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dc.contributor.authorDeibler, Richard Wendel
dc.contributor.authorMann, Jennifer K.
dc.contributor.authorSumners, De Witt L.
dc.contributor.authorZechiedrich, Lynn
dc.date.accessioned2011-11-29T06:58:19Z
dc.date.issued2007
dc.identifier.citationDeibler, Richard W., Jennifer K. Mann, De Witt L. Sumners, and Lynn Zechiedrich. 2007. Hin-mediated DNA knotting and recombining promote replicon dysfunction and mutation. BMC Molecular Biology 8: 44.en_US
dc.identifier.issn1471-2199en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:5355105
dc.description.abstractBackground: The genetic code imposes a dilemma for cells. The DNA must be long enough to encode for the complexity of an organism, yet thin and flexible enough to fit within the cell. The combination of these properties greatly favors DNA collisions, which can knot and drive recombination of the DNA. Despite the well-accepted propensity of cellular DNA to collide and react with itself, it has not been established what the physiological consequences are. Results: Here we analyze the effects of recombined and knotted plasmids in E. coli using the Hin site-specific recombination system. We show that Hin-mediated DNA knotting and recombination (i) promote replicon loss by blocking DNA replication; (ii) block gene transcription; and (iii) cause genetic rearrangements at a rate three to four orders of magnitude higher than the rate for an unknotted, unrecombined plasmid. Conclusion: These results show that DNA reactivity leading to recombined and knotted DNA is potentially toxic and may help drive genetic evolution.en_US
dc.language.isoen_USen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofdoi://10.1186/1471-2199-8-44en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1904230/pdf/en_US
dash.licenseLAA
dc.titleHin-Mediated DNA Knotting and Recombining Promote Replicon Dysfunction and Mutationen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalBMC Molecular Biologyen_US
dash.depositing.authorDeibler, Richard Wendel
dc.date.available2011-11-29T06:58:19Z
dash.affiliation.otherHMS^Systems Biologyen_US
dc.identifier.doi10.1186/1471-2199-8-44*
dash.contributor.affiliatedDeibler, Richard Wendel


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