Mer2 interacts directly with meiotic chromatin, axial proteins, and the DNA break forming machinery to facilitate the formation of meiotic double-strand breaks.

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

Genetic analysis combined with whole genome sequencing elucidates mechanisms and pathways that form and prevent a specific class of genome rearrangements, foldback inversions, seen in many human cancers.

The human genome is unpackaged to allow DNA breaks to be joined back together, and then repackaged into chromosomes afterwards.

Genome-wide mapping of heteroduplex DNA (a recombination intermediate) formed during mitotic recombination in yeast demonstrates that the "classical" model of double-strand DNA break repair is inadequate to explain several aspects of mitotic recombination.

Genetic and physical analyses reveal that DNA-RNA hybrids form fortuitously at DNA double-strand breaks during transcription and need removal to allow repair by homologous recombination.

Kinesin Kif2C is recruited to DNA damage sites, modulates the mobility and dynamics of DNA damage foci, and promotes DNA double strand break repair.

During meiosis, budding yeast use a checkpoint involving the protein Mec1 to prevent the formation of double-strand breaks in DNA that has not completed replication.

PLK-1/2-mediated SYP-4 phosphorylation is dependent on crossover precursor formation, triggering a switch in the dynamic state of the synaptonemal complex that reduces the formation of further double-strand breaks at late meiotic prophase.

Mapping DNA replication timing, allied to genetic analysis of a RecQ repair helicase, reveals that antigenic variation in the African trypanosome may be initiated by locus-specific, replication-derived sequence instability.