Trends in Microbiology
Volume 12, Issue 9, September 2004, Pages 401-404
Journal home page for Trends in Microbiology

Research Focus
Antibiotic-induced lateral transfer of antibiotic resistance

https://doi.org/10.1016/j.tim.2004.07.003Get rights and content

As do many temperate bacteriophages, integrating conjugative elements (ICEs) recruit the SOS DNA damage response to mobilize themselves from the bacterial chromosome and infect other cells. This transfers resistance to multiple antibiotics. Several commonly used antibiotics induce the SOS response, potentially hastening genetic change and the evolution to resistance of pathogenic populations. The use of such antibiotics should be reconsidered.

Section snippets

The SOS DNA damage response, antibiotics, genetic change and resistance

The SOS system (reviewed in Refs. 8, 9) controls a set of approximately 42 genes that share an upstream sequence, known as the SOS box, which is bound by the transcriptional repressor LexA. When single-stranded DNA (ssDNA), a hallmark of DNA damage, is present in a cell, it is bound by RecA to form a nucleoprotein filament – the activated form of the RecA coprotease (RecA*), which catalyzes the autocleavage of the LexA repressor to a form that no longer binds to the SOS box. The SOS response

Induction of dormant DNA elements

Initially described for bacteriophage λ, many temperate phages (i.e. phages that can lie dormant as a plasmid or by integrating into the host chromosome) are repressed by a phage-encoded repressor that undergoes autocleavage in the presence of RecA*. The repressor prevents expression of most phage genes and phage replication, so that the virus is passed on as part of the host. Cleavage of the repressor prevents it from binding to the operator and the phage is then induced (i.e. enters the lytic

Concluding remarks

DNA-damaging agents accelerate the evolution of bacterial genomes in several different ways. This should be taken into consideration in the design of antibiotic therapy. Some of the possible precautions are: (i) that the use of SOS-inducing antibiotics might be reduced and confined to situations in which there is no alternative; (ii) that the use of such antibiotics might be limited to closely supervised situations to reduce the chances of incomplete treatment; and (iii) that prophylactic use

Acknowledgements

We thank Joseph Petrosino for comments on the manuscript. Supported by a postdoctoral fellowship from the Natural Sciences and Engineering Research Council of Canada (AS) and US National Institutes of Health grants R01-GM64022 (PJH) and R01GM53158 (SMR).

References (24)

  • Walker, G.C. (1996) The SOS response of Escherichia coli In Escherichia coli and Salmonella: Cellular and Molecular...
  • M.D. Sutton

    The SOS response: recent insights into umuDC-dependent mutagenesis and DNA damage tolerance

    Annu. Rev. Genet.

    (2000)
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