Hin-Mediated DNA Knotting and Recombining Promote Replicon Dysfunction and Mutation
Citation
Deibler, 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.Abstract
Background: 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.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1904230/pdf/Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAACitable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:5355105
Collections
- HMS Scholarly Articles [17875]
Contact administrator regarding this item (to report mistakes or request changes)