The SOS Response Controls Integron Recombination

Émilie Guerin, Guillaume Cambray, Neus Sanchez-Alberola, Susana Campoy, Ivan Erill, Sandra Da Re, Bruno Gonzalez-Zorn, Jordi Barbé, Marie-Cécile Ploy, and Didier Mazel

Science, May 2009 p 1034, Vol. 324, No. 5930.

An ever-growing concern in the medical world is the rise of antibiotic-resistant pathogens. One source of comfort that we have had in this fight against the spread of resistance is that the expression of resistance genes confers a cost to bacteria. In the absence selection for antibiotics it is thought that this cost will give a selective advantage to non-resistant bacteria, and so bacterial populations will loose resistance over time in the absence of antibiotics. The authors of this paper suggest that this is unfortunately not always the case.

In the words of Jurassic Park, “Nature will find a way.” For bacteria, one of the weapons in their arsenal against antibiotics is the SOS response. Under normal conditions the protein LexA binds to the operator region controlling SOS genes to repress their expression. In the event of DNA damage LexA is cleaved from this region and a series of DNA repair mechanisms are activated, some of which are low- fidelity and therefore lead to an increase of mutations, some of which may be beneficial in resisting further DNA damage.

In terms of antibiotic resistance, this paper explains that LexA repression and SOS expression also influences recombination of genes cassettes (which often code for antibiotic resistance. During SOS expression cassette recombination is induced. This can result in either silencing or reactivation of cassettes. In other words, a cassette carrying resistance genes can be reactivated through recombination under times of stress and then revert to a “dormant” form that provides no cost to the bacterium once the SOS response is again repressed.


Additional Reading:
Erill, S. Campoy, J. Barbe, FEMS Microbiol. Rev. 31, 637 (2007).
C. M. Collis, R. M. Hall, Antimicrob. Agents Chemother. 39, 155 (1995).
A. Aertsen, C. W. Michiels, Trends Microbiol. 14, 421 (2006).
D. I. Andersson, Curr. Opin. Microbiol. 9, 461 (2006).


Julie Hughes,
Graduate Student, University of Idaho