Excision Repair Characteristics of recB − res − and uvrC − Strains of Escherichia coli
Author(s) -
Takesi Kato
Publication year - 1972
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.112.3.1237-1246.1972
Subject(s) - pyrimidine dimer , escherichia coli , recbcd , biology , dna , strain (injury) , microbiology and biotechnology , mutant , incubation , photolyase , irradiation , centrifugation , dna damage , dna repair , biochemistry , anatomy , gene , physics , nuclear physics
AnEscherichia coli strain carrying therecB21 andres-1 mutations showed an abnormally low level of colony-forming ability although it grew essentially normally in liquid medium. TherecB21 res-1 strain showed little, if any, of the ultraviolet (UV)-induced deoxyribonucleic acid (DNA) breakdown characteristic of theres-1 mutant. Nevertheless, the double mutant was far more sensitive to UV than either theres-1 or therecB21 strain. When compared with a wild-type strain, the rate of release of dimers from UV-irradiated DNA was very slow in therecB21 res-1 , but normal in theres-1 recB + orrecB21 res + mutants. However, the ratio of dimer-to-thymine released into the acid-soluble fraction was three times higher than the wild type inrecB21 res + andrecB21 res-1 and only one-tenth as high as the wild type inres-1 rec + . Alkaline sucrose gradient centrifugation revealed occurrence of single-strand incision of UV-irradiated DNA and the restitution of nicked DNA at a similar rate in therecB21 res-1 andrecB21 res + strains. MutantsuvrC − showed increased amounts of nicks in their DNA with increasing incubation time after UV irradiation, although no detectable amounts of dimers were excised from UV-irradiated DNA. From these results, it is concluded that the increased sensitivity of theres-1 strain to UV light is due to a reduced ability to excise dimers from UV-irradiated DNA and that the high rate of UV-induced breakdown of DNA is not the primary cause. A possible role ofuvrC gene in the excision repair is discussed.
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