Fig. 6. Summary of afd1 phenotypes. In the wild type, AEs are recruited and elongate along the entire chromosome. Telomere clustering requires elongated AEs. RAD51 is recruited and forms paired foci during recognition of homologous chromosomes. The bouquet, RAD51 and other unknown factors contribute to homologous pairing and synapsis. In afd1-1, AEs are recruited but their elongation is arrested. This impacts on both bouquet formation, RAD51 polymerization, homologous pairing and synapsis. In afd1-4, AEs are recruited and 50% of normal AEs elongation occurs. These AEs are sufficiently long to allow bouquet formation in 20% of the meiocytes. However, RAD51 polymerization is impaired and homologous pairing and synapsis does not occur. Therefore, homologous pairing and synapsis do not solely rely on the presence of elongated AEs and the bouquet. On the basis of these data, we propose that AFD1/REC8 controls the extent of AE elongation prior to the proper distribution of the recombination machinery, leading to pairing of homologous chromosomes independently of bouquet formation.