Affiliation:
1. Department of Bacteriology and TSEs, Central Veterinary Institute of Wageningen UR, 8219 PH Lelystad, The Netherlands
2. Department of Infectious Diseases and Immunology, Utrecht University, 3584 CL Utrecht, The Netherlands
3. WHO Collaborating Centre for Campylobacter/OIE Reference Laboratory for Campylobacteriosis Utrecht, The Netherlands
Abstract
ABSTRACT
The presence and functionality of DNA repair mechanisms in
Campylobacter jejuni
are largely unknown. In silico analysis of the complete translated genome of
C. jejuni
NCTC 11168 suggests the presence of genes involved in methyl-directed mismatch repair (MMR), nucleotide excision repair, base excision repair (BER), and recombinational repair. To assess the functionality of these putative repair mechanisms in
C. jejuni
,
mutS
,
uvrB
,
ung
, and
recA
knockout mutants were constructed and analyzed for their ability to repair spontaneous point mutations, UV irradiation-induced DNA damage, and nicked DNA. Inactivation of the different putative DNA repair genes did not alter the spontaneous mutation frequency. Disruption of the UvrB and RecA orthologues, but not the putative MutS or Ung proteins, resulted in a significant reduction in viability after exposure to UV irradiation. Assays performed with uracil-containing plasmid DNA showed that the putative uracil-DNA glycosylase (Ung) protein, important for initiation of the BER pathway, is also functional in
C. jejuni
. Inactivation of
recA
also resulted in a loss of natural transformation. Overall, the data indicate that
C. jejuni
has multiple functional DNA repair systems that may protect against DNA damage and limit the generation of genetic diversity. On the other hand, the apparent absence of a functional MMR pathway may enhance the frequency of on-and-off switching of phase variable genes typical for
C. jejuni
and may contribute to the genetic heterogeneity of the
C. jejuni
population.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
34 articles.
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