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dc.contributor.authorRothman, Roberten_US
dc.contributor.authorMargossian, Lindaen_US
dc.contributor.authorClark, Alvinen_US
dc.date.accessioned2006-08-22T16:24:30Zen_US
dc.date.available2006-08-22T16:24:30Zen_US
dc.date.issued1979-01en_US
dc.identifier.citationMolecular and General Genetics 169N3 (1979) 279-287en_US
dc.identifier.issn1432-1874en_US
dc.identifier.urihttp://hdl.handle.net/1850/2418en_US
dc.description.abstractW-reactivation is reduced by recF143 and recF144 mutations and is undetectable if a second mutation at either the uvrA or uvrB locus is combined with recF143. The uvrA and uvrB mutations alone block W-reactivation partially. A recL152 mutation also partially blocks W-reactivation by itself. In combination with a uvrB5 mutation, recL125 blocks W-reactivation completely but in combination with recF143, significant residual W-reactivation ability remains. We suggest that the phenomenon of W-reactivation is the result of at least two modes or pathways. The observation that recF143 uvrB5 and recF143 uvrA6 strains permit normal levels of mutagenesis (Kato et al., 1977) but completely block all W-reactivation leads us to suggest further that the mechanism(s) of W-reactivation is at least partly different from that of UV mutagenesis.en_US
dc.format.extent43151 bytesen_US
dc.format.mimetypeapplication/pdfen_US
dc.language.isoen_USen_US
dc.publisherSpringer: Molecular and General Geneticsen_US
dc.titleW-reactivation of phage lambda in recF, recL, uvrA, and uvrB mutants of E. coli K-12en_US
dc.typeArticleen_US
dc.identifier.urlhttp://dx.doi.org/10.1007/BF00382274


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