| Literature DB >> 32703440 |
Santina Snow1, Emily Bacon1, Jennifer Bergeron1, David Katzman1, Amelia Wilhelm1, Owen Lewis1, Deepsing Syangtan1, Andrew Calkins1, Linda Archambault1, Melissa L Anacker2, Paula Jean Schlax3.
Abstract
The causative agent of Lyme disease, Borrelia burgdorferi, requires shifts in gene expression to undergo its natural enzootic cycle between tick and vertebrate hosts. mRNA decay mechanisms play significant roles in governing gene expression in other bacteria, but are not yet characterized in B. burgdorferi. RNase III is an important enzyme in processing ribosomal RNA, but it also plays a role in mRNA decay in many bacteria. We compared RNA decay profiles and steady-state abundances of transcripts in wild-type Borrelia burgdorferi strain B31 and in an RNase III null (rnc-) mutant. Transcripts encoding RNA polymerase subunits (rpoA and rpoS), ribosomal proteins (rpsD, rpsK, rpsM, rplQ, and rpsO), a nuclease (pnp), a flagellar protein (flaB), and a translational regulator (bpuR) decayed more rapidly in the wild-type strain than in the slow growing rnc- mutant indicating that RNA turnover is mediated by RNase III in the bacterium that causes Lyme disease. Additionally, in wild type bacteria, RNA decay rates of rpoS, rpoN, ospA, ospC, bpuR and dbpA transcripts are only modestly affected by changes in the osmolarity.Entities:
Keywords: Borrelia burgdorferi; Lyme disease; RNase III; mRNA decay
Year: 2020 PMID: 32703440 PMCID: PMC7427566 DOI: 10.1016/j.bbrc.2020.05.201
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575