Most genetic characteristics of T4 recombination (the effects of chromosomal termini on recombination, heterozygosity, high negative interference, base mismatch repair, polarized segregation, and the stimulation or depression of recombination in response to phage mutations or external perturbations) can be expressed adequately in terms of our present understanding of the molecular events of T4 infection cycles. T4 DNA replication begins and ends with linear chromosomes and does not require a circular intermediate. Replication is bi-directional, possibly from multiple origins. Two phases of replication are distinguishable: (a) an early mode during which about 20 progeny copies of infecting chromosomes are made prior to (b) a recombination-dependent mode during which progeny molecules associate to form covalently joined linear concatemers. Further replication is generally arrested if concatemerization is prevented. T4 DNA recombination depends on the production of single-stranded gaps and termini. If replication is inhibited, the single-stranded regions are produced by deoxyribonuclease activities. In contrast, during partial replication of damaged chromosomes, during slow replication when enzymes or subtrates are limited, and during normal replication, they are formed by strand-displacement DNA polymerization. As a rule, any agents or perturbations that cause an accumulation of single-stranded regions stimulate recombination, whereas efficient repair of such regions depresses it. Both the preservation and pairing of single-stranded regions are facilitated by the gene-32 single-stranded DNA binding protein. Covalent repair of strand interruptions between recombined DNA segments requires polymerases or nucleases as well as ligases.