Multiple mutant strains have been tested for their mimicry of the UV-mutagenesis deficiency of a recA single mutant. Revertants to histidine prototrophy and clear plaque mutants of lambda were scored to determine capacity for UV-mutagenesis. Nearly normal capacity was shown by a uvr+ recB- recF - strain, which shows almost no recA-dependent recombination, by uvr- recB+ recF - strains, which show almost no recA-dependent repair and by a uvrA- recB- recF- strain, which shows neither recA-dependent recombination nor repair. Since the uvr mutants can be assumed to show additionally no excision repair, these results may mean that UV-mutagenesis occurs during processes other than recombination and repair. Alternative hypotheses are discussed. The slight difference in mutagenic capacity was traced to the recF single mutation, which blocks the production of unmixed bursts of clear-plaque lambda mutants. Since this accounts for only about 10% of the mutations leading to clear-plaque mutants, it is suggested that there is more than one UV-mutagenic process.

Publication Date



Article may be found at: http://www.genetics.org/cgi/reprint/87/1/1 ROBERT H. ROTHMAN was a predoctoral trainee supported by Public Health Service Predoctoral Training Grant 5T01-GM00367-14. This research was supported by Public Health Service Research Grant AI 05371 from the National Institute of Allergy and Infectious Diseases.ISSN:0016-6731 Note: imported from RIT’s Digital Media Library running on DSpace to RIT Scholar Works in February 2014.

Document Type


Department, Program, or Center

Thomas H. Gosnell School of Life Sciences (COS)


RIT – Main Campus