Abstract

Temperature-sensitive and amber mutations in T4 gene 49 were suppressed by a second mutation at either of two different loci on the T4 genome. We call these loci fdsA and fdsB. From a series of two and three factor crosses with amber mutations in known genes, fdsA was located between genes 41 and 42, and fdsB between genes 24 and 25. Phage mutated at both suppressor loci complemented their neighboring genes and, hence, are not likely to be mutant in those genes. The suppressor mutations occurred at a frequency two to three orders of magnitude greater than the reversion frequency of most amber mutants. Complementation results indicated that fds + was partially dominant over fds (both A and B). Also, fdsA appeared defective in the synthesis of an early protein, and synthesized a new protein of a lower molecular weight. From these observations it appeared that the mutations resulting in 49-suppression caused the partial or complete inactivation of a gene product. Both suppressors either in the presence or absence of the 49-mutation displayed an arrest in the rate of DNA synthesis 15–20 min after infection. The expression of late phage functions appeared to be necessary for this turnoff of DNA synthesis. This DNA-arrest phenotype helps explain the small burst size of phage carrying the suppressors. In addition, the suppressors were found to be as sensitive to ultraviolet irradiation as phage isolated for such sensitivity.

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