{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T16:56:25Z","timestamp":1778864185797,"version":"3.51.4"},"reference-count":43,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Microbiol"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>The bacterium <jats:italic>Borrelia burgdorferi<\/jats:italic>, the causative agent of Lyme disease, is a limited-genome organism that must obtain many of its biochemical building blocks, including N-acetylglucosamine (GlcNAc), from its tick or vertebrate host. GlcNAc can be imported into the cell as a monomer or dimer (chitobiose), and the annotation for several <jats:italic>B. burgdorferi<\/jats:italic> genes suggests that this organism may be able to degrade and utilize chitin, a polymer of GlcNAc. We investigated the ability of <jats:italic>B. burgdorferi<\/jats:italic> to utilize chitin in the absence of free GlcNAc, and we attempted to identify genes involved in the process. We also examined the role of RpoS, one of two alternative sigma factors present in <jats:italic>B. burgdorferi<\/jats:italic>, in the regulation of chitin utilization.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Using fluorescent chitinase substrates, we demonstrated an inherent chitinase activity in rabbit serum, a component of the <jats:italic>B. burgdorferi<\/jats:italic> growth medium (BSK-II). After inactivating this activity by boiling, we showed that wild-type cells can utilize chitotriose, chitohexose or coarse chitin flakes in the presence of boiled serum and in the absence of free GlcNAc. Further, we replaced the serum component of BSK-II with a lipid extract and still observed growth on chitin substrates without free GlcNAc. In an attempt to knockout <jats:italic>B. burgdorferi<\/jats:italic> chitinase activity, we generated mutations in two genes (<jats:italic>bb0002<\/jats:italic> and <jats:italic>bb0620<\/jats:italic>) predicted to encode enzymes that could potentially cleave the \u03b2-(1,4)-glycosidic linkages found in chitin. While these mutations had no effect on the ability to utilize chitin, a mutation in the gene encoding the chitobiose transporter (<jats:italic>bbb04<\/jats:italic>, <jats:italic>chbC<\/jats:italic>) did block utilization of chitin substrates by <jats:italic>B. burgdorferi<\/jats:italic>. Finally, we provide evidence that chitin utilization in an <jats:italic>rpoS<\/jats:italic> mutant is delayed compared to wild-type cells, indicating that RpoS may be involved in the regulation of chitin degradation by this organism.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>The data collected in this study demonstrate that <jats:italic>B. burgdorferi<\/jats:italic> can utilize chitin as a source of GlcNAc in the absence of free GlcNAc, and suggest that chitin is cleaved into dimers before being imported across the cytoplasmic membrane via the chitobiose transporter. In addition, our data suggest that the enzyme(s) involved in chitin degradation are at least partially regulated by the alternative sigma factor RpoS.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2180-10-21","type":"journal-article","created":{"date-parts":[[2010,1,27]],"date-time":"2010-01-27T07:14:36Z","timestamp":1264576476000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["The chitobiose transporter, chbC, is required for chitin utilization in Borrelia burgdorferi"],"prefix":"10.1186","volume":"10","author":[{"given":"Ryan G","family":"Rhodes","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janet A","family":"Atoyan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David R","family":"Nelson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2010,1,26]]},"reference":[{"issue":"10","key":"977_CR1","first-page":"1","volume":"57","author":"RM Bacon","year":"2008","unstructured":"Bacon RM, Kugeler KJ, Mead PS: Surveillance for Lyme Disease - United States, 1992-2006. 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