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Three Star Mutants of Coliphage T2
Abstract
SUMMARY: Star mutants of coliphages produce irregularly-shaped plaques which harbour mixed phage clones consisting of two or more phage genotypes: one type which forms star plaques identical in morphology and genetic constitution to those of the primary star mutant and other types which form regular genetically-homo-geneous plaques. The peculiar morphology and genetic heterogeneity of star plaques is due to the appearance and subsequent selection in every such plaque of secondary mutants with growth properties superior to those of the primary star mutant. In the present work, the genetic structure of three such primary star mutants of coliphage T2 and of the secondary, regular mutants which they sport has been examined. The ‘bromouracil’ star mutant s 8 owes its star character to a single mutation at a locus s 8, which is not closely linked to any known genetic marker of coliphage T2. The secondary, regular mutants found in every plaque of s 8 harbour reverse mutations to s 8 + wild-type at the mutated star locus itself. The ‘extended-host-range’ star mutant h′ owes its star character to the h′ allele of the host range locus h. The secondary, regular mutants found in every plaque of h′ harbour suppressor mutations to h′ at a definite locus i 1 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′ upon the coliphage T2. The ‘P32-decay’ star mutant hrs harbours a mutation rs which extends over a considerable sector of the T2 genome situated between the distantly linked loci r 7 and r 1. The star phenotype of this mutant derives from an interaction between the host-range locus h and the rs mutation so that some genetic states of the host range locus confer poor plaque development on phage particles in which they exist in conjunction with rs . The secondary, regular mutants found in every plaque of hrs harbour one of a set of non-allelic h + or ht mutations in the h locus, which abolish the plaque growth-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 r 7 with their r + alleles by crosses of hrs to wild-type. One may suppose that star mutants should be encountered with all those plaque-forming virus types which can sport with sufficiently high probability, i.e. soon enough during the development of each plaque, secondary mutants of growth characteristics superior to those of the parent type.
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© Society for General Microbiology, 1958