For simplification, the diagram shows a pair of telocentric chromosomes (with the centromere located at one of the chromosomal ends) that form a single CO during meiosis. This single CO, together with sister chromatid cohesion, ensures that the homologues remain attached following the disassembly of the synaptonemal complex (SC). SC disassembly is coordinated with a remodeling of meiotic chromosomes. Together, these processes promote the acquisition of a chromosome structure that allows the correct orientation of the homologues on the metaphase I plate. At the onset of anaphase I, the selective release of sister chromatid cohesion allows the segregation of the homologues to different poles of the spindle. This is followed by the second meiotic division in which the sister chromatids are separated (in a manner similar to a regular mitotic division), thereby producing four haploid gametes. The second line of the diagram depicts an example of how the failure to form COs can cause a pair of homologues to missegregate during meiosis. Note how the homologues lacking a CO fail to align properly on the metaphase I plate, and this results in both homologues migrating to the same pole, which ultimately results in the formation of aneuploid gametes (this example displays one of the possible segregation patterns that can occur in the absence of COs). The bottom part of the diagram shows the same pair of chromosomes undergoing a mitotic division. Note how in contrast with meiotic metaphase I, the centromeres of the sister chromatids are oriented towards different poles of the spindle during mitotic metaphase. The complete release of sister chromatid cohesion allows for the separation of the sister chromatids, resulting in the formation of two daughter nuclei with an identical chromosome complement to the mother cell.

The diagram shows a single sister chromatid (as a double stranded DNA molecule) from each homologue. After the topoisomerase-like enzyme Spo11 forms a meiotic DSB, the DSB site is processed by removal of the covalently bound Spo11 and resection of the ends in a 5′ to 3′ orientation. This results in the formation of 3′ single-stranded tails with which the Rad51 and Dmc1 strand-exchange proteins associate. These nucleoprotein filaments proceed to invade a homologous intact template for repair, resulting in the formation of a nascent D-loop structure. These unstable strand invasions can be dismantled by SGS1, however, CO-fated DSBs are protected from the action of SGS1 by the ZMM proteins, which promote the formation of single end invasions. Second end capture, followed by DNA synthesis and ligation, results in the formation of a double Holliday junction (dHJ) intermediate, which is resolved as a CO by an unknown dHJ resolvase. Although not depicted in the diagram, dHJs may also be resolved as NCOs. Nascent D-loops that are not stabilized by the ZMM proteins can be repaired by a mechanism known as synthesis-dependent strand annealing (SDSA). This requires DNA synthesis and the displacement of the invading strand, which might be promoted by RTEL1. Annealing of the displaced strand with the other DSB end is followed by DNA synthesis and ligation, resulting in the formation of NCOs. The anti-recombination activity of SGS1 is needed to prevent the formation of aberrant joint molecules that occur when secondary strand invasions take place. Some of the aberrant joint molecules that are not disassembled by SGS1 are resolved as COs by MUS81. Apart from this late role, MUS81 may also play earlier roles in the resolution of aberrant joint molecules.