Phage modification of the capacity of γ-irradiated Escherichia coli to support virus growth

Abstract

The capacity of Escherichia coli to support the growth of T-even phages is more radiation resistant than it is to support the growth of T-odd phages. Since the differential effect is seen using the same irradiated cell culture, this effect must somehow be due to the characteristics of the phage. Here we have investigated the phospholipid metabolism in γ-irradiated E. coli B cells infected with T4 and T7 phage with the viewpoint that phospholipid synthesis, hence maintenance of membrane integrity, may be an essential factor in determining the capacity of cells to support phage growth. Results obtained using cells preirradiated with 100 krads show that the rate and amount of de novo phospholipid synthesis, as followed by 32P labeling, in T4-infected cells are greater than in T7-infected cells. The rate continually increases from 0–15 min after infection, whereas in the latter cells there is a shut-off of synthesis beginning at around 10 min into infection. Using similarly irradiated cells, we found the course of turnover in T4-infected cells of phospholipids, prelabeled with [ 14C]acetate prior to infection, to show a pattern opposite that in T7-infected cells. The T4-infected cells show indications of redirection of synthesis, whereas the T7-infected cells show continued degradation starting at 5 min after infection. We conclude that there is a correlation between the ability of the phage to redirect the phospholipid metabolism of the cells, which ability the T4 phage is known to have, and the capacity of the irradiated cells to support a complete cycle of infection. The threshold γ-ray dose within which the capacity of E. coli B for supporting a normal plaquing efficiency of T4 is 300 krads, whereas that capacity for T7 declines exponentially with dose. However, within this dose range, the burst size and RNA synthesis of T4-infected cells decreases exponentially with dose, while those cells still surviving capacity loss for T7 growth give roughly normal bursts of this phage. The capacity of E. coli B for T4rII growth is similar in radiation resistance to that for T4r + growth. The rate and amount of de novo phospholipid synthesis in rII-infected cells (where the cells were also irradiated with 100 krads prior to infection) are similar to those found in T4r +-infected cells for the first 10 min of infection, but thereafter diminishes in rate.