Affiliation:
1. Department of Microbiology, Cornell University, Ithaca, New York 14853-8101
Abstract
ABSTRACT
Bacitracin resistance is normally conferred by either of two major mechanisms, the BcrABC transporter, which pumps out bacitracin, or BacA, an undecaprenol kinase that provides C
55
-isoprenyl phosphate by de novo synthesis. We demonstrate that the
Bacillus subtilis bcrC
(
ywoA
) gene, encoding a putative bacitracin transport permease, is an important bacitracin resistance determinant. A
bcrC
mutant strain had an eightfold-higher sensitivity to bacitracin. Expression of
bcrC
initiated from a single promoter site that could be recognized by either of two extracytoplasmic function (ECF) σ factors, σ
X
or σ
M
. Bacitracin induced expression of
bcrC
, and this induction was dependent on σ
M
but not on σ
X
. Under inducing conditions, expression was primarily dependent on σ
M
. As a consequence, a
sigM
mutant was fourfold more sensitive to bacitracin, while the
sigX
mutant was only slightly sensitive. A
sigX sigM
double mutant was similar to a
bcrC
mutant in sensitivity. These results support the suggestion that one function of
B. subtilis
ECF σ factors is to coordinate antibiotic stress responses.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
107 articles.
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