Abstract
In animal systems, the only case of third meiotic division without a prior round of DNA replication has been described in Drosophila males carrying mutations in roughex, a gene encoding an inhibitor of Cdk1 activity. Here, we describe another Drosophila gene, terno (teo), that regulates meiotic exit in males. In teo mutants, meiosis I and II are regular, but in many germline cysts, the 64 haploid spermatids undergo an extra division. Additionally, teo mutants are defective in sperm individualization. Teo interacts with cyclin A and B, Fizzy (Cdc20), and the anaphase-promoting complex/cyclosome components Cdc16 and Cdc27. In teo mutant testes, the cyclin A and B levels are higher than in wild type, and downregulation of either cyclin rescues the teo mutant phenotypes. These results suggest that Teo facilitates targeted degradation of the cyclins, so that in teo mutants, there is an increase in Cdk1-CycA and Cdk1-CycB activities, resulting in both the extra meiotic division and the sperm maturation defect.
