RNase III processing of rRNA in the Lyme disease spirochete Borrelia burgdorferi

ABSTRACT The rRNA genes of Borrelia (Borreliella) burgdorferi are unusually organized; the spirochete has a single 16S rRNA gene that is more than 3 kb from a tandem pair of 23S-5S rRNA operons. We generated an rnc null mutant in B. burgdorferi that exhibits a pleiotropic phenotype, including decreased growth rate and increased cell length. Here, we demonstrate that endoribonuclease III (RNase III) is, as expected, involved in processing the 23S rRNA in B. burgdorferi. The 5′ and 3′ ends of the three rRNAs were determined in the wild type and rnc Bb mutants; the results suggest that RNase III in B. burgdorferi is required for the full maturation of the 23S rRNA but not for the 5S rRNA nor, curiously, for the 16S rRNA. IMPORTANCE Lyme disease, the most common tick-borne zoonosis in the Northern Hemisphere, is caused by the bacterium Borrelia (Borreliella) burgdorferi, a member of the deeply branching spirochete phylum. B. burgdorferi carries a limited suite of ribonucleases, enzymes that cleave RNA during processing and degradation. Several ribonucleases, including RNase III, are involved in the production of ribosomes, which catalyze translation and are a major target of antibiotics. This is the first study to dissect the role of an RNase in any spirochete. We demonstrate that an RNase III mutant is viable but has altered processing of rRNA.