{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:35:31Z","timestamp":1790224531121,"version":"4.1.0"},"reference-count":73,"publisher":"National Academy of Sciences","issue":"40","license":[{"start":{"date-parts":[[2023,9,26]],"date-time":"2023-09-26T00:00:00Z","timestamp":1695686400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000266","name":"UKRI | Engineering and Physical Sciences Research Council","doi-asserted-by":"publisher","award":["EP\/T017856\/1"],"award-info":[{"award-number":["EP\/T017856\/1"]}],"id":[{"id":"10.13039\/501100000266","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2023,10,3]]},"abstract":"<jats:p>\n                    Antibiotics, by definition, reduce bacterial growth rates in optimal culture conditions; however, the real-world environments bacteria inhabit see rapid growth punctuated by periods of low nutrient availability. How antibiotics mediate population decline during these periods is poorly understood. Bacteria cannot optimize for all environmental conditions because a growth-longevity tradeoff predicts faster growth results in faster population decline, and since bacteriostatic antibiotics slow growth, they should also mediate longevity. We quantify how antibiotics, their targets, and resistance mechanisms influence longevity using populations of\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    and, as the tradeoff predicts, populations are maintained for longer if they encounter ribosome-binding antibiotics doxycycline and erythromycin, a finding that is not observed using antibiotics with alternative cellular targets. This tradeoff also predicts resistance mechanisms that increase growth rates during antibiotic treatment could be detrimental during nutrient stresses, and indeed, we find resistance by ribosomal protection removes benefits to longevity provided by doxycycline. We therefore liken ribosomal protection to a \u201cTrojan horse\u201d because it provides protection from an antibiotic but, during nutrient stresses, it promotes the demise of the bacteria. Seeking mechanisms to support these observations, we show doxycycline promotes efficient metabolism and reduces the concentration of reactive oxygen species. Seeking generality, we sought another mechanism that affects longevity and we found the number of doxycycline targets, namely, the ribosomal RNA operons, mediates growth and longevity even without antibiotics. We conclude that slow growth, as observed during antibiotic treatment, can help bacteria overcome later periods of nutrient stress.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2221507120","type":"journal-article","created":{"date-parts":[[2023,9,26]],"date-time":"2023-09-26T15:35:57Z","timestamp":1695742557000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":8,"title":["Ribosome-binding antibiotics increase bacterial longevity and growth efficiency"],"prefix":"10.1073","volume":"120","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9133-9119","authenticated-orcid":false,"given":"Emily","family":"Wood","sequence":"first","affiliation":[{"name":"Biosciences, College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4QD, United Kingdom"},{"name":"Engineering and Physical Sciences Research Council Hub for Quantitative Modelling in Healthcare, University of Exeter, Exeter EX4 4QJ, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1413-913X","authenticated-orcid":false,"given":"Hinrich","family":"Schulenburg","sequence":"additional","affiliation":[{"name":"Evolutionary Ecology and Genetics, Zoologisches Institut, Christian-Albrechts-Universit\u00e4t zu Kiel, Am Botanischen Garten 1-9, Kiel 24118, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9692-8828","authenticated-orcid":false,"given":"Philip","family":"Rosenstiel","sequence":"additional","affiliation":[{"name":"Instituts f\u00fcr Klinische Molekularbiologie, Dekanat der Medizinischen Fakult\u00e4t, Christian-Albrechts-Universit\u00e4t zu Kiel, Christian-Albrechts-Platz 4, Kiel D-24118, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5396-4346","authenticated-orcid":false,"given":"Tobias","family":"Bergmiller","sequence":"additional","affiliation":[{"name":"Biosciences, College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4QD, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dyan","family":"Ankrett","sequence":"additional","affiliation":[{"name":"Biosciences, College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4QD, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivana","family":"Gudelj","sequence":"additional","affiliation":[{"name":"Biosciences, College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4QD, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Beardmore","sequence":"additional","affiliation":[{"name":"Biosciences, College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4QD, United Kingdom"},{"name":"Engineering and Physical Sciences Research Council Hub for Quantitative Modelling in Healthcare, University of Exeter, Exeter EX4 4QJ, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2023,9,26]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2005.02.016"},{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio764"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.02463-14"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1521291113"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0034953"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms19124078"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00047.2010"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002158"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.2001586"},{"key":"e_1_3_4_10_2","first-page":"307","volume-title":"Effects of Antibiotic Resistance on Bacterial Fitness, Virulence, and Transmission","author":"Andersson D. 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Beardmore E. Wood rebear217\/AbxIncrease Longevity: Phenotypic data: Ribosome-binding antibiotics increase bacterial longevity and growth efficiency. Zenodo. https:\/\/zenodo.org\/record\/8334696. 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