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Cambray G, Sanchez-Alberola N, Campoy S, et al. Prevalence of SOS-mediated control of integron integrase expression as an adaptive trait of chromosomal and mobile integrons. Mob DNA. 2011;2(1):6doi: 10.1186/1759-8753-2-6.
Cambray, G., Sanchez-Alberola, N., Campoy, S., Guerin, �. �., Da Re, S., González-Zorn, B., Ploy, M. C., Barbé, J., Mazel, D., & Erill, I. (2011). Prevalence of SOS-mediated control of integron integrase expression as an adaptive trait of chromosomal and mobile integrons. Mobile DNA, 2(1), 6. https://doi.org/10.1186/1759-8753-2-6
Cambray, Guillaume, et al. "Prevalence of SOS-mediated control of integron integrase expression as an adaptive trait of chromosomal and mobile integrons." Mobile DNA vol. 2,1 (2011): 6. doi: https://doi.org/10.1186/1759-8753-2-6
Cambray G, Sanchez-Alberola N, Campoy S, Guerin É, Da Re S, González-Zorn B, Ploy MC, Barbé J, Mazel D, Erill I. Prevalence of SOS-mediated control of integron integrase expression as an adaptive trait of chromosomal and mobile integrons. Mob DNA. 2011 Apr 30;2(1):6. doi: 10.1186/1759-8753-2-6. PMID: 21529368; PMCID: PMC3108266.
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Mob DNA. 2011 Apr 30;2(1):6. doi: 10.1186/1759-8753-2-6.

Prevalence of SOS-mediated control of integron integrase expression as an adaptive trait of chromosomal and mobile integrons.

Mobile DNA

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

Affiliations

  1. Institut Pasteur, Unité Plasticité du Génome Bactérien, CNRS URA 2171, 75015 Paris, France.
  2. Departament de Genètica i de Microbiologia, Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain.
  3. Department of Biological Sciences, University of Maryland Baltimore County, Baltimore 21228, USA.
  4. Université de Limoges, Faculté de Médecine, EA3175, INSERM, Equipe Avenir, Limoges 87000, France.
  5. Departamento de Sanidad Animal, Facultad de Veterinaria, and VISAVET, Universidad Complutense de Madrid, 28040 Madrid, Spain.

PMID: 21529368 PMCID: PMC3108266 DOI: 10.1186/1759-8753-2-6

Abstract

BACKGROUND: Integrons are found in hundreds of environmental bacterial species, but are mainly known as the agents responsible for the capture and spread of antibiotic-resistance determinants between Gram-negative pathogens. The SOS response is a regulatory network under control of the repressor protein LexA targeted at addressing DNA damage, thus promoting genetic variation in times of stress. We recently reported a direct link between the SOS response and the expression of integron integrases in Vibrio cholerae and a plasmid-borne class 1 mobile integron. SOS regulation enhances cassette swapping and capture in stressful conditions, while freezing the integron in steady environments. We conducted a systematic study of available integron integrase promoter sequences to analyze the extent of this relationship across the Bacteria domain.

RESULTS: Our results showed that LexA controls the expression of a large fraction of integron integrases by binding to Escherichia coli-like LexA binding sites. In addition, the results provide experimental validation of LexA control of the integrase gene for another Vibrio chromosomal integron and for a multiresistance plasmid harboring two integrons. There was a significant correlation between lack of LexA control and predicted inactivation of integrase genes, even though experimental evidence also indicates that LexA regulation may be lost to enhance expression of integron cassettes.

CONCLUSIONS: Ancestral-state reconstruction on an integron integrase phylogeny led us to conclude that the ancestral integron was already regulated by LexA. The data also indicated that SOS regulation has been actively preserved in mobile integrons and large chromosomal integrons, suggesting that unregulated integrase activity is selected against. Nonetheless, additional adaptations have probably arisen to cope with unregulated integrase activity. Identifying them may be fundamental in deciphering the uneven distribution of integrons in the Bacteria domain.

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