Journal
ANNUAL REVIEW OF MICROBIOLOGY, VOL 65
Volume 65, Issue -, Pages 479-499Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.micro.112408.134040
Keywords
RpoS; spirochete; sigma factor; Lyme borreliosis; gene expression; enzootic cycle
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Funding
- NIAID NIH HHS [AI051486, R01 AI051486] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI051486] Funding Source: NIH RePORTER
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Borrelia burgdorferi, the spirochete that causes Lyme disease, is maintained in nature via an enzootic cycle that comprises a tick vector and a vertebrate host. Transmission from the tick to the mammal, acquisition from the mammal back to the tick, and adaptation to the two disparate environments require sensing signals and responding by regulating programs of gene expression. The molecular mechanisms utilized to effect these lifestyle changes have begun to be elucidated and feature an alternative sigma factor cascade in which RpoN (sigma(54)) and RpoS (sigma(S)) globally control the genes required for the different phases of the enzootic cycle. The RpoN-RpoS pathway is surprisingly complex, entailing Rrp2, an unusual enhancer-binding protein and two-component regulatory system response regulator activated by acetyl phosphate; BosR, an unorthodox DNA-binding protein; DsrA(Bb), a small noncoding RNA; and Hfq and CsrA, two RNA-binding proteins. B. burgdorferi also has a c-di-GMP signaling system that regulates the tick side of the enzootic cycle and whose function is only beginning to be appreciated.
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