We have investigated the in vivo roles of T4 gene- 32 protein in recombination. We have studied the effects of gene- 32 mutations under conditions that allow normal DNA replication and are permissive for progeny production. Under these conditions, certain gene- 32 mutations specifically reduce insertion-type (short-interval) recombination but none affect crossover-type (long-interval) recombination (see Figure 5). Heterozygote frequencies in all gene-32 mutants are similar to or higher than in a gene-32+ background and are not correlated with recombination deficiencies. "Recombination-deficient" alleles are dominant or codominant over the "recombination-proficient" gene-32 mutation tsL171. This explains apparent discrepancies between a gene-32 map deduced from two-factor crosses and the map derived from three-factor crosses.