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.