Abstract
It was discovered that the mutation in the rII region of phage T4 have a characteristic in common which sets them apart from the mutations in all other parts of the map. This characteristic is a host-range reduction, namely, a failure to produce plaques on a host (K) lysogenic for phage A. The mutant phage particles adsorb to and kill K, but normal lysis and phage release do not occur. All mutants with this property are located within a sharply defined portion of the phage linkage map. Within that region, however, their locations are widely scattered. An unambiguous seriation of the mutants, with roughly additive distances, can be accomplished, except for certain anomalous cases. The simultaneous presence of a wild-type phage particle in K enables the multiplication of rII mutants to proceed, apparently by supplying a function in which the mutant is deficient. A heterozygous diploid in the trans configuration is simulated by a mixed infection of K with 2 mutant types. The application of the phenotype test to pairs of rII mutants leads to the division of the region into 2 functionally separable segments. Spontaneous reversion to wild-type had been observed for most of these mutants. It remains to be seen whether these are genuine reversions. Each mutant reverts at a characteristic rate, but the rates for different mutants differ enormously. Partial reversions to intermediate types are also observed. The mutants differ greatly in degree of residual ability to grow on K. There is no evident correlation between map position, reversion rate, and degree of residual activity of the various mutants. The selective feature of K for wild-type re-combinants offers the possibility of extending the recombina-. tion studies to an analysis of the fine details of the region. Preliminary studies of this type indicate that the units of recombination are not larger than the order of one dozen nucle-otide pairs and that mutations may involve various lengths of chromosome.

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