The Cohen lab has been instrumental in defining the role of the DNA mismatch repair (MMR) pathway in mammalian meiosis. Using mouse mutants for each of the mammalian MMR orthologs, we have determined that MSH4/MSH5 heterodimers recruit MLH1/MLiH3 to class I crossover sites in order to specify the appropriate number and spacing of crossover events in the mammalian genome.
Our continued research in this area focuses on how these crossover mediators of the class I pathway interact with mediators of the class II pathway, through recruitment and integration via key helicases and endonucleases such as BLM, EXO1, and SLX4. In addition, we are currently investigating the role of the cyclin n-terminal domain containing protein-1 (CNTD1) in controlling class I crossing over. For more details click on image.