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dc.contributor.advisorRothman, Robert H.
dc.contributor.authorFried, Barry
dc.date.accessioned2021-09-07T21:02:42Z
dc.date.available2021-09-07T21:02:42Z
dc.date.issued6/1/1982
dc.identifier.urihttp://hdl.handle.net/20.500.12648/4497
dc.description.abstractWild-type strains of E. coli possess both short and long patch repair mechanisms to correct UV-induced pyrimidine dimers. Short patch repair is the predominant mode, and long patch repair is recA+ -dependent, requires de novo protein synthesis, and is UV-inducible. Excision repair in a recI.152 mutant is characterized by slow dimer excision and the exhibition of primarily large patches. Residual excision repair in the recI.152 mutant was studied by introducing a recA.56 mutation into the recI.152 strain. Analysis of cell survival, host-cell reactivation, Weigle-reactivation, and the rate of dimer release in both the recL152 single mutant and the recA56 recL152 double mutant reveals that residual excision repair detected in the recL152 strain is recA+ -independent and non-inducible. These data indicate that long patch repair replication in the recL152 mutant is not the same as the long patches seen in wild-type cells, and possibly represents altered regulation of the more important short patch system.
dc.subjectWild-Type Strains
dc.subjectPyrimidine Dimers
dc.subjectPatch Repair
dc.subjectCell Reactivation
dc.subjectWeigle-Reactivation
dc.titlerecA-Independence of Residual Dimer Excision in a recI.152 Mutant of Esherichia C01.1 K-12
dc.typethesis
refterms.dateFOA2021-09-07T21:02:42Z
dc.description.institutionSUNY Brockport
dc.description.departmentBiological Sciences
dc.description.degreelevelMaster of Science (MS)
dc.source.statuspublished
dc.description.publicationtitleBiology Master’s Theses
dc.contributor.organizationThe College at Brockport
dc.languate.isoen_US


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