{"doi":"10.1128/mbio.00355-24","title":"Initiation of H1-T6SS dueling between\n            <i>Pseudomonas aeruginosa</i>","abstract":"<jats:title>ABSTRACT</jats:title>\n          <jats:sec>\n            <jats:title/>\n            <jats:p>\n              The Type VI secretion system (T6SS) is a multicomponent apparatus, present in many Gram-negative bacteria, which can inhibit bacterial prey in various ecological niches.\n              <jats:italic>Pseudomonas aeruginosa</jats:italic>\n              assembles one of its three T6SS (H1-T6SS) to respond to attacks from adjacent competing bacteria. Surprisingly, repeated assemblies of the H1-T6SS, termed dueling, were described in a monoculture in the absence of an attacker strain; however, the underlying mechanism was unknown. Here, we explored the role of H2-T6SS of\n              <jats:italic>P. aeruginosa</jats:italic>\n              in triggering H1-T6SS assembly. We show that H2-T6SS inactivation in\n              <jats:italic>P. aeruginosa</jats:italic>\n              causes a significant reduction in H1-T6SS dueling and that H2-T6SS activity directly triggers retaliation by the H1-T6SS. Intraspecific competition experiments revealed that elimination of H2-T6SS in non-immune prey cells conferred protection from H1-T6SS. Moreover, we show that the H1-T6SS response is triggered independently of the characterized lipase effectors of the H2-T6SS, as well as those of\n              <jats:italic>Acinetobacter baylyi</jats:italic>\n              and\n              <jats:italic>Vibrio cholerae</jats:italic>\n              . Our results suggest that H1-T6SS response to H2-T6SS in\n              <jats:italic>P. aeruginosa</jats:italic>\n              can impact intraspecific competition, particularly when the H1-T6SS effector-immunity pairs differ between strains, and could determine the outcome of multistrain colonization.\n            </jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE</jats:title>\n              <jats:p>\n                The opportunistic pathogen\n                <jats:italic>Pseudomonas aeruginosa</jats:italic>\n                harbors three different Type VI secretion systems (H1, H2, and H3-T6SS), which can translocate toxins that can inhibit bacterial competitors or inflict damage to eukaryotic host cells. Unlike the unregulated T6SS assembly in other Gram-negative bacteria, the H1-T6SS in\n                <jats:italic>P. aeruginosa</jats:italic>\n                is precisely assembled as a response to various cell damaging attacks from neighboring bacterial cells. Surprisingly, it was observed that neighboring\n                <jats:italic>P. aeruginosa</jats:italic>\n                cells repeatedly assemble their H1-T6SS toward each other. Mechanisms triggering this “dueling” behavior between sister cells were unknown. In this report, we used a combination of microscopy, genetic and intraspecific competition experiments to show that H2-T6SS initiates H1-T6SS dueling. Our study highlights the interplay between different T6SS clusters in\n                <jats:italic>P. aeruginosa</jats:italic>\n                , which may influence the outcomes of multistrain competition in various ecological settings such as biofilm formation and colonization of cystic fibrosis lungs.\n              </jats:p>\n            </jats:sec>\n          </jats:sec>","journal":"mBio","year":2024,"id":676949,"datarank":0.4943755299006494,"base_score":3.295836866004329,"endowment":3.295836866004329,"self_citation_contribution":0.4943755299006494,"citation_network_contribution":0.0,"self_endowment_contribution":0.4943755299006494,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":26,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1513595,"name":"S. Narayanan","orcid":"0009-0004-3479-8097","position":1,"is_corresponding":false},{"id":1768715,"name":"A. Tejada-Arranz","orcid":"0000-0002-8452-8245","position":2,"is_corresponding":false},{"id":1768722,"name":"A. Plack","orcid":null,"position":3,"is_corresponding":false},{"id":277870,"name":"Marek Basler","orcid":"0000-0001-5414-2088","position":4,"is_corresponding":false},{"id":8826,"name":"M. George","orcid":"0009-0006-4935-3079","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Initiation of H1-T6SS dueling between\n            <i>Pseudomonas aeruginosa</i>","abstract":"<jats:title>ABSTRACT</jats:title>\n          <jats:sec>\n            <jats:title/>\n            <jats:p>\n              The Type VI secretion system (T6SS) is a multicomponent apparatus, present in many Gram-negative bacteria, which can inhibit bacterial prey in various ecological niches.\n              <jats:italic>Pseudomonas aeruginosa</jats:italic>\n              assembles one of its three T6SS (H1-T6SS) to respond to attacks from adjacent competing bacteria. Surprisingly, repeated assemblies of the H1-T6SS, termed dueling, were described in a monoculture in the absence of an attacker strain; however, the underlying mechanism was unknown. Here, we explored the role of H2-T6SS of\n              <jats:italic>P. aeruginosa</jats:italic>\n              in triggering H1-T6SS assembly. We show that H2-T6SS inactivation in\n              <jats:italic>P. aeruginosa</jats:italic>\n              causes a significant reduction in H1-T6SS dueling and that H2-T6SS activity directly triggers retaliation by the H1-T6SS. Intraspecific competition experiments revealed that elimination of H2-T6SS in non-immune prey cells conferred protection from H1-T6SS. Moreover, we show that the H1-T6SS response is triggered independently of the characterized lipase effectors of the H2-T6SS, as well as those of\n              <jats:italic>Acinetobacter baylyi</jats:italic>\n              and\n              <jats:italic>Vibrio cholerae</jats:italic>\n              . Our results suggest that H1-T6SS response to H2-T6SS in\n              <jats:italic>P. aeruginosa</jats:italic>\n              can impact intraspecific competition, particularly when the H1-T6SS effector-immunity pairs differ between strains, and could determine the outcome of multistrain colonization.\n            </jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE</jats:title>\n              <jats:p>\n                The opportunistic pathogen\n                <jats:italic>Pseudomonas aeruginosa</jats:italic>\n                harbors three different Type VI secretion systems (H1, H2, and H3-T6SS), which can translocate toxins that can inhibit bacterial competitors or inflict damage to eukaryotic host cells. Unlike the unregulated T6SS assembly in other Gram-negative bacteria, the H1-T6SS in\n                <jats:italic>P. aeruginosa</jats:italic>\n                is precisely assembled as a response to various cell damaging attacks from neighboring bacterial cells. Surprisingly, it was observed that neighboring\n                <jats:italic>P. aeruginosa</jats:italic>\n                cells repeatedly assemble their H1-T6SS toward each other. Mechanisms triggering this “dueling” behavior between sister cells were unknown. In this report, we used a combination of microscopy, genetic and intraspecific competition experiments to show that H2-T6SS initiates H1-T6SS dueling. Our study highlights the interplay between different T6SS clusters in\n                <jats:italic>P. aeruginosa</jats:italic>\n                , which may influence the outcomes of multistrain competition in various ecological settings such as biofilm formation and colonization of cystic fibrosis lungs.\n              </jats:p>\n            </jats:sec>\n          </jats:sec>","is_dataset_classified":null,"base_score":3.1780538303479458,"endowment":3.1780538303479458,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"38990002","pmcid":"PMC11323562","openalex_id":"https://openalex.org/W4400542375","authors":[],"funders":[{"funder_name":"EC | European Research Council","grant_id":"865105","title":"Mechanisms of dynamic localization of the bacterial Type 6 secretion system assembly"},{"funder_name":"Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung","grant_id":"51NF40_180541","title":null},{"funder_name":"European Molecular Biology Organization","grant_id":"ALTF 905-2017","title":null},{"funder_name":"Swiss National Science Foundation","grant_id":"180541","title":"NCCR AntiResist (phase I)"}],"total_grants":4,"fwci":8.9899,"citation_percentile":0.98736611,"influential_citations":0,"citation_trend":[{"year":2024,"count":3},{"year":2025,"count":15},{"year":2026,"count":5}],"oa_status":"gold","license":"cc-by","oa_locations":[{"url":"https://doi.org/10.1128/mbio.00355-24","host_type":"journal"},{"url":"https://doi.org/10.1128/mbio.00355-24","host_type":"publisher"},{"url":"https://journals.asm.org/doi/pdf/10.1128/mbio.00355-24","host_type":"publisher"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38990002","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/11323562","host_type":"repository"},{"url":"https://doaj.org/article/6896466620974f80b9136d4010fa34b0","host_type":"repository"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC11323562/pdf/mbio.00355-24.pdf","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC11323562","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC11323562?pdf=render","host_type":"Europe_PMC"},{"url":"http://dx.doi.org/10.1128/mbio.00355-24","host_type":""}],"fields_of_study":["Vibrio bacteria research studies","Antibiotic Resistance in Bacteria","Yersinia bacterium, plague, ectoparasites research","0301 basic medicine","03 medical and health sciences","Pseudomonas aeruginosa","Type VI Secretion Systems","Acinetobacter","Bacterial Proteins","Vibrio cholerae","Microbial Interactions","Acinetobacter baylyi"],"mesh_terms":["Type VI Secretion Systems","Acinetobacter","Bacterial Proteins","Pseudomonas aeruginosa","Vibrio cholerae","Microbial Interactions"],"keywords":["Type VI secretion system","Pseudomonas aeruginosa","Microbiology","Biology","Competition (biology)","Effector","Biofilm","Bacteria","Cell biology","Virulence","Genetics","Ecology","Competition","toxins","Bacterial Interactions","T6ss","Acinetobacter","Type VI Secretion Systems","QR1-502","Bacterial Proteins","Microbial Interactions","Vibrio cholerae","Research Article"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Life in Land"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[{"name":"doi"}],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-17T03:23:44.630932Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}