<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335556/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Pseudomonas aeruginosa</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE335556</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>A Pseudomonas aeruginosa LysR-type transcriptional regulator, PA3321, essential for productive biofilm and influences virulence and pathogenesis</name><description>The transposon insertion mutation of regulator PA3321 (PA3321∷Tn) significantly reduced biofilm formation, while enhancing virulence in Drosophila melanogaster fruit fly and BALB/C mouse infection models. This regulator influenced bacterial motility, c-di-GMP signaling, and the RhlI-RhlR and Pseudomonas quinolone signal (PQS) quorum-sensing (QS) systems. We used RNA-seq assays to identify the regulatory mechanisms of PA3321. We observed that 391 genes were up-regulated and 114 genes were down-regulated in the absence of PA3321, many of which are involved in rhamnolipid synthesis, type II, type III, and type VI secretion systems, and QS systems.</description><dates><publication>2026/06/16</publication></dates><accession>GSE335556</accession><cross_references><GSM>GSM9815495</GSM><GSM>GSM9815496</GSM><GSM>GSM9815493</GSM><GSM>GSM9815494</GSM><GSM>GSM9815491</GSM><GSM>GSM9815492</GSM><GPL>18287</GPL><GSE>335556</GSE><taxon>Pseudomonas aeruginosa</taxon></cross_references></HashMap>