<i>Borrelia burgdorferi</i> tolerates alteration to P66 porin function in a murine infectivity model.

ABSTRACT: Borrelia burgdorferi exists in a complex enzootic life cycle requiring differential gene regulation. P66, a porin and adhesin, is upregulated and essential during mammalian infection, but is not produced or required within the tick vector. We sought to determine whether the porin function of P66 is essential for infection. Vancomycin treatment of B. burgdorferi cultures was used to screen for P66 porin function and found to generate spontaneous mutations in p66 (bb0603). Three novel, spontaneous, missense P66 mutants (G175V, T176M, and G584R) were re-created by site-directed mutagenesis in an infectious strain background and tested for infectivity in mice by ID₅₀ experiments. Two of the three mutants retained infectivity comparable to the isogenic con

SUBMITTER: Fierros CH 

PROVIDER: S-EPMC11790652 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature