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Center for the Study of Reproduction and Departments of Molecular Genetics, Obstetrics, Gynecology and Women's Health, and Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, U.S.A.; Current affiliation: Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, U.S.A.
* To whom correspondence should be addressed. E-mail: pollard{at}aecom.yu.edu.
Meiosis is a double division process that is preceded by only one DNA replication event to produce haploid gametes. The defining event in meiosis is prophase 1, during which chromosome pairs locate each other, become physically connected and exchange genetic information. While many aspects of this process have been elucidated in lower organisms there has been scant information available until now about the process in mammals. Recent advances in genetic analysis especially in mice and humans, has revealed many genes that play essential roles in meiosis in mammals. These include cell cycle regulatory proteins that couple exit from the premeiotic DNA synthesis to the progression through prophase1, the chromosome structural proteins involved in synapsis and the repair and recombination proteins that process the recombination events. Failure to adequately repair the DNA damage caused by recombination triggers meiotic checkpoints that results in ablation of the germ cells by apoptosis. These analyses have revealed surprising sexual dimorphism in the requirements of different gene products and a much less stringent checkpoint regulation in females. This may provide an explanation for the10 fold increase in meiotic errors in females compared with males. This review provides a comprehensive analysis of the use of genetic manipulation particularly in mice but also of the analysis of mutations in humans, to elucidate the mechanisms that are required for traverse through prophase 1.
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