The role of mcm5 and mad2 in the Pachytene checkpoint in Drosophila females. Anshu A. Paul, Kim S. McKim. Waksman Institute of Microbiology, Rm 206, Genetics, Rutgers, New Brunswick, New Brunswick, NJ.

   The meiotic recombination pathway in Drosophila females is monitored by the presence of several checkpoints. Checkpoints serve as error correction mechanisms present at different stages of meiosis to monitor the fidelity of various ongoing processes. One of these checkpoints, called the Pachytene checkpoint, oversees the processes that lead up to the formation of crossovers. In the presence of a defect, the checkpoint is not satisfied and it leads to a delay in meiotic progression which allows the cell additional time to repair its defects and generate crossovers. I am characterizing the roles of two candidate genes, mcm5 and mad2, as they relate to the Pachytene checkpoint. The gene mcm5, which was previously known to function in DNA replication, transcription activation, and chromosome condensation, is also one of the precondition genes in the meiotic recombination pathway. Furthermore, it was found to be similar in sequence to the gene mei-218, which is involved in the Pachytene checkpoint. Similarly, the gene mad2, which was previously known to function in mitotic checkpoint activation, may have a role in meiotic checkpoint activation. In order to determine the function of these genes in the Pachytene checkpoint, I combined each of these mutations with a mei-9 mutation, which typically fails to satisfy the checkpoint and has a meiotic prophase delay. If the double mutants have a meiotic delay, indicating the activation of the Pachytene checkpoint, then mcm5 and mad2 are not involved in checkpoint activation. On the other hand, if there is no delay in my double mutants, indicating that the checkpoint was not activated despite the presence of a crossover defect, then mcm5 or mad2 function in checkpoint activation. My results showed that mcm5, even when combined with the crossover defective mutant mei-9, did not result in a Pachytene delay, suggesting that mcm5 does indeed play a role in the activation of the Pachytene checkpoint. Experiments are currently being performed on the mad2 mutants to characterize their function in the Pachytene checkpoint.