Yeast transformation is a model system for studying recombination. DNA molecules that integrate into yeast chromosomes during transformation do so through homologous recombination. Circular and linear DNA molecules recombine with homologous chromosomal sequences, with DNA ends being highly recombinogenic and interacting directly with homologous sequences. Circular hybrid plasmids integrate via a single reciprocal crossover but at low frequency. Restriction enzyme digestion within a homologous region enhances integration efficiency. Deleted-linear molecules can still transform at high frequency, and their integration replaces the missing segment using chromosomal information. Integration of linear and gapped-linear molecules, but not circular molecules, is blocked by the rad52-1 mutation. RAD52 is likely involved in DNA repair synthesis required for these processes. Transformation of yeast with defined DNA sequences provides a powerful approach to study recombination. Plasmid integration occurs via homologous recombination. The Meselson-Radding model suggests that recombination begins with a nick on one molecule, followed by repair synthesis and displacement of the nicked strand to promote heteroduplex formation. Experiments show that DNA ends are highly recombinogenic and interact directly with homologous sequences. Double-stranded gaps in linear molecules are repaired during integration. The rad52-1 mutation blocks linear but not circular molecule integration. RAD52 may be involved in DNA repair synthesis necessary for linear plasmid integration, double-strand break repair, and gene conversion. The integration of linear and gapped-linear molecules is blocked by the rad52-1 mutation, suggesting that RAD52 is involved in DNA repair synthesis. The integration of gapped-linear molecules results in replacement of the missing segment using chromosomal information. The structure of integrated transformants from linear and circular molecules is identical. The integration of gapped-linear molecules is always accompanied by repair of the missing information using chromosomal information as a template. The integration of linear plasmids cut within homologous yeast DNA sequences is analogous to double-strand break repair, a process requiring RAD52. The integration of circular plasmids occurs via a different mechanism, as RAD52 is not required for circular molecule integration. The model for circular plasmid integration involves strand invasion from a nick on either chromosomal or plasmid DNA. The integration of linear plasmids requires the break to be within a sequence homologous to chromosomal DNA. The model for linear plasmid integration is formally equivalent to Resnick's model for double-strand break repair. The results have practical applications in the isolation of integrated derivatives of autonomously replicating plasmids, cloning of mutant alleles, and fine-structure genetic mapping. The repair of gapped plasmids from chromosomal information facilitates the cloning of mutant alleles. Transformation with gapped plasmids is useful for fine-structure genetic mapping. The integration of complex plasmids at specific chromosomal loci can be targeted by restriction enzyme digestionYeast transformation is a model system for studying recombination. DNA molecules that integrate into yeast chromosomes during transformation do so through homologous recombination. Circular and linear DNA molecules recombine with homologous chromosomal sequences, with DNA ends being highly recombinogenic and interacting directly with homologous sequences. Circular hybrid plasmids integrate via a single reciprocal crossover but at low frequency. Restriction enzyme digestion within a homologous region enhances integration efficiency. Deleted-linear molecules can still transform at high frequency, and their integration replaces the missing segment using chromosomal information. Integration of linear and gapped-linear molecules, but not circular molecules, is blocked by the rad52-1 mutation. RAD52 is likely involved in DNA repair synthesis required for these processes. Transformation of yeast with defined DNA sequences provides a powerful approach to study recombination. Plasmid integration occurs via homologous recombination. The Meselson-Radding model suggests that recombination begins with a nick on one molecule, followed by repair synthesis and displacement of the nicked strand to promote heteroduplex formation. Experiments show that DNA ends are highly recombinogenic and interact directly with homologous sequences. Double-stranded gaps in linear molecules are repaired during integration. The rad52-1 mutation blocks linear but not circular molecule integration. RAD52 may be involved in DNA repair synthesis necessary for linear plasmid integration, double-strand break repair, and gene conversion. The integration of linear and gapped-linear molecules is blocked by the rad52-1 mutation, suggesting that RAD52 is involved in DNA repair synthesis. The integration of gapped-linear molecules results in replacement of the missing segment using chromosomal information. The structure of integrated transformants from linear and circular molecules is identical. The integration of gapped-linear molecules is always accompanied by repair of the missing information using chromosomal information as a template. The integration of linear plasmids cut within homologous yeast DNA sequences is analogous to double-strand break repair, a process requiring RAD52. The integration of circular plasmids occurs via a different mechanism, as RAD52 is not required for circular molecule integration. The model for circular plasmid integration involves strand invasion from a nick on either chromosomal or plasmid DNA. The integration of linear plasmids requires the break to be within a sequence homologous to chromosomal DNA. The model for linear plasmid integration is formally equivalent to Resnick's model for double-strand break repair. The results have practical applications in the isolation of integrated derivatives of autonomously replicating plasmids, cloning of mutant alleles, and fine-structure genetic mapping. The repair of gapped plasmids from chromosomal information facilitates the cloning of mutant alleles. Transformation with gapped plasmids is useful for fine-structure genetic mapping. The integration of complex plasmids at specific chromosomal loci can be targeted by restriction enzyme digestion