Bacteriophage T4 bypass31 mutations that make gene 31 nonessential for bacteriophage T4 replication: mapping bypass31 mutations by UV rescue experiments

Abstract

The product of gene 31 is normally required for assembly of the T4 capsid. Two mutations that each bypass that requirement are shown to be located at separate sites in gene 23, which encodes the major structural protein of the capsid. A second phenotypic effect that characterizes both bypass3l mutant strains is the ability to multiply in host-defective strains, such as hdB3-1 and groEL mutants, on which wild-type T4 is unable to assemble capsids. The genetic data indicate that both phenotypic effects are due to the bypass3l mutation. Elimination of the requirement for both the phage protein, gp3l, and the host protein, GroEL, by either of two single mutations in gene 23 indicates that GroEL and gp3l are normally needed to interact with gp23 in capsid assembly of wild-type T4.

Bacteriophage T4 bypass31 mutations that make gene 31 nonessential for bacteriophage T4 replication: isolation and characterization

“…This function probably promotes a specific type of association among gp23 molecules. The fact that byp3l mutations are located in T4 gene 23, as shown in the accompanying paper (8), indicates that conformational changes in gp23 can lead to interactions among gp23 molecules similar to those promoted by the gp3l-gpGroEL complex.…”

“…as discussed in the accompanying paper (8), that a single mutation results in both of the byp3l phenotypes-the ability to assemble capsids in the absence of gp3l and the ability to assemble capsids in host-defective groEL mutants-lead us to suggest that gp3l and gpGroEL together perform a single function essential for T4+ capsid assembly. This function probably promotes a specific type of association among gp23 molecules.…”