Show simple item record

Recombination-induced suppression of cell division following P1-mediated generalized transduction in Klebsiella aerogenes

dc.contributor.authorSambucetti, Lidia C.en_US
dc.contributor.authorBender, Robert A.en_US
dc.date.accessioned2006-09-11T19:06:46Z
dc.date.available2006-09-11T19:06:46Z
dc.date.issued1983-03en_US
dc.identifier.citationBender, Robert A.; Sambucetti, Lidia C.; (1983). "Recombination-induced suppression of cell division following P1-mediated generalized transduction in Klebsiella aerogenes ." MGG Molecular & General Genetics 189(2): 263-268. <http://hdl.handle.net/2027.42/47551>en_US
dc.identifier.issn1617-4623en_US
dc.identifier.issn0026-8925en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/47551
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6343791&dopt=citationen_US
dc.description.abstractKlebsiella aerogenes recombinants resulting from bacteriophage P1-mediated generalized transduction failed to increase in number for approximately six generations after transduction. Nevertheless these recombinants continued to grow and became sensitive to penicillin after a transient resistance, suggesting that the cells were growing as long, non-dividing filaments. When filamentous cells were isolated from transduced cultures by gradient centrifugation, recombinants were 1000-fold more frequent among the filaments than among the normal-sized cells. The suppression of cell-division lasted for six generations whether markers near the origin ( gln, ilv ) or terminus ( his, trp ) of chromosome replication were used, despite a 50-fold difference in transduction frequencies for these markers. The suppression of cell division was a host response to recombination rather than to P1 invasion since cells lysogenized by P1 in these same experiments showed only a short (two generation) suppression of cell division. We speculate that the suppression of cell-division is an SOS response triggered by the degraded DNA not incorporated in the final recombinant. We demonstrate that both the filamentation and the transient penicillin resistance of recombinant cells can be exploited to enrich greatly for recombinants, raising transduction frequencies to as high as 10 -3 .en_US
dc.format.extent633369 bytes
dc.format.extent3115 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherSpringer-Verlag; Springer-Verlag GmbH & Co. KGen_US
dc.subject.otherMicrobial Genetics and Genomicsen_US
dc.subject.otherLife Sciencesen_US
dc.subject.otherCell Biologyen_US
dc.subject.otherBiochemistry, Generalen_US
dc.titleRecombination-induced suppression of cell division following P1-mediated generalized transduction in Klebsiella aerogenesen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelGeneticsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Cellular and Molecular Biology, Division of Biological Sciences, University of Michigan, 48109, Ann Arbor, MI, USAen_US
dc.contributor.affiliationotherDepartment of Molecular Biology, Albert Einstein College of Medicine, 10461, Bronx, NY, USAen_US
dc.contributor.affiliationumcampusAnn Arboren_US
dc.identifier.pmid6343791en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/47551/1/438_2004_Article_BF00337815.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1007/BF00337815en_US
dc.identifier.sourceMGG Molecular & General Geneticsen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.