Antitoxin CrlA of CrlTA Toxin–Antitoxin System in a Clinical Isolate Pseudomonas aeruginosa Inhibits Lytic Phage Infection

Frontiers in Microbiology

Muyang Ni¹  Mei He¹  Yunxue Guo³  Jianzhong Lin⁴  Shituan Lin⁴  Jiayu Gu⁴ 

[1] Key Laboratory of Exploration Technologies for Oil and Gas Resources, Ministry of Education, School of Resources and Environment, Yangtze University, Wuhan, China;Key Laboratory of Tropical Marine Bio-Resources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, Innovation Academy of South China Sea Ecology and Environmental Engineering, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China;Southern Marine Science and Engineering Guangdong Laboratory, Guangzhou, China;University of Chinese Academy of Sciences, Beijing, China;

关键词: toxin–antitoxin system;    autoregulation;    degradation;    phage infection;    Pseudomonas aeruginosa;   

DOI  :  10.3389/fmicb.2022.892021

来源: DOAJ

【 摘 要 】

Pseudomonas aeruginosa 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 P. aeruginosa 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 P. aeruginosa WK172. CrlA neutralized the toxicity of the toxin CrlA (CrlT) which cleaves mRNA, and they formed a type II TA system. Specifically, crlA and crlT 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, crlTA is induced in the stationary phase, and crlA is expressed at higher levels than crlT. The excess CrlA inhibits the infection of lytic Pseudomonas phages. CrlA is widely distributed among Pseudomonas and in other bacterial strains and may provide antiphage activities.

【 授权许可】

Unknown