Abstract
Our understanding of the molecular mechanisms behind bacteria-phage interactions remains limited. Here we report that a small protein, SrpA, controls core cellular processes in response to phage infection and environmental signals in Pseudomonas aeruginosa. We show that SrpA is essential for efficient genome replication of phage K5, and controls transcription by binding to a palindromic sequence upstream of the phage RNA polymerase gene. We identify potential SrpA-binding sites in 66 promoter regions across the P. aeruginosa genome, and experimentally validate direct binding of SrpA to some of these sites. Using transcriptomics and further experiments, we show that SrpA, directly or indirectly, regulates many cellular processes including cell motility, chemotaxis, biofilm formation, pyocyanin synthesis and protein secretion, as well as virulence in a Caenorhabditis elegans model of infection. Further research on SrpA and similar proteins, which are widely present in many other bacteria, is warranted.
Highlights
Our understanding of the molecular mechanisms behind bacteria-phage interactions remains limited
A small number of mutants show wild-type adsorption rate (WAR) with genetic mutations occurring in metabolic pathways that are essential for various phage infection stages, such as genome injection, transcription, replication, and packaging[7,8,9]
These results indicated that the bacterial srpA gene is required for a successful infection by the phage K5
Summary
Our understanding of the molecular mechanisms behind bacteria-phage interactions remains limited. During a long history of reciprocal competition with phages, bacteria have evolved several genetic systems that actively stop phage attacks, such as restriction-modification (R-M) system, CRISPR-Cas system, abortive infection (Abi) system, toxin-antitoxin (TA) system, and bacteriophage exclusion (BREX) system[2, 3]. The QS system can affect cell physiological state and cell populations, leading to attenuated phage reproduction[5] Extracellular polymers, such as exopolysaccharides, lipopolysaccharide (LPS), capsule, and proteinaceous layer, may function as physical shields against phage adsorption by masking phage receptors[6, 7]. A small number of mutants show wild-type adsorption rate (WAR) with genetic mutations occurring in metabolic pathways that are essential for various phage infection stages, such as genome injection, transcription, replication, and packaging[7,8,9]. A Tn5G transposon library of P. aeruginosa PAK-AR2 was constructed and screened for bacterial genes required for the phage K5 infection[10]
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