{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T16:03:58Z","timestamp":1781107438183,"version":"3.54.1"},"reference-count":0,"publisher":"National Academy of Sciences","issue":"3","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1995,1,31]]},"abstract":"<jats:p>We present evidence that human immunodeficiency virus (HIV) reverse transcriptase (RT) can substitute for DNA polymerase I in bacteria. Expression of HIV RT enables an Escherichia coli mutant, polA12 recA718, containing a temperature-sensitive mutation in DNA polymerase I, to grow at a nonpermissive temperature. The plasmid pBR322 contains a DNA polymerase I-dependent origin of replication. Expression of HIV RT enables the same E. coli mutant to maintain this plasmid at a nonpermissive temperature. Furthermore, expression of HIV RT in this mutant renders it sensitive to 3'-azido-3'-deoxythymidine, a commonly used anti-AIDS drug that targets HIV RT. These combined findings on the genetic complementation of DNA polymerase I by HIV RT provide a bacterial assay to screen for drugs directed against HIV RT. Genetic complementation provides a method for positive selection of large numbers of functional HIV RT mutants for studies on structure-function relationships.<\/jats:p>","DOI":"10.1073\/pnas.92.3.684","type":"journal-article","created":{"date-parts":[[2006,5,31]],"date-time":"2006-05-31T04:26:33Z","timestamp":1149049593000},"page":"684-688","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":23,"title":["Human immunodeficiency virus reverse transcriptase substitutes for DNA polymerase I in Escherichia coli."],"prefix":"10.1073","volume":"92","author":[{"given":"B","family":"Kim","sequence":"first","affiliation":[{"name":"Joseph Gottstein Memorial Cancer Research Laboratory, Department of Pathology, University of Washington, Seattle 98195."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L A","family":"Loeb","sequence":"additional","affiliation":[{"name":"Joseph Gottstein Memorial Cancer Research Laboratory, Department of Pathology, University of Washington, Seattle 98195."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1995,1,31]]},"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.92.3.684","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,13]],"date-time":"2022-04-13T13:59:51Z","timestamp":1649858391000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/full\/10.1073\/pnas.92.3.684"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,1,31]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1995,1,31]]}},"alternative-id":["10.1073\/pnas.92.3.684"],"URL":"https:\/\/doi.org\/10.1073\/pnas.92.3.684","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,1,31]]},"assertion":[{"value":"1995-01-31","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}