The physiological manifestation of conditional lethal mutations in the genes involved in the formation of the T4 head have been re-examined. If the product of genes 20 or 40 is defective, open-ended tubular structures (polyheads) are synthesized. Infection with mutants in gene 22 leads to the formation of polyheads, about 70% of which consist of two or more concentric layers (multilayered polyheads). Cells infected with mutants in gene 21 and 24 yield a mixed burst of capsid-like particles (τ-particles) and polyheads, many of which have hemispherical caps.

High resolution micrographs of τ-particles reveal a substructure similar to that seen on micrographs of polyheads, in contrast to normal capsids on whose surface no detail can be visualized.

Studies of the kinetics of formation of the head-related structures show that the absence or malfunctioning of a particular gene product results in an efficient use of the late phage proteins for the formation of either polyheads or τ-partieles. Furthermore, kinetic studies of multilayered polyhead formation suggest that single-layered polyheads can serve as a “core” onto which subsequent layers are added.

The minimum number of head genes whose active product is needed to form the various head-related structures has been determined by examining infection by a series of double mutants. Multilayered polyheads produced when the product of gene 22 is defective need for their assembly the active product of only two of the seven head genes studied, namely, genes 23 and 31. Single-layered polyheads, however, which are produced in cells infected either with mutants in gene 20 or 40 need, in addition to genes 23 and 31, the product of gene 22. The so-called τ-particles appear if the genes 21 and 24 are mutated either singly or together and require for their formation the functional product of all the other head genes.

These results suggest that some of the gene products have a shape-specifying role. Gene 22 is associated with the initiation process in capsid formation and genes 20 and 40 with the formation of the hemispherical cap. Genes 21 and 24 appear to determine the size and surface structure of the capsids thus rendering them susceptible to DNA integration. It is also possible that their primary function is to act as a condensing factor for phage DNA.