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This makes the rise of bacteria exhibiting polymyxin E (colistin) resistance, largely through modification of lipid A moieties, concerning and suggests that it is important to document the potential sources of the corresponding resistance genes. This study searched for potential emerging colistin resistance genes from the environment by investigating a previously performed functional metagenomic selection for colistin resistance of a goose fecal microbiome. We found that the selection captured\n                      <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                      sp. DNA fragments that all contained\n                      <jats:italic toggle=\"yes\">eptA<\/jats:italic>\n                      genes. We confirmed their ability to confer significant colistin resistance in\n                      <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                      via modification of lipid A in the outer membrane. Furthermore, we found evidence for mobilization of closely related\n                      <jats:italic toggle=\"yes\">eptA<\/jats:italic>\n                      genes in\n                      <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                      genomes, marking them as potential\n                      <jats:italic toggle=\"yes\">mcr<\/jats:italic>\n                      genes or their precursors. This study highlights the potential for functional metagenomic selections for colistin resistance to capture genes from unexpected environmental sources such as the goose fecal microbiome.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Colistin is an important antibiotic of last resort, and increasing resistance to this drug via mobile phosphoethanolamine transferase genes, such as\n                        <jats:italic toggle=\"yes\">mcr-1<\/jats:italic>\n                        , threatens its clinical utility. Given the discovery of\n                        <jats:italic toggle=\"yes\">mcr-1<\/jats:italic>\n                        in pigs, the ability of animals to act as vectors in the spread of colistin resistance is alarming. We show here that functionally selected\n                        <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                        phosphoethanolamine transferase genes from the goose microbiome have the ability to confer clinical levels of colistin resistance when transferred into\n                        <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                        . While the genes are annotated as\n                        <jats:italic toggle=\"yes\">eptA<\/jats:italic>\n                        homologs, closer study of these genes suggests that they may be mobilized within the\n                        <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                        genus, suggesting that they may be\n                        <jats:italic toggle=\"yes\">mcr<\/jats:italic>\n                        genes of concern instead.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/aem.02468-25","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T13:01:01Z","timestamp":1786021261000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["A functionally selected\n                    <i>Acinetobacter<\/i>\n                    sp. phosphoethanolamine transferase gene from the goose fecal microbiome confers colistin resistance in\n                    <i>E. coli<\/i>"],"prefix":"10.1128","volume":"92","author":[{"given":"Elizabeth","family":"Bernate","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02y3ad647","id-type":"ROR","asserted-by":"publisher"}],"name":"College of Veterinary Medicine, University of Florida","place":["Gainesville, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yijun","family":"Shi","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/047426m28","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Animal Sciences, University of Illinois at Urbana-Champaign","place":["Urbana, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ezabelle","family":"Franck","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05g3dte14","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biomedical Sciences, Florida State University","place":["Tallahassee, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2302-502X","authenticated-orcid":true,"given":"Terence S.","family":"Crofts","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/047426m28","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Animal Sciences, University of Illinois at Urbana-Champaign","place":["Urbana, USA"]},{"id":[{"id":"https:\/\/ror.org\/047426m28","id-type":"ROR","asserted-by":"publisher"}],"name":"Carl R. 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