DOI: 10.1128/jb.00551-25 ISSN: 0021-9193

The bacterial SOS response promotes the expression of the transposase encoded by IS CR mobile genetic elements

Claire Lallement, Thomas Jové, Cécile Pasternak, Sandra Da Re, Marie-Cécile Ploy

ABSTRACT

Insertion sequences (IS) are widely involved in bacterial genomic plasticity by disrupting, adding, moving genomic sequences, or by activating or extinguishing gene expression. A specific family of IS, IS CR (for insertion sequence of Common Region), is thought to be involved in the dissemination of antibiotic resistance genes (ARGs). While some IS CR members are commonly found in bacteria isolated in clinical settings and can contribute to downstream ARG expression, the mechanisms regulating the IS CR -encoded transposase expression have remained uncharacterized. Here, we investigated the expression of the transposase genes of IS CR1 , IS CR2, and IS CR8 and its regulation in Escherichia coli . Using in silico analyses and in vitro experiments, we showed that the expression levels were extremely low, as observed for most IS transposases. We further demonstrated the direct role of DNA damages and the key SOS response repressor, LexA, in controlling the activity of the transposase promoter. These results provide evidence that the mobility of at least some IS CR elements may be promoted upon bacterial exposure to antibiotics inducing the SOS response.

IMPORTANCE

Mobile genetic elements (MGEs) are the most prevalent cause of antibiotic resistance emergence. Among these mobile elements, insertion sequences (IS) are well known to allow the dissemination of antibiotic resistance genes (ARGs) through the action of their transposase. Here, we studied the regulation of the transposase expression in a specific family of IS, the IS CR family, some members of which are known to be involved in antibiotic resistance. Characterizing the regulation of transposase expression is an important starting point for understanding how these IS can contribute, through their movement, to the spread and expression of antibiotic resistance.

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