{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE311nnn/GSE311345/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Homo sapiens"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311345"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Bacterial effector modifies host messenger RNA to promote virulence","description":"Bacterial pathogens harbor specialized secretion systems that inject effector proteins into the host cell to establish infection and disease. While many bacterial effectors post-translationally modify proteins to influence host responses, the extent to which effectors modify host RNA is currently unknown. Here we performed RNA-interactome capture (RIC) to isolate effectors bound to host cellular messenger RNA (mRNA) during Legionella pneumophila infection. RIC identified an uncharacterized effector, FadA (Lpw16921), which localized to the host-cell nucleus and interacted with host mRNAs at uracil (U)-rich RNA motifs. FadA exhibited NADPH-oxidase activity that mediated 8-oxo-guanine (oxo8G) modifications of mRNA substrates, resulting in oxidative damage and inhibition of translation. Infection with L. pneumophila harboring wild-type FadA, but not a catalytically inactive mutant, increased oxo8G modifications, suppressed cytokine responses, and promoted bacterial persistence in vivo. Our findings demonstrate the potential for a secreted Q2 effector to post-transcriptionally modify host mRNA as a mechanism to promote bacterial virulence.","dates":{"publication":"2026/08/13"},"accession":"GSE311345","cross_references":{"GSM":["GSM9323843","GSM9323842","GSM9323841","GSM9323840","GSM9323845","GSM9323844"],"GPL":["30173"],"GSE":["311345"],"taxon":["Homo sapiens"]}}