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CCORDING to the theory proposed by BARRICELLI (1956, 1960), multiplicity A reactivation of bacteriophage takes place to a large extent (see below) through recombinations that permit the replacement of damaged genetic material by undamaged homologous segments contributed by the other phages present. This would require an increase of recombination frequency, at least if the normal recombination rate is insufficient for multiplicity reactivation (m) . A stimulation of recombination in multiplicity reactivated complexes is therefore expected according to this theory. ‘To illustrate this, we consider the two irradiated ( h phage lethal hits) homologous phage genomes present in a doubly infected bacterium. Let us start at some point in one of the genomes and follow the two genomes in one direction (Figure 1 ) . When we arrive at a locus which is damaged in one of the two genomes, there is a 50% probability that the damage will be in the genome of the phage we are following, and a 50% probability that it will be in the genome of the other phage present. If it is in the genome of the phage we are following a crossover will be required in order to circumvent the damage and make an intact genome. Since

STIMULATION OF RECOMBINATION IN MULTIPLICITY-REACTIVATED BICOMPLEXES AND THE GENETIC MAP LENGTH OF PHAGE T4