Three Star Mutants of Coliphage T2
- 1 April 1958
- journal article
- research article
- Published by Microbiology Society in Journal of General Microbiology
- Vol. 18 (2), 346-363
- https://doi.org/10.1099/00221287-18-2-346
Abstract
Star mutants of coliphages produce irregularly-shaped plaques which harbor mixed phage clones consisting of two or more phage genotypes: one type, which again forms star plaques, and other types which form genetically-homogeneous plaques. The morphology and genetic heterogeneity of star plaques is due to the appearance and selection of secondary mutants with growth properties superior to those of the star mutant. The genetic structure of three star mutants of coliphage T2 and of the secondary mutants was examined. (1) The "bromouracil" star mutant s8 owes its star character to a single mutation at a locus s8 which is not closely linked to any known genetic marker of coliphage T2. The secondary mutants found in every plaque of s8, harbor reverse mutations to s8+ wild-type. (2) The "extended-host-range" star mutant h'' owes its star character to the h'' allele of the host range locus h. The secondary mutants have suppressor mutations at locus il closely linked to h. These suppressor mutations abolish only the star effect of the h'' allele without affecting the extended-host-range conferred by h''. (3) The "p32-decay" star mutant hrs harbors a mutation rs which extends over a considerable sector of the T2 genome situated between the distantly linked loci r7 and r1. The star phenotype of this mutant derives from an interaction between the host-range locus h and the rs mutation so that some states of the host range locus confer poor plaque development if present in conjunction with rs. The secondary mutants found in plaques of hrs harbor one of a set of non-allelic h+ or ht mutations in the h locus, which abolish the plaque inhibiting interaction of h with the rs mutation, and which also affect the host range. It is possible to replace variable sectors of the rs mutation proximal to r7 with their r+ alleles by crosses of hrs to wild-type.Keywords
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