Affiliation:
1. Department of Medical Microbiology and Immunology, University of Wisconsin—Madison School of Medicine and Public Health, Madison, Wisconsin
Abstract
ABSTRACT
Most strains of
Neisseria gonorrhoeae
carry the 57-kb gonococcal genetic island (GGI), as do a few strains of
Neisseria meningitidis
. The GGI is inserted into the chromosome at the
dif
site (
difA
) and is flanked by a partial repeat of the
dif
site (
difB
). Since
dif
is a sequence recognized by the site-specific recombinases XerC and XerD and the GGI shows evidence of horizontal acquisition, we hypothesized that the GGI may be acquired or lost by XerCD-mediated site-specific recombination. We show that while the GGI flanked by wild-type
dif
sites,
difA
and
difB
, is not readily lost from the gonococcal chromosome, the substitution of
difB
with another copy of
difA
allows the frequent excision and loss of the GGI. In mutants carrying two
difA
sites (
difA
+
difA
+
), the GGI can be detected as an extrachromosomal circle that exists transiently. A mutation of
xerD
diminished GGI excision from the chromosome of a
difA
+
difA
+
strain, while mutations in
recA
or type IV secretion genes had no effect on the loss of the GGI. These data indicate that the GGI is maintained by the replication of the chromosome and that GGI excision and loss are dependent upon the
dif
sequence and
xerD
. The detection of a circular form of the GGI in a wild-type strain suggests that GGI excision may occur naturally and could function to facilitate GGI transfer. These data suggest a model of GGI excision and loss explaining the absence of the GGI from some gonococcal strains and the maintenance of variant GGIs in some gonococcal and meningococcal isolates.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
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