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. To ensure accurate crossover formation, meiosis-specific protein complexes regulate the degree in which each pathway is used. One such complex is the mei-MCM complex, which contains MCM (mini-chromosome maintenance) and MCM-like proteins REC (ortholog of Mcm8), MEI-217, and MEI-218, collectively called the mei-MCM complex. The mei-MCM complex genetically promotes Class I crossovers and inhibits Class II crossovers in Drosophila, but it is unclear how individual mei-MCM proteins contribute to crossover regulation. In this study, we perform genetic analyses to understand how specific regions and motifs of mei-MCMs contribute to Class I and II crossover formation and distribution. Our analyses show that the long, disordered N-terminus of MEI-218 is dispensable for crossover formation, and that REC’s predicted ability to bind and hydrolyze ATP is differentially required for Class I and Class II crossover formation. Results indicate that REC’s predicted ability to hydrolyze ATP, in trans with an additional, unknown subunit is required for promoting the formation of Class I crossovers. However, the inhibition of Class II crossovers depends on REC’s predicted abilities to both bind and hydrolyze ATP. Overall, our results suggest that REC forms multiple complexes that exhibit differential REC-dependent ATP binding and hydrolyzing requirements. These results provide genetic insight into the mechanism in which mei-MCMs, a conserved class of meiotic proteins, promote Class I crossovers and inhibit Class II crossovers.