Experiments with a mutant of T4, tsL97, temperature sensitive for gene 43, showed that T4 DNA polymerase was necessary in vivo to repair gaps in recombinant molecules. CsCl density gradient experiments showed that molecular recombinants were not repaired when the T4tsL97-infected cells were shifted to 42 C after replication and recombination had taken place. Repair was almost complete when the same procedure was followed with the wild-type T4, or when the T4tsL97-infected cells were incubated at the permissive temperature, 36 C. Long-single-strand production was also affected similarly by the T4tsL97 mutation. All the results were consistent with the theory that gaps exist in many recombinant molecules at the recombinant joint, that T4 DNA polymerase is the enzyme that repairs these gaps in vivo, and that covalent repair of the recombinants leads to extensive long-single-strand production.