Abstract
The protein products of at least 21 phage genes are needed for the formation of the tail of bacteriophage T4. Cells infected with amber mutants defective in these genes are blocked in the assembly process. By characterizing the intermediate structures and unassembled proteins accumulating in mutant‐infected cells, we have been able to delineate most of the gene‐controlled steps in tail assembly. Both the organized structures and unassembled proteins serve as precursors for in vitro tail assembly.
We review here studies on the initiation, polymerization, and termination of the tail tube and contractile sheath and the genetic control of these processes. These studies make clear the importance of the baseplate; if baseplate formation is blocked (by mutation) the tube and sheath subunits remain essentially unaggregated, in the form of soluble subunits.
Seventeen of the 21 tail genes specify proteins involved in baseplate assembly. The genes map contiguously in two separate clusters, one of nine genes and the other of eight genes. Recent studies show that the hexagonal baseplate is the end‐product of two independent subassembly pathways. The proteins of the first gene cluster interact to form a structure which probably represents one‐sixth of the outer radius. The products of the other gene cluster interact to form the central part of the baseplate.
Most of the phage tail precursor proteins appear to be synthesized in a non‐aggregating form; they are converted to a reactive form upon incorporation into preformed substrate complexes, without proteolytic cleavage. Thus reactive sites are limited to growing structures.