The effects of P32 disintegration in the Hfr donor cell on the genetic recombination of Escherichia coli K 12 have been studied. The dose-response relationship for the transfer of markers at a distance x from the chromosomal origin, N/N0 = e−αxD, which summarizes the findings of Fuerst et al. (1956) for early markers of Hfr H, has been found to hold true to a good approximation for more distal selected markers in this strain, as well as for selected markers of Hfr CS, which transfers its chromosome in the opposite direction. The inheritance by recombinants of non-selected male markers located between the origin and the selected marker is not affected at all by prior P32 dose to the Hfr. The sensitivity of each Hfr strain studied to the lethal effects of P32 decay corresponds to the sensitivity to transfer effects of a male marker located about one-third of the total chromosomal length away from the origin. Genetic and lethal effects in Hfr H showed the same dependence on storage temperature during P32 decay. Our data, therefore, supports the concept of a common origin for the lethal and genetic effects of P32 decay.

The quantitative predictions of current models for chromosome transfer with regard to radiation mating experiments have been examined. A simple model, involving no DNA synthesis, as well as the replicon model of Jacob et al. (1963) predict exponential marker inactivation curves of the kind found experimentally. The model of Bouck & Adelberg (1963) predicts a more complex dose dependence, but one not nearly so different from that of the other two models as was anticipated by Jacob et al. It appears unjustified to attempt to exclude any of the three models on the basis of presently available data from radiation mating experiments.