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Abstract

The accurate repair of DNA double‐strand breaks (DSBs) is crucial for the maintenance of genome stability and the prevention of tumours. Homologous recombination (HR) is a complex process used by cells to repair DSBs that arise spontaneously during DNA replication or after exposure to DNA‐damaging agents. HR is also fundamental for DSB‐initiated DNA transactions, which occur during meiosis, V(D)J recombination and mating‐type switching. During the past decade, many HR components have been identified using genetic and biochemical approaches (Jasin, 2002; Keeney, 2001; Lisby & Rothstein, 2004, 2005; Liu & West, 2004; West, 2003); the main challenge now is to define how known HR components function at the molecular level. The first workshop on recombination was held in 1968 and was a highly stimulating meeting that focused on how DNA could be manipulated to achieve recombination. Since then, the field has expanded considerably. This was reflected in the most recent meeting, which brought together scientists studying many areas of DNA metabolism that either use or have a direct effect on HR. The main difference between HR‐mediated DSB repair in mitotic and meiotic cells is that repair in mitotic cells occurs through an intact sister chromatid, whereas meiotic cells preferentially use a paired homologue as a template to generate a crossover that is essential for homologue disjunction at the first meiotic division. Meiotic DSBs are generated in a highly controlled manner through the nucleolytic action of the meiosis‐specific sporulation protein 11 (Spo11). This process also depends on a complex of interacting proteins including the yeast orthologue (Xrs2) of mammalian Nijmegen breakage syndrome 1 (NBS1), meiotic recombination 2 (Mer2) and recombination 114 (Rec114). S. Keeney (New York, NY, USA) reported on Mer2, which associates with chromosomes prior to synaptonemal complex formation, and is phosphorylated by cell‐division cycle 28 …