“…Since genetic disruption of either one of the meiosis‐specific cohesin subunits leads to infertility with different phenotypes of chromosome structure, each of them plays an essential role in chromosome dynamics during meiosis (Bannister, Reinholdt, Munroe, & Schimenti, ; Fukuda, Fukuda, Agostinho, Hernandez‐Hernandez, & Kouznetsova, ; Herran, Gutierrez‐Caballero, Sanchez‐Martin, Hernandez, & Viera, ; Hodges, Revenkova, Jessberger, Hassold, & Hunt, ; Hopkins, Hwang, Jacob, Sapp, & Bedigian, ; Ishiguro, Kim, Shibuya, Hernandez‐Hernandez, & Suzuki, ; Llano, Gomez, Garcia‐Tunon, Sanchez‐Martin, & Caburet, ; Revenkova et al., ; Winters, McNicoll, & Jessberger, ; Xu, Beasley, Warren, Horst, & McKay, ). The accessory proteins, PDS5B (Fukuda & Hoog, ), WAPL (Adelfalk, Janschek, Revenkova, Blei, & Liebe, ; Brieno‐Enriquez, Moak, Toledo, Filter, & Gray, ; Zhang, Hakansson, Kuroda, & Yuan, ) and SORORIN (Gomez, Felipe‐Medina, Ruiz‐Torres, Berenguer, & Viera, ; Jordan, Eyster, Chen, Pezza, & Rankin, ), also appear on chromosomes during meiotic prophase I and regulate the stability of the binding of cohesin on the chromatin. Thus, in addition to a canonical somatic cell‐type cohesin complex, different combinations of subunits generate distinct cohesin complexes during meiosis, which provide specialized functions for generating meiotic chromosomes.…”