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• W829138746 abstract "An effort was made to define the gene functions that are in­ volved in the multiplicity reactivation of damaged T*f phage particles. First, wild type phage were either treated with nitrous acid or ex­ posed to ultraviolet irradiation. The treated phage were used to in­ fect two populations of bacteria: one population was singly infected by the phage and is referred to as monocomplexes, the second popula­ tion was infected with an average of two or more damaged phage and is referred to as multicomplexes. When the log of the fractional survival was plotted as a function of increasing dosage it was found that the multicomplexes were inactivated less rapidly than the monocomplexes. This increased survival ability of the multicomplexes is referred to as multiplicity reactivation. Then phage carrying mutations in genes whose products had previously been shown to be needed for normal levels of genetic recombination were used. These phage mutants were defective either in gene ^7, ^6, 32, jsx or Growth of host-phage monocomplexes and multicomplexes was carried out at semi-permissive or semi-restrictive conditions. At semi-restrictive growth conditions, levels of multiplicity reactivation were substantially reduced, while under semi-permissive conditions multiplicity reactivation returned to a level closer to that of wild type. When phage were used which had mutations in genes v, 30 or Mf, multiplicity reactivation of nitrous acid damaged phage occurred at the wild type level. These results viii indicate that the same gene functions that are required for marker ex­ change are also required for multiplicity reactivation which implies that both processes occur by the same or similar recombination path­ ways. In addition, it was found that host-phage monocomplexes formed from phage that are defective in gene ^6, W? or 32 were more sensitive to nitrous acid inactivation than monocomplexes formed from wild type phage. Quantitation of this increased sensitivity revealed that about 20% of the nitrous acid induced lethal lesions remain unrepaired in the mutant monocomplexes. These results sire indicative of a postreplicative recombination repair pathway in bacteriophage Ik." @default.
• W829138746 created "2016-06-24" @default.
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• W829138746 date "1977-01-01" @default.
• W829138746 modified "2023-09-27" @default.
• W829138746 title "MULTIPLICITY REACTIVATION AND REPAIR OF LETHAL LESIONS INDUCED BY NITROUS ACID OR ULTRAVIOLET IRRADIATION IN BACTERIOPHAGE T4" @default.
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