tick bite. However, those studies could not differentiate whether motor rotation or merely the possession of the periplasmic flagella was crucial for cellular morphology and host persistence. Here, we constructed and characterized a motB mutant that is nonmotile but retains its periplasmic flagella. Even though ΔmotB bacteria assembled flagella, part of the mutant cell is rod shaped. Cryoelectron tomography revealed that the flagellar ribbons are distorted in the mutant cells, indicating that motor rotation is essential for spirochetal flat-wave morphology. The ΔmotB cells are unable to infect mice, survive in the vector, or migrate out of the tick. Coinfection studies determined that the presence of these nonmotile ΔmotB cells has no effect on the clearance of wild-type spirochetes during murine infection and vice versa. Together, our data demonstrate that while flagellar motor rotation is necessary for spirochetal morphology and motility, the periplasmic flagella display no additional properties related to immune clearance and persistence within relevant hosts.
authors.affiliation: Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA.
authors.forename: Syed Z
authors.initials: SZ
authors.lastname: Sultan
authors.affiliation: Department of Medical Microbiology and Immunology, University of Toledo College of Medicine, Toledo, Ohio, USA.
authors.forename: Padmapriya
authors.initials: P
authors.lastname: Sekar
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, Houston, Texas, USA.
authors.forename: Xiaowei
authors.initials: X
authors.lastname: Zhao
authors.affiliation: Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA.
authors.forename: Akarsh
authors.initials: A
authors.lastname: Manne
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, Houston, Texas, USA.
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Medical Microbiology and Immunology, University of Toledo College of Medicine, Toledo, Ohio, USA.
authors.forename: R Mark
authors.initials: RM
authors.lastname: Wooten
authors.affiliation: Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA motalebm@ecu.edu.
authors.forename: M A
authors.initials: MA
authors.lastname: Motaleb
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics; D025065:Borrelia burgdorferi / Q000502:physiology* / Q000648:ultrastructure; D020285:Cryoelectron Microscopy; D004195:Disease Models, Animal; D055032:Electron Microscope Tomography; D005407:Flagella / Q000378:metabolism* / Q000648:ultrastructure; D017353:Gene Deletion; D018884:Ixodes / Q000382:microbiology*; D008124:Locomotion; D008193:Lyme Disease / Q000382:microbiology / Q000473:pathology; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D020409:Molecular Motor Proteins / Q000378:metabolism*; D012399:Rotation
chemical_list: D001426:Bacterial Proteins; D020409:Molecular Motor Proteins; C064779:MotB protein, Bacteria