A phage P22 gene controlling integration of prophage
dc.contributor.author | Smith, Hamilton O. | en_US |
dc.contributor.author | Levine, Myron | en_US |
dc.date.accessioned | 2006-04-17T16:13:45Z | |
dc.date.available | 2006-04-17T16:13:45Z | |
dc.date.issued | 1967-02 | en_US |
dc.identifier.citation | Smith, Hamilton O., Levine, Myron (1967/02)."A phage P22 gene controlling integration of prophage." Virology 31(2): 207-216. <http://hdl.handle.net/2027.42/33387> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WXR-4CK888F-6K/2/e472514da787d9365b6aeb3fc82fde16 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/33387 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6021093&dopt=citation | en_US |
dc.description.abstract | A mutually noncomplementing group of phage P22 mutants (L mutants) have been isolated which cannot accomplish a late step necessary for prophage integration. L mutants produce turbid plaques and lead to cell survival on high multiplicity infection, but the infecting phage genomes are incapable of integrating as prophage and are progressively diluted among the segregating cells. L mutants can become prophage by complementation with L+ phage. The L+ gene apparently produces a diffusible product which acts trans to accomplish integration. Experiments with temperature sensitive L mutants show that the gene begins acting late, after the infected cells have recovered and begun to divide, and does not accomplish its effect in all the cells until at least the third generation. L lysogens formed by complementation are stable. The L+ gene is thus necessary for integration but not for maintenance of the lysogenic state. | en_US |
dc.format.extent | 897644 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | A phage P22 gene controlling integration of prophage | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Human Genetics, and the Lawrence D. Buhl Research Center for Human Genetics, University of Michigan, Ann Arbor, Michigan, USA | en_US |
dc.contributor.affiliationum | Department of Human Genetics, and the Lawrence D. Buhl Research Center for Human Genetics, University of Michigan, Ann Arbor, Michigan, USA | en_US |
dc.identifier.pmid | 6021093 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/33387/1/0000786.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0042-6822(67)90164-X | en_US |
dc.identifier.source | Virology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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