Abstract
Crossover formation as a result of meiotic recombination is vital for proper segregation of homologous chromosomes at the end of meiosis I. In most organisms, crossovers are generated through two crossover pathways: Class I and Class II. Meiosis-specific protein complexes ensure accurate crossover placement and formation by promoting and inhibiting the formation of crossovers in both crossover pathways. In Drosophila, Class I crossovers are promoted and Class II crossovers are prevented by a complex that contains MCM (mini-chromosome maintenance) and MCM-like proteins, REC (ortholog of Mcm8), MEI-217, and MEI-218, collectively called the mei-MCM complex. However, little is known about how the mei-MCMs function within the Class I and II crossover pathways. In this study, we perform genetic analysis to understand how specific regions and motifs of REC and MEI-218 contribute to crossover formation and distribution. We see that while the N-terminus of MEI-218 is dispensable for crossover formation, REC’s conserved AAA ATPase motifs exhibit differential requirements for Class I and Class II crossover formation. REC-dependent ATP hydrolysis, but not ATP binding, is required for promoting the formation of Class I, MEI-9 dependent crossovers. Conversely, the ability for REC to both bind and hydrolyze ATP is required for REC’s Class II anti-crossover role, yet to varying degrees, suggesting that REC forms multiple complexes that require different REC-dependent ATP binding functions. These results provide genetic insight into the mechanism in which mei-MCMs promote Class I crossovers and inhibit Class II crossovers.