{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329327/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Shewanella glacialimarina"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329327"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Queuosine promotes wecB-dependent phage resistance and biofilm formation in marine bacterium Shewanella glacialimarina","description":"Transfer RNA (tRNA) modifications critically fine-tune translational accuracy and efficiency, influencing bacterial adaptation to environmental challenges. Among these, the queuosine (Q) modification has recently emerged as a regulator of biofilm formation, yet its role during phage infection remains unknown. Here, we investigate how Q modification links host translational control to phage infection. We show that phage infection activates the Q biosynthetic pathway, leading to elevated Q levels and enhanced translation of NAT-biased genes. This shift drives two interconnected outcomes, namely increased biofilm formation and enhanced mutagenesis mediated by translesion synthesis polymerases. We further identify conserved, slippage-prone regions within surface-related genes that act as hotspots for adaptive variation. Together, our findings uncover a novel mechanistic link between tRNA modification and phage-driven bacterial diversification.","dates":{"publication":"2026/04/28"},"accession":"GSE329327","cross_references":{"GSM":["GSM9701795","GSM9701798","GSM9701799","GSM9701796","GSM9701797","GSM9701802","GSM9701800","GSM9701801"],"GPL":["36874"],"GSE":["329327"],"taxon":["Shewanella glacialimarina"]}}