Affiliation:
1. Burnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, Florida, USA
Abstract
ABSTRACT
The Lyme disease spirochete
Borrelia burgdorferi
is dependent on purine salvage from the host environment for survival. The genes
bbb22
and
bbb23
encode purine permeases that are essential for
B. burgdorferi
mouse infectivity. We now demonstrate the unique contributions of each of these genes to purine transport and murine infection. The affinities of spirochetes carrying
bbb22
alone for hypoxanthine and adenine were similar to those of spirochetes carrying both genes. Spirochetes carrying
bbb22
alone were able to achieve wild-type levels of adenine saturation but not hypoxanthine saturation, suggesting that maximal hypoxanthine uptake requires the presence of
bbb23
. Moreover, the purine transport activity conferred by
bbb22
was dependent on an additional distal transcriptional start site located within the
bbb23
open reading frame. The initial rates of uptake of hypoxanthine and adenine by spirochetes carrying
bbb23
alone were below the level of detection. However, these spirochetes demonstrated a measurable increase in hypoxanthine uptake over a 30-min time course. Our findings indicate that
bbb22
-dependent adenine transport is essential for
B. burgdorferi
survival in mice. The
bbb23
gene was dispensable for
B. burgdorferi
mouse infectivity, yet its presence was required along with that of
bbb22
for
B. burgdorferi
to achieve maximal spirochete loads in infected mouse tissues. These data demonstrate that both genes,
bbb22
and
bbb23
, are critical for
B. burgdorferi
to achieve wild-type infection of mice and that the differences in the capabilities of the two transporters may reflect distinct purine salvage needs that the spirochete encounters throughout its natural infectious cycle.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
19 articles.
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