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Department of Microbial and Molecular Pathogenesis, and Department of Systems Biology and Translational Medicine, Texas A&M University Health Science Center, College Station, Texas 77843-1114
* To whom correspondence should be addressed. Email:
jskare{at}medicine.tamhsc.edu.
The etiologic agent of Lyme disease, Borrelia burgdorferi, must adapt to the distinct environments of the arthropod vector and mammalian host during its complex lifecycle. B. burgdorferi alters gene expression and protein synthesis in response to temperature, pH and other uncharacterized environmental factors. The hypothesis tested in this study is that dissolved gases, including CO2, serve as a signal for B. burgdorferi to alter protein production and gene expression. This study focused on the characterization of in vitro anaerobic (5% CO2, 3% H2, 0.087 PPM O2) and microaerophilic (1% CO2, 3.48 PPM O2) growth conditions and how they modulate protein synthesis and gene expression in B. burgdorferi. Several immunoreactive proteins were synthesized at higher levels under anaerobic conditions, including BosR, NapA, DbpA, OspC, BBK32 and RpoS. Previous studies demonstrated that NapA is produced at lower levels when microaerophilic cultures were purged with nitrogen gas to displace oxygen and CO2. This study identifies CO2 as a contributing factor to the observed change in NapA synthesis. Specifically, the reduction of dissolved CO2, independent of O2 levels, resulted in reduced NapA synthesis. BosR, DbpA, OspC and RpoS synthesis was also decreased with the displacement of CO2. Quantitative RT-PCR indicated that dbpA, ospC and bbk32 transcripts are increased in the presence of CO2 indicating that these putative borrelial virulence determinants are regulated at the transcriptional level. As such, dissolved CO2 may be an additional cue for borrelial host-adaptation and gene regulation.
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Borrelia burgdorferi alters its gene expression and antigenic profile in response to CO2 levels
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Abstract
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