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J Virol. 1970 December; 6(6): 727-737
Copyright © 1970 American Society for Microbiology. All Rights Reserved.

Synthesis of Messenger Ribonucleic Acid After Bacteriophage T1 Infection ¹

Department of Microbiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14620

ABSTRACT

Synthesis of host-specific and phage-specific messenger ribonucleic acid (mRNA) was studied in bacteria infected by unmodified (T1 · B) or modified [T1 · B(P1)] bacteriophage T1. In a "standard" infection of Escherichia coli B by T1 · B (no host-controlled modification involved), the rate and amount of T1 mRNA synthesis was intermediate between those values reported for infections by a virulent phage such as T4 or a temperate phage such as lambda. The initial rate of mRNA synthesis was slightly increased after T1 · B(P1) infection of E. coli B in comparison with T1 · B infection of the same host. Little or no phage mRNA synthesis could be detected in T1 · B infection of E. coli B(P1). Phage mRNA synthesis in T1 · B(P1)-infected E. coli B(P1) cells was approximately the same in amount as that seen in T1 · B(P1) infection of E. coli B. Synthesis of host-specific mRNA continued throughout the latent period in all infections studied. However, the enzyme ß-galactosidase could not be induced, except after T1 · B infection of E. coli B(P1). In an attempt to understand the apparent differences in mRNA synthesis after infection of E. coli B by phages T1 · B or T1 · B(P1), the effect of altered T1 deoxyribonucleic acid (DNA) methylation on mRNA synthesis was studied. Methyl-deficient T1 DNA, made in cells infected with ultraviolet-irradiated phage T3, inhibited ¹⁴C-uridine incorporation more strongly than normal T1. One passage of methyl-deficient T1 through E. coli B restored uracil incorporation rates to those seen with ordinary T1. This suggests that methylation of T1 DNA can influence the rate of phage mRNA synthesis. However, attempts to relate the difference in mRNA synthesis seen between T1 · B and T1 · B(P1) in E. coli B to the activity of the P1 modification gene were not conclusive.

² U.S. Public Health Service postdoctoral fellow. Present address: Department of Microbiology, University of Colorado Medical Center, Denver, Colo. 80220.

¹ Part of this paper is based on a Ph.D. Thesis submitted by C. J. M. to the University of Rochester. A preliminary report was presented at the Annual Meeting of the American Society for Microbiology, and appeared in Bacteriological Proceedings (1967).