Summary
The effects were studied of three clear plaque mutations of phage P22 (cir4-1, cir5-1 and cir6-1) on antirepressor synthesis. The mutant site cir4-1 has no influence on the expression of gene ant. The cir5-1 and cir6-1 mutations prevent the repression of early ant synthesis shortly after infection: P22 cir5-1 exhibits a strong ant-overproduction because it renders the cir5 repressor protein defective for turning off early ant expression (Harvey et al. 1981). P22 cir6-1 exhibits only a low level of constitutive ant synthesis insensitive to cir5-directed repression. Complementation experiments between P22 wild type or mutant in the cir5 or cir6 sites reveal the following phenotypes of the cir6-1 mutation: (1) The cir6-1 site behaves as a weak promotor site insensitive to cir5-directed repression of ant synthesis. (2) In the P22 cir5-1 cir6-1 double recombinant the cir6-1 site is cis dominant preventing ant overproduction as observed in simple P22 cir5-1 infections. (3) Some of the deficient phenotypes of P22 cir6-1 can be complemented by co-infecting P22 mutants carrying a cir6 + allele. These results are explained by the following model: The active cir5 repressor protein is a dimer (or oligomer) and the cir5-1 and cir6-1 mutations map in different domains influencing the repressing as well as the dimer forming activities of this protein. Which particular cir6-1 phenotype is observed depends on the experimental conditions employed, and on the promotor site (either p ANT or cir6-1) from which ant expression procedes. P22 cir5-1 antam19 in su -bacteria does not produce any traceable amount of ant amber protein fragments, and an antam19 allele in trans to ant + restrains synthesis of ant protein.
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Prell, H.H., Auer, J. & Soška, J. The immI region of Salmonella phage P22. Molec Gen Genet 198, 110–115 (1984). https://doi.org/10.1007/BF00328709
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DOI: https://doi.org/10.1007/BF00328709