The uvrD252 mutation leads to increased UV sensitivity, diminished dimer excision and host cell reactivation capacity, and an increase in the average patch size after repair replication. A recA56 uvrD252 double mutant was far more resistant to UV than was a recA56 uvrB5 double mutant. Its host cell reactivation capacity was identical to that of uvrD252 single mutant and was far greater than that of the uvrB5 single mutant. The strain showed no Weigle reactivation. From these results, we concluded that the double mutant has no inducible DNA repair (including long-patch excision repair) but retains dimer excision capabilities comparable to the uvrD252 single mutant. It appears, therefore, that the long patches detected in the uvrD mutant were not identical to the recA-dependent patches seen in wild-type cells.

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Article may be found at: http://jb.asm.org/cgi/reprint/158/2/749 Research was supported by a faculty research fellowship and grant-in-aid from the Research Foundation of State University of New York.ISSN:1098-5530 Note: imported from RIT’s Digital Media Library running on DSpace to RIT Scholar Works in February 2014.

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Department, Program, or Center

Thomas H. Gosnell School of Life Sciences (COS)


RIT – Main Campus