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When a protein involved in DNA repair malfunctions, it can anneal RNA molecules to DNA molecules, creating hybrids that increase the frequency of mutations in the DNA.

Biochemical and genetic approaches uncover a chromatin remodeler for PRDM9 binding and the parallel local epigenetic modification of cytosines in mouse spermatocytes.

The LIN37-DREAM complex has a critical role in regulating DNA double-strand break end processing and suppressing aberrant homology-directed repair in quiescent cells.

The meiotic DNA recombination landscape is locally influenced by the kinetochore to minimize potentially deleterious pericentromeric crossover recombination.

The discovery of a mechanism that causes DNA deletions during non-canonical DNA replication termination is described.

Unloading the polymerase sliding clamp PCNA from DNA by Elg1 promotes recombination at the RTS1 replication fork barrier by limiting Fbh1 and Srs2 activity.

Genomic deletions and gene conversions, caused by template switching associated with restarted DNA replication, are detected downstream of a collapsed replication fork and are suppressed by several conserved DNA helicases.

D-loops are critical intermediates in homologous recombination, and the novel D-loop mapping assay defines position, length, and distribution of D-loops with near base-pair resolution.

Recombinant mitochondrial genomes can be selected, traits can be genetically mapped and new genetic combinations can be made.

Homologous recombination is the default response to replication impedance by the RTS1 barrier, leading to restarted replication forks that suffer frequent collapse, triggering further rounds of recombination downstream of the barrier.