Antitoxin CrlA of CrlTA Toxin-Antitoxin System in a Clinical Isolate Inhibits Lytic Phage Infection.

is an important opportunistic pathogen in cystic fibrosis patients and immunocompromised individuals, and the toxin-antitoxin (TA) system is involved in bacterial virulence and phage resistance. However, the roles of TA systems in are relatively less studied and no phage Cro-like regulators were identified as TA components. Here, we identified and characterized a chromosome-encoded prophage Cro-like antitoxin (CrlA) in the clinical isolate WK172. CrlA neutralized the toxicity of the toxin CrlA (CrlT) which cleaves mRNA, and they formed a type II TA system. Specifically, and are co-transcribed and their protein products interact with each other directly. The autorepression of CrlA is abolished by CrlT through the formation of the CrlTA complex. Furthermore, is induced in the stationary phase, and is expressed at higher levels than . The excess CrlA inhibits the infection of lytic phages. CrlA is widely distributed among and in other bacterial strains and may provide antiphage activities.