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A Highly Polymorphic Meiotic Recombination Mouse Hot Spot Exhibits Incomplete Repair

Department of Cancer Biology, Genome Plasticity Laboratory, The Scripps Research Institute, 5353 Parkside Drive RE107, Jupiter, Florida 33458, and INSERM U674, Functional Genomics of Solid Tumors, 27 rue Juliette Dodu, 75010 Paris, France

Received 17 May 2007/ Returned for modification 19 June 2007/ Accepted 7 August 2007

The recent mapping of recombination hot spots in the human genome has demonstrated that crossover is a nonrandom process that occurs at well-defined positions along chromosomes. However, the mechanisms that direct hot-spot turnover in complex mammalian genomes are poorly understood. Analyses of the human genome are impaired by the inability to genetically dissect and molecularly manipulate recombinogenic regions to test their roles in regulating hot spots. Here, using the BXD recombinant inbred strains as a crossover library, three new recombination hot spots have been identified on mouse chromosome 19. Analyses of a highly polymorphic recombination hot spot (HS22) revealed that approximately 4% of recombinant molecules display complex and incomplete repair with discontinuous conversion tracts, as well as persistent heteroduplex DNA at crossover sites in mature spermatozoa. Also, sequence analysis of the wild house mouse revealed instability at the center of this hot spot. This suggests that complete repair is not required for completion of mammalian meiosis, a scenario that leaves duplex DNA containing mismatches at crossover sites.

Published ahead of print on 20 August 2007.