Recombineering, the use of endogenous homologous recombination systems to recombine DNA in vivo, is a commonly used technique for genome editing in microbes. Recombineering has not yet been developed for animals, where non-homology-based mechanisms are thought to dominate DNA repair. Here, we demonstrate that in C. elegans, linear DNAs with micro-homologies (35 bases) participate in a robust local gene conversion mechanism that can be exploited for recombineering. We find that double-stranded PCR amplicons and bridging single-stranded oligonucleotides (ssODNs) recombine readily to form novel DNA assemblies in vivo that can repair double-strand breaks induced by CRISPR/Cas9 on chromosomes. We use this method to create precise GFP knock-in alleles using a universal linear GFP template and two gene-specific “bridge” ssODNs linking GFP to the Cas9 cleavage site. In vivo assembly can also be used to assemble novel knock-in fusions and gene replacements, and is efficient enough for use without selection (scarless edits). Our findings are consistent with the budding yeast models for synthesis-dependent strand annealing and template switching during repair-induced DNA replication. We conclude that, like microbes, metazoans possess robust homology-dependent repair mechanisms that can be harnessed for recombineering and genome editing.