{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T16:32:27Z","timestamp":1787157147735,"version":"build-2736575974"},"reference-count":33,"publisher":"Microbiology Society","issue":"8","license":[{"start":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T00:00:00Z","timestamp":1787097600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100005825","name":"National Institute of Food and Agriculture","doi-asserted-by":"crossref","award":["1023966"],"award-info":[{"award-number":["1023966"]}],"id":[{"id":"10.13039\/100005825","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,8,19]]},"abstract":"<jats:p>\n                    For the clinical treatment of infections with\n                    <jats:italic>Enterobacteriaceae<\/jats:italic>\n                    , the development of resistance to last-resort antimicrobials like colistin is of concern, as it limits treatment options. Since 2015, ten families of\n                    <jats:italic>mobile colistin resistance<\/jats:italic>\n                    (\n                    <jats:italic>mcr<\/jats:italic>\n                    ) genes have been discovered; however, our understanding of MCR remains limited because (i)\n                    <jats:italic>mcr-1<\/jats:italic>\n                    is the most studied variant, (ii)\n                    <jats:italic>mcr<\/jats:italic>\n                    variants are rarely compared and (iii)\n                    <jats:italic>mcr<\/jats:italic>\n                    variants are primarily studied in\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    , even though studies have shown that\n                    <jats:italic>mcr<\/jats:italic>\n                    variants can confer significantly different phenotypes and that lipid A (i.e. the target of colistin and\n                    <jats:italic>mcr-<\/jats:italic>\n                    modification) structurally differs between bacterial species. To fill this gap, we examined how\n                    <jats:italic>mcr-3<\/jats:italic>\n                    and\n                    <jats:italic>mcr-9<\/jats:italic>\n                    , as two less frequently studied\n                    <jats:italic>mcr<\/jats:italic>\n                    variants, impact the colistin resistance of laboratory-adapted and real-world (i.e. clinical or food) isolates of\n                    <jats:italic>E. coli<\/jats:italic>\n                    ,\n                    <jats:italic>Salmonella enterica<\/jats:italic>\n                    and\n                    <jats:italic>Klebsiella pneumoniae<\/jats:italic>\n                    . We found that while\n                    <jats:italic>mcr-3<\/jats:italic>\n                    consistently conferred colistin resistance to all tested strains,\n                    <jats:italic>mcr-9<\/jats:italic>\n                    only conferred resistance to two strains. The fold-change in colistin minimum inhibitory concentrations was significantly impacted by both the bacterial species and the\n                    <jats:italic>mcr<\/jats:italic>\n                    variant but not by whether a strain was a laboratory-adapted or real-world isolate. Overall, our results suggest that while laboratory-adapted strains may provide a good estimate of\n                    <jats:italic>mcr<\/jats:italic>\n                    -mediated colistin resistance of real-world isolates, findings of\n                    <jats:italic>mcr<\/jats:italic>\n                    -mediated phenotypes in one bacterial species should not be extrapolated to another.\n                  <\/jats:p>","DOI":"10.1099\/mic.0.001759","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T16:15:26Z","timestamp":1787156126000},"source":"Crossref","is-referenced-by-count":0,"title":["MCR-3 and MCR-9 confer species-specific increases in colistin MICs"],"prefix":"10.1099","volume":"172","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3627-9966","authenticated-orcid":false,"given":"Anna","family":"Schumann","sequence":"first","affiliation":[{"name":"Department of Food Science, Cornell University, Ithaca, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4168-5662","authenticated-orcid":false,"given":"Martin","family":"Wiedmann","sequence":"additional","affiliation":[{"name":"Department of Food Science, Cornell University, Ithaca, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"345","reference":[{"key":"R1","article-title":"Antimicrobial Resistance","year":"2023"},{"key":"R2","article-title":"Antibiotic resistance threats in the United States","year":"2019"},{"key":"R3","article-title":"Antimicrobial Resistance Threats in the United States","year":"2025"},{"key":"R4","article-title":"Federal Scientists Find in U.S. Samples the MCR-1 Gene Responsible for Colistin 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