Summary
The clearish plaque mutants λvirC which were isolated from λ true-virulent, λvirLvirCvirR (λvirLCR), do not complement CI mutants but CII, CIII and λ mutant (λc 42) for lysogenization. No complementation for lysogenization was observed between λvirCR and any CI, CII, CIII or y mutants. No lysogen was obtained when λvirC or λvirC carrying susN, susO or susP was infected to λ-sensitive sup - host. This was also true for λvirCR. Infection of λind - lysogen with λvirCRsusNO(P) or λvirCsusNO(P) results in marked prophage induction. Effect of λvirCRsusNO(P) on prophage induction is stronger than that of λvirCsusNO(P). These results suggest the existence of gene(s) for anti-repressor. When λvirCsusNO(P) or λvirCRsusNO(P) was infected to W3350 sup - at high m.o.i., lysogen in anti-immune state and that in weak-immune state was obtained, respetively. Wild type λ phage forms clear plaque on λvirCsusNO(P) lysogen with e.o.p. of one and no plaque on λvirCRsusNO(P) lysogen. T4rII can plate on both lysogens. This weak-immunity caused by λvirCRsusNO(P) prophage is different from CI immunity and not abolished by irradiation of ultraviolet light (hereafter this is referred to as the vir-immunity). Action of anti-immunity and vir-immunity are almost λ specific. Possible functional sites for anti-and vir-immunity substances are suggested to be virL and virR regions. A hypothesis was presented that the vir-immunity may caused by the overproduced anti-immunity substance coded from x region.
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Communicated by H. Ozeki
This material has been published as an abstract in Jap. J. Genetics 45, 479 (1970).
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Koga, H., Horiuchi, T. Studies on lambda virulent mutants. Molec. Gen. Genet. 124, 219–232 (1973). https://doi.org/10.1007/BF00293093
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DOI: https://doi.org/10.1007/BF00293093