General genetic recombination in bacteriophage T4 : DNA exchange, DNA- protein-protein interactions

Abstract

We will discuss current models of genetic recombination emphasizing their general aspects and the specific points which have been demonstrated in phage T4. Recombination in this phage occurs preferentially (although not exclusively) near chromosomal ends. It depends on single-stranded regions (which are formed either by partial degradation or by partial synthesis). DNA replication stimulates recombination in T4 mainly because it generates single-stranded termini in partially replicated chromosomes. Such single-stranded termini invade homologous regions of duplex molecules, thereby generating recombinational forks. These forks can be resolved to yield insertion-type or crossover-type recombinants. Alternatively, they can be reconverted to replication forks. Thus, no clear-cut distinction between replicative or recombinational forks can be made. Because the T4 chromosomes are circularly permuted, growing points reach ends and recombinational forks accumulate soon after the onset of DNA replication. The invading single-strands generate a network of DNA whose complexity increases with increasing numbers of infecting particles and with time after infection. The conversion of these forks to replication forks rapidly accelerates overall DNA synthesis in viral infected cells. The networks are finally resolved during maturation. The interconversion of recombinational and replication forks is facilitated by the multiple roles of several proteins in replication and recombination. Activities of these proteins in both processes are modulated by specific interactions with the T4 gene-32 protein. This protein, which presumably coats all intracellular single-stranded DNA regions provides an ordering principle for the coordinated action, in time and space, of the other proteins acting on DNA. Additional stabilization of these interactions occurs by the interaction of these proteins with membrane components.