Class 1 integrons in Acinetobacter baumannii: a weak expression of gene cassettes to counterbalance the lack of LexA-driven integrase repression

• Published in: International journal of antimicrobial agents 2019-04, Vol.53 (4), p.491-499
• Main Authors: Couvé-Deacon, Elodie, Jové, Thomas, Afouda, Pamela, Barraud, Olivier, Tilloy, Valentin, Scaon, Erwan, Hervé, Bastien, Burucoa, Christophe, Kempf, Marie, Marcos, Javier Yugueros, Ploy, Marie-Cécile, Garnier, Fabien
• Format: Article
• Language: English
• Subjects: Acinetobacter baumannii; Cancer; Cassette promoter; Integrase; Integron; Life Sciences; PcS; Regulation
• ISSN: 0924-8579; 1872-7913
• DOI: 10.1016/j.ijantimicag.2018.11.012

•Predominance of the PcS gene cassette promoter variant (strong Pc) in Acinetobacter baumannii•Gene cassette array diversity is low in A. baumannii class 1 integrons•The strength of class 1 integron Pc promoters is weaker in A. baumannii than in E. coli•Integrons with PcS might be selected to limit the integrase cost in A. baumannii Integrons recruit resistance genes through integrase-driven recombination events that are regulated by the bacterial SOS response and require the repressor LexA. Class 1 integrons genes are expressed from a common promoter, Pc, of which at least 5 predominant variants, classified from weak to strong, have been described. In Escherichia coli, there is an intertwined regulation between gene cassette expression and integrase activity: the stronger the promoter, the weaker the integrase. Class 1 integrons have been frequently described in Acinetobacter baumannii. However, Acinetobacter spp. lack the LexA repressor, suggesting that the integrase is constitutively expressed. We characterized the integron content of 83 clinical and environmental A. baumannii strains. We found a predominance of Pc variants described as strong in E. coli. The Pc expression level was 2- to 4-fold lower in A. baumannii than in E. coli, and the diversity of the gene cassette array was low. In A. baumannii, integrons with a PcS promoter might have been selected to enable sufficient resistance while avoiding the toxicity of a highly active integrase. Furthermore, a transcriptional interference between PcS and PintI1 (as shown in E. coli) may limit the expression of the integrase and thus counterbalance the lack of LexA-driven integrase repression to prevent the cost of the integrase.