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Journal of Bacteriology, March 2008, p. 1912-1921, Vol. 190, No. 6
0021-9193/08/$08.00+0     doi:10.1128/JB.01421-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Borrelia burgdorferi Uniquely Regulates Its Motility Genes and Has an Intricate Flagellar Hook-Basal Body Structure

Department of Microbiology, Immunology, and Cell Biology, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, West Virginia 26506-9177,¹ Department of Oral Biology, State University of New York at Buffalo, Buffalo, New York 14214,² Prefectural University of Hiroshima, Department of Life Sciences, 562 Nanatsuka, Shobara, Hiroshima, 727-0023, Japan,³ CREST Soft-Nano Machine Project, Innovation Plaza, Hiroshima, 3-10-23 Kagamiyama, Higashi-Hiroshima, 739-0046, Japan⁴

Received 2 September 2007/ Accepted 3 January 2008

Borrelia burgdorferi is a flat-wave, motile spirochete that causes Lyme disease. Motility is provided by periplasmic flagella (PFs) located between the cell cylinder and an outer membrane sheath. The structure of these PFs, which are composed of a basal body, a hook, and a filament, is similar to the structure of flagella of other bacteria. To determine if hook formation influences flagellin gene transcription in B. burgdorferi, we inactivated the hook structural gene flgE by targeted mutagenesis. In many bacteria, completion of the hook structure serves as a checkpoint for transcriptional control of flagellum synthesis and other chemotaxis and motility genes. Specifically, the hook allows secretion of the anti-sigma factor FlgM and concomitant late gene transcription promoted by ²⁸. However, the control of B. burgdorferi PF synthesis differs from the control of flagellum synthesis in other bacteria; the gene encoding ²⁸ is not present in the genome of B. burgdorferi, nor are any ²⁸ promoter recognition sequences associated with the motility genes. We found that B. burgdorferi flgE mutants lacked PFs, were rod shaped, and were nonmotile, which substantiates previous evidence that PFs are involved in both cell morphology and motility. Although most motility and chemotaxis gene products accumulated at wild-type levels in the absence of FlgE, mutant cells had markedly decreased levels of the flagellar filament proteins FlaA and FlaB. Further analyses showed that the reduction in the levels of flagellin proteins in the spirochetes lacking FlgE was mediated at the posttranscriptional level. Taken together, our results indicate that in B. burgdorferi, the completion of the hook does not serve as a checkpoint for transcriptional regulation of flagellum synthesis. In addition, we also present evidence that the hook protein in B. burgdorferi forms a high-molecular-weight complex and that formation of this complex occurs in the periplasmic space.

Published ahead of print on 11 January 2008.