TWO SEQUENTIAL REPRESSIONS OF DNA SYNTHESIS IN THE ESTABLISHMENT OF LYSOGENY BY PHAGE P22 AND ITS MUTANTS

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Abstract
The rate of DNA synthesis in complexes infected with wild type and mutants of phage P22 was followed by H3-thymidine pulse labeling. The essential features of the c+ infection, which gives high-frequency lysogeny, are (1) early onset of phage-specific DNA synthesis, continuing until the sixth minute of the infection; (2) a sharp depression in the over-all rate of DNA synthesis, both phage and host, starting at the sixth minute, reaching nearly zero rate at about the sixteenth minute; (3) recovery of host synthesis which eventually parallels the rate of uninfected control cells at about 45 min, when infected cells begin to divide and give rise to lysogenic progeny. Cells infected with c1 mutants, which give only a lytic response, fail to show the depression of synthesis at 6 min. The rate continues to increase rapidly until about 25 min when the cells begin to lyse and liberate progeny particles. On the other hand, c2-infected cells, which also give only lysis, do show the early inhibition, which is followed by a sharp rise at 16 min which greatly exceeds control rates, reaching a peak at 50 min when cell lysis starts. Mixedly infected cells, which produce high frequency of lysogeny, show a pattern of DNA synthesis similar to that of c+-infected complexes. The functions of the c1 and C2 loci are interpreted as controlling DNA synthesis during infection leading to lysogeny. The c1 locus represses phage DNA synthesis in the first few minutes of the infection, and the c2 locus maintains the repressed state after the recovery of cellular replication.