CLXN and situs inversus: Keita Sasaki, Kogiku Shiba, Akihiro Nakamura et al. show that mice lacking calaxin have intact fertility despite showing primary cilia dyskinesia and abnormal 9 + 0 nodal cilia formation, while loss of calaxin in zebrafish causes situs inversus but does not affect 9 + 2 axonemal formation.