During Drosophila oogenesis, the activation of a meiotic checkpoint couples progression through meiosis to specific developmental processes. In particular, the checkpoint affects accumulation of Gurken protein, a transforming growth factor alpha-like signaling molecule, central to the establishment of the dorsal-ventral axis of the oocyte. Mutations in double-stranded DNA repair enzymes, activate a checkpoint that, in turn, prevents Gurken translation presumably through post-translational modification of vasa, an eIF4A-like translation initiation factor. One of the checkpoint genes required to arrest meiosis in response to the presence of DSB is mei-41, a Drosophila homologue of the mammalian ATM tumor suppressor, DNA damage cell-cycle checkpoint protein. The ATM kinase is critical for the regulation of G1/S and G2/M checkpoints in response to genotoxic agents. In yeast and vertebrates, it was shown that ATM protein regulates these checkpoints through two downstream protein kinases, Chk1 and Chk2. Chk1, is encoded by the Drosophila grapes locus and Chk2, by the Drosophila mnk locus. Using biochemical, molecular and genetic analysis, we find that the meiotic checkpoint is dependent only on mnk, and it may act through a post-translational modification process. To further characterize the meiotic checkpoint, the role of other DNA damage checkpoint proteins in this process is being studied.