Recombinational repair of alkylation lesions in phage T4

Abstract

Treatment of phage T4-host adsorption complexes by MNNG increased recombination between two rII markers by about three-fold. Temperature sensitive mutants defective in genes 32, 46 and 47, which cause reductions in recombination at semirestrictive temperature, proved to be substantially more sensitive to MNNG at such temperatures than wild-type phage. In addition, the recombination defective mutants xm(uvsX) and y10(y) were sensitive to MNNG than wild-type, whereas mutants defective in genes 45 and denV, which are apparently not involved in recombination, were not MNNG sensitive. These findings suggest that a recombination pathway involving the products of genes 32, 46, 47, uvsX and y is employed in repairing MNNG-induced lethal lesions. This mechanism is effective in cells infected by single phage, implying post-replication recombinational repair between daughter chromosomes. MNNG-induced lesions are subjects to multiplicity reactivation, but mutants defective in genes 46 to 47 showed the same degree of multiplicity reactivation as wild-type phage. The gene 32 and gene 47 recombination defective mutants were tested for their effects of MNNG-induced reversion of an rII marker. No reduction in induced reversion was found. Thus, it appears that the postulated recombinational repair pathway employing the products of genes 32 and 47 does not contribute substanitally to induced mutagenesis.

Damage in DNA of an infecting phage T4 shifts reproduction from asexual to sexual allowing rescue of its genes

“…In the laboratory, recombination is known to be increased by DNA damage but in these cases mating is forced by reversible K.CN poisoning or starvation. (See table 3 in Schneider, Bernstein & Bernstein, 1978, for a list of eight cases in which this was demonstrated in phage T4.) Under natural conditions, however, without starvation or simultaneous double infections, immunity strongly promotes asexual reproduction in phage T4.…”

Deoxyribonucleic acid repair in bacteriophage.

“…Phage T4-host complexes are inactivated by MNNG with single-hit kinetics (220). When a mutant defective in gene 32, 46, 47, uvsX, or y is used, single-hit inactivation is again observed, but the rate of inactivation in all cases is greater than the rate for the wild type (155). There was no initial shoulder on these MNNG inactivation curves, indicating that the repair pathway(s) coded for by these genes is not saturable, in contrast to what was found upon treatment with EMS.…”

“…The increases in recombination per lethal hit were calculated for a number of inactivating agents from data in the literature (58). These values are 15% for mp decay (186), 22% for X rays (67), 41% for EMS (88), 43% for UV irradiation (49), 140% for HNO2 (58), and 660% for MNNG (155). Presumably, these increases in recombination reflect recombinational repair which goes on during MR.…”