{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T13:46:34Z","timestamp":1792071994512,"version":"4.4.0"},"reference-count":92,"publisher":"American Society for Microbiology","license":[{"start":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:00:00Z","timestamp":1792022400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:00:00Z","timestamp":1792022400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["RC2DK122394, R35GM131762"],"award-info":[{"award-number":["RC2DK122394, R35GM131762"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P41GM135018, R01GM038784"],"award-info":[{"award-number":["P41GM135018, R01GM038784"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U01CA264071"],"award-info":[{"award-number":["U01CA264071"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSystems"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Gut-resident bacteria must withstand membrane-disrupting stresses, such as bile acids, to persist in the intestinal environment. The Bacteroidota are a dominant phylum of the human gut microbiota. However, the genes responsible for the synthesis of membrane lipids in this phylum remain relatively uncharacterized.\n                      <jats:italic toggle=\"yes\">Bacteroides fragilis<\/jats:italic>\n                      is a prevalent member of this phylum and encodes two predicted cardiolipin synthase family proteins, ClsA and ClsB. We previously identified both\n                      <jats:italic toggle=\"yes\">cls<\/jats:italic>\n                      genes as bile-acid fitness factors in\n                      <jats:italic toggle=\"yes\">B. fragilis<\/jats:italic>\n                      P207, but the contributions of\n                      <jats:italic toggle=\"yes\">clsA<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">clsB<\/jats:italic>\n                      to cell physiology remained unclear. Here, we combine targeted gene deletion with high-resolution lipidomics, metabolomics, and elemental mass spectrometry to show that ClsA and ClsB have distinct and non-redundant functions in the cell. Each\n                      <jats:italic toggle=\"yes\">cls<\/jats:italic>\n                      gene differs in its growth-phase expression pattern, and deletion of each gene produces distinct effects on cell morphology, fitness under membrane-perturbing stress, and the broader metabolome.\n                      <jats:italic toggle=\"yes\">clsA<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">clsB<\/jats:italic>\n                      strongly influence the levels of different glycyl-seryl peptidolipids, a\n                      <jats:italic toggle=\"yes\">Bacteroides<\/jats:italic>\n                      lipid family that includes immune-active lipids, and whose loss impairs bile acid resistance and gut colonization. In contrast to the acute ion-gradient disruption caused by the secondary bile acid deoxycholate, deletion of\n                      <jats:italic toggle=\"yes\">clsA<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">clsB<\/jats:italic>\n                      did not measurably alter steady-state intracellular ion levels under standard growth conditions. Together, these results define related but non-redundant roles for two cardiolipin synthase family proteins in a common member of the human gut microbiota.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        The gut bacterium\n                        <jats:italic toggle=\"yes\">Bacteroides fragilis<\/jats:italic>\n                        is a normal member of the human intestinal microbiota that can also bloom to high abundance in inflamed guts. To survive within the gut,\n                        <jats:italic toggle=\"yes\">B. fragilis<\/jats:italic>\n                        must maintain the integrity and function of its cell membrane. In this study, we report that the two cardiolipin synthase family genes in the\n                        <jats:italic toggle=\"yes\">B. fragilis<\/jats:italic>\n                        genome impact the cell\u2019s lipid profile in distinct ways and contribute differently to how\n                        <jats:italic toggle=\"yes\">B. fragilis<\/jats:italic>\n                        responds to membrane stress. Our work provides insight into how a common gut bacterium adapts to conditions encountered in the intestine and improves understanding of membrane biology in this important group of gut microbes.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msystems.00749-26","type":"journal-article","created":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T13:01:27Z","timestamp":1792069287000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Non-redundant cardiolipin synthase family proteins shape lipid composition and stress resilience in\n                    <i>Bacteroides fragilis<\/i>"],"prefix":"10.1128","author":[{"given":"Matthew K.","family":"Schnizlein","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05hs6h993","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Genetics & Immunology, Michigan State University","place":["East Lansing, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bongjin","family":"Hong","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05hs6h993","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Genetics & Immunology, Michigan State University","place":["East Lansing, USA"]},{"id":[{"id":"https:\/\/ror.org\/05hs6h993","id-type":"ROR","asserted-by":"publisher"}],"name":"Elemental Health Institute, Michigan State University","place":["East Lansing, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4557-1638","authenticated-orcid":true,"given":"Jennifer N. 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