Furthermore, all SYCP3 mutations reported in human male infertility and female recurrent pregnancy loss affect the C-terminal sequence of the protein (Miyamoto et al., 2003; Bolor et al., 2009; Nishiyama et al., 2011); our structural analysis shows that these mutations would block higher order assembly whilst retaining tetramer formation, confirming a key role for meiotic chromosome organisation by SYCP3 in human fertility. Here, SYCP3 is linked to male infertility.