RecT Affects Prophage Lifestyle and Host Core Cellular Processes in Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a notorious pathogen that causes various nosocomial infections. Several prophage genes located on the chromosomes of P. aeruginosa have been reported to contribute to bacterial pathogenesis via host phenotype transformations, such as serotype conversion and antibiotic resistance. However, our understanding of the molecular mechanism behind host phenotype shifts induced by prophage genes remains largely unknown. Here, we report a systematic study around a hypothetical recombinase, Pg54 (RecT), located on a 48-kb putative prophage (designated PP9W) of a clinical P. aeruginosa strain P9W. Using a Δ mutant (designated P9D), we found that RecT promoted prophage PP9W excision and gene transcription via the inhibition of the gene expression level of , which encodes a CI-like repressor protein. Further transcriptomic profiling and various phenotypic tests showed that RecT modulated like a suppressor to some transcription factors and vital genes of diverse cellular processes, providing multiple advantages for the host, including cell growth, biofilm formation, and virulence. The versatile functions of RecT hint at a strong impact of phage proteins on host P. aeruginosa phenotypic flexibility. Multidrug-resistant and metabolically versatile P. aeruginosa are difficult to eradicate by anti-infective therapy and frequently lead to significant morbidity and mortality. This study characterizes a putative recombinase (RecT) encoded by a prophage of a clinical P. aeruginosa strain isolated from severely burned patients, altering prophage lifestyle and host core cellular processes. It implies the potential role of RecT in the coevolution arm race between bacteria and phage. The excised free phages from the chromosome of host bacteria can be used as weapons against other sensitive competitors in diverse environments, which may increase the lysogeny frequency of different P. aeruginosa subgroups. Subsequent analyses revealed that RecT both positively and negatively affects different phenotypic traits of the host. These findings concerning RecT functions of host phenotypic flexibility improve our understanding of the association between phage recombinases and clinical P. aeruginosa, providing new insight into mitigating the pathogen infection.