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A MUTANT OF ESCHERZCHZA COLI K12 EXHIBITING VARYING ULTRAVIOLET SENSITIVITIES DEPENDING ON THE TEMPERATURE OF INCUBATION AFTER IRRADIATION *
Author(s) -
SUZUKI KENSHl,
SAlTO ETSUKO,
MORIMYO MlTSUOKl
Publication year - 1969
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.1751-1097.1969.tb07290.x
Subject(s) - lysogenic cycle , mutant , bacteria , incubation , chloramphenicol , prophage , bacteriophage , irradiation , escherichia coli , ultraviolet light , microbiology and biotechnology , chemistry , biology , biochemistry , genetics , gene , photochemistry , nuclear physics , physics
— A mutant, URT‐43, was isolated from E. coli C600 dar + . The mutant has a characteristic feature in that its sensitivity to ultraviolet (u.v.) light is greatly influenced by the temperature at which irradiated bacteria are incubated. On the basis of dose‐reduction factor, URT‐43 is approximately ten times more sensitive at 42° than at 30°C, even though unirradiated bacteria are not thenno‐sensitive, The mutant could not repair u.v.‐irradiated bacteriophage Λ vir in the dark either at 30° or at 42°C, indicating that it is defective in host‐cell reactivation. In contrast, the same bacteriophage was reactivated in preirradiated URT‐43 if the host‐bacteriophage complex was plated at 30° but there was no reactivation at 42°C. Therefore u.v.reactivation was positive at 30° but negative at 42°C. The induction of prophage by URT‐43(Λ h ) was achieved by much lower doses of U.V. light than that required for the induction of lysogenic wild type bacteria. Experiments were performed in which irradiated URT‐43 was first incubated for various periods in liquid media and plated both at 30° and 42°C. It was found that irradiated bacteria came to be resistant to subsequent plating at 42° only when they were preincubated in the liquid medium containing necessary amino acids and at 30°C. Since this phenomenon was completely inhibited by chloramphenicol, the process seemed to require de novo protein synthesis. An hypothesis was proposed that there are at least two independent dark‐repair mechanisms in E. coli; one is responsible for host‐cell reactivation and the other is responsible for U.V. reactivation.