<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Saleh DO</submitter><funding>Deutscher Akademischer Austauschdienst</funding><funding>European Research Council</funding><funding>Volkswagen Foundation</funding><funding>Ministry of Scientific Research, Egypt</funding><pagination>e1011451</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10298799</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(6)</volume><pubmed_abstract>Both the bacterial flagellum and the evolutionary related injectisome encoded on the Salmonella pathogenicity island 1 (SPI-1) play crucial roles during the infection cycle of Salmonella species. The interplay of both is highlighted by the complex cross-regulation that includes transcriptional control of the flagellar master regulatory operon flhDC by HilD, the master regulator of SPI-1 gene expression. Contrary to the HilD-dependent activation of flagellar gene expression, we report here that activation of HilD resulted in a dramatic loss of motility, which was dependent on the presence of SPI-1. Single cell analyses revealed that HilD-activation triggers a SPI-1-dependent induction of the stringent response and a substantial decrease in proton motive force (PMF), while flagellation remai</pubmed_abstract><journal>PLoS pathogens</journal><pubmed_title>SPI-1 virulence gene expression modulates motility of Salmonella Typhimurium in a proton motive force- and adhesins-dependent manner.</pubmed_title><pmcid>PMC10298799</pmcid><funding_grant_id>864971</funding_grant_id><funding_grant_id>91705821</funding_grant_id><pubmed_authors>Saleh DO</pubmed_authors><pubmed_authors>Erhardt M</pubmed_authors><pubmed_authors>Klotzsch E</pubmed_authors><pubmed_authors>Weber W</pubmed_authors><pubmed_authors>Giralt-Zuniga M</pubmed_authors><pubmed_authors>Durairaj AC</pubmed_authors><pubmed_authors>Kaganovitch E</pubmed_authors><pubmed_authors>Strowig T</pubmed_authors><pubmed_authors>Horstmann JA</pubmed_authors></additional><is_claimable>false</is_claimable><name>SPI-1 virulence gene expression modulates motility of Salmonella Typhimurium in a proton motive force- and adhesins-dependent manner.</name><description>Both the bacterial flagellum and the evolutionary related injectisome encoded on the Salmonella pathogenicity island 1 (SPI-1) play crucial roles during the infection cycle of Salmonella species. The interplay of both is highlighted by the complex cross-regulation that includes transcriptional control of the flagellar master regulatory operon flhDC by HilD, the master regulator of SPI-1 gene expression. Contrary to the HilD-dependent activation of flagellar gene expression, we report here that activation of HilD resulted in a dramatic loss of motility, which was dependent on the presence of SPI-1. Single cell analyses revealed that HilD-activation triggers a SPI-1-dependent induction of the stringent response and a substantial decrease in proton motive force (PMF), while flagellation remai</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2025-04-26T04:54:45.55Z</modification><creation>2025-04-06T11:14:21.607Z</creation></dates><accession>S-EPMC10298799</accession><cross_references><pubmed>37315106</pubmed><doi>10.1371/journal.ppat.1011451</doi></cross_references></HashMap>