Effects of radiophosphorus decay in bacteriophage T4D. II. The mechanism of marker rescue

When bacteriophage T4D is inactivated by decay of incorporated 32P, about 40 percent of the phage lethal hits (PLH) completely destroy the ability of the damaged phage to contribute genes to the progeny of a mixed infection with a genetically distinct and viable helper phage. The other 60 percent of the PLH inactivate some but not all of the phage genome. The inactivated portions, or knockouts, vary from less than 5 percent to more than 95 percent of the genome in size. Not all portions of the genome are equally sensitive to 32P decay. The topography of marker rescue from 32P-damaged phage is similar to that previously observed for ultraviolet-irradiated T4. This topography cannot result from the initial distribution of lethal damages (double-strand breaks), since these are produced at random positions by 32P decay. It is shown that the topography of rescue also does not result from preferential injection of the regions of high rescue, nor is it due to high recombination frequencies in these regions. Other models that can explain the rescue topography are presented