The Fur homologue BosR requires Arg39 to activate rpoS transcription in Borrelia burgdorferi and thereby direct spirochaete infection in mice.

ABSTRACT: Borrelia burgdorferi is the causative agent of Lyme disease. In B. burgdorferi, RpoS controls the expression of virulence genes needed for mammalian infection. The Fur homologue BosR regulates the transcription of rpoS and therefore BosR determines, albeit indirectly, the infection status of the spirochaete. Transcription of rpoS in B. burgdorferi is complex: rpoS can be transcribed either from an RpoD-dependent promoter to yield a long transcript or from an RpoN-dependent promoter to yield a short transcript. This study shows that BosR repressed synthesis of the long transcript while at the same time activating synthesis of the short transcript. How BosR does this is unclear. To address this, spirochaetes were engineered to express either BosR or the naturally occurring variant BosRR39K.

SUBMITTER: Katona LI 

PROVIDER: S-EPMC4806591 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature