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ACTION SPECTRA FOR PHOTOREACTIVATION OF KILLING AND MUTATION TO PROTOTROPHY IN U.V.‐SENSITIVE STRAINS OF ESCHERICHIA COLI POSSESSING AND LACKING PHOTOREACTIVATING ENZYME *
Author(s) -
Kondo Sohei,
Kato Takesi
Publication year - 1966
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1966.tb05929.x
Subject(s) - photolyase , auxotrophy , pyrimidine dimer , escherichia coli , mutation , microbiology and biotechnology , strain (injury) , enzyme , chemistry , biology , dna , dna repair , genetics , stereochemistry , biochemistry , gene , anatomy
— Ultraviolet‐sensitive strains of E. coli , Hs30 ( uvr ‐ phr ‐ arg ‐ ), lacking the ability to repair ultraviolet damage in the dark ( uvr ‐ ), lacking photoreactivating‐enzyme activity ( phr ‐ ), and lacking the ability to synthesize arginine ( arg ‐ ), and H s 30–R ( uvr ‐ phr + arg ‐ ), having the same auxotrophic marker and the same high u.v.‐sensitivity, were derived, respectively, from resistant strain H/r30 ( uvr + phr ‐ urg ‐ ) and its revertant H/r30–R ( uvr + phr + urg ‐ ). H s 30 and H s 30–R have about 25 and 35 times higher sensitivity than H/r30 and H/r30–R for u.v.‐induced killing and mutation to prototrophy, respectively. Efficiency of photoreactivation (PR) of mutation in strain H s 30–R is about ten times higher than the PR efficiency in the parent strain H/r30–R at wavelengths between 3341 and 4358 Å but not that much higher at 3132 Å. On the other hand, H s 30 shows no PR at any of these wavelengths, although the parent strain H/r30 does show PR of mutation around 3341 Å., These results support the. previously described model that PR in H/r30 is an indirect effect of PR light which enhances dark repair. It is concluded that H s 30 and H s 30–R lack dark‐repair capacity for u.v.‐induced mutational damage and that the same type of photoreactivable DNA lesions as those responsible for U.V. killing, i.e. pyrimidine dimers, are the primary cause of u.v.‐induced mutation in the uvr‐ strains. PR spectra for killing in H s 30–R and mutation in H/r30–R and H/r30 were obtained and compared, and the quantitative conclusions reached are discussed in connection with the hypothesis that the same kind of lesion (pyrimidine dimer) is the primary cause of mutation in the uvr + strains as well.