By contrast, noncrossovers can be generated by a combination of repair pathways such as synthesis-dependent strand annealing. The mechanism for repairing DSBs to generate crossovers during meiotic prophase probably involves some kind of double Holliday junction, an intermediate in genetic recombination involving a mobile junction between four strands of DNA. DSBs that do not become crossovers are repaired as noncrossovers, often referred to as 'gene conversions' (Joyce, 2009a). DSBs are believed to be catalyzed by the Spo11 protein, a suspected paralog of a type II topoisomerase from archaebacteria. The formation of crossovers depends on the repair of programmed DNA double-strand breaks (DSBs) through homologous recombination (McKim, 1998 Keeney, 2001). Therefore, it is not surprising that crossover formation is a tightly regulated process. In the absence of chiasmata, homologs may segregate randomly, resulting in aneuploidy, which can lead to infertility, severe developmental consequences, or lethality. Meiotic crossovers promote genetic variation and mature into chiasmata, which hold the homologous chromosomes together at metaphase I and direct their segregation at anaphase I. Interestingly, PCH2-dependent delays in prophase may allow additional crossovers to form (Joyce, 2009a). Furthermore, the PCH2-dependent checkpoint is activated by these events and pachytene progression is delayed until the DSB repair complexes required to generate crossovers are assembled. It is proposed that the sites and/or conditions required to promote crossovers are established independently of DSB formation early in meiotic prophase. Surprisingly, two lines of evidence suggest that the PCH2-dependent checkpoint does not reflect the accumulation of unprocessed recombination intermediates: the delays in meiotic progression do not depend on DSB formation or on mei-41, the Drosophila ATR homolog, which is required for the checkpoint response to unrepaired DSBs. The PCH2-dependent delays also require proteins thought to regulate the number and distribution of crossovers, suggesting that this checkpoint monitors events leading to crossover formation.

Consistent with the hypothesis that a checkpoint has been activated, the delays in meiotic progression are suppressed by a mutation in the conserved AAA+ ATPase pch2. This study shows that mutations in Drosophila genes required to process DSBs into crossovers delay two important steps in meiotic progression: a chromatin-remodeling process associated with DSB formation and the final steps of oocyte selection. This process is usually monitored by one or more checkpoints that ensure that DSBs are repaired prior to the meiotic divisions. Crossovers mature into chiasmata, which hold and orient the homologous chromosomes on the meiotic spindle to ensure proper segregation at meiosis I. Genetic map position - 3R: 4,385,880.4,387,451 ĭuring meiosis, programmed DNA double-strand breaks (DSBs) are repaired to create at least one crossover per chromosome arm. Keywords - meiotic checkpoint, meiotic chromosome crossovers

Chiasmata crossover definition