title: The coiled tail of the round-headed spermatozoa appears during epididymal passage in GOPC-deficient mice.
abstract: Male mice deleting the gene encoding GOPC (Golgi-associated PDZ- and coiled-coil motif-containing protein) are infertile, showing globozoospermia with a coiled tail (Yao et al., 2002). We confirmed how and where tail anomalies were produced in spermatids and epididymal spermatozoa by light and electron microscopy. During spermiogenesis, tail formation occurred normally, but a defect was found at the posterior ring. Thereafter, remarkable sperm tail deformations were induced during epididymal passage. In the proximal caput epidiymidis, the tails remained normal and straight, but most of them coiled around the nucleus in the cauda epididymidis. Coiling is presumed to occur with the migration of the cytoplasmic droplet by the absence of the posterior ring. The connecting piece of the coiled tail was often dislocated or separated from the implantation fossa. Many mitochondria were separated from the outer dense fibers (ODFs) and formed a stratified mitochondrial sheath. Due to this, the distal part of the midpiece became bared of the mitochondrial sheath. The bared ODFs were often bent and disorganized. Tail deformities are attributed to weak or incomplete adhesion between the following structures: 1) plasma membrane and nuclear envelope at the posterior ring, 2) connecting piece and implantation fossa, and 3) mitochondria and ODFs. These defects result in a coiled tail, tail dislocation from the implantation fossa, and the stratified mitochondrial sheath accompanying bared ODFs in the midpiece, respectively. Thus the posterior ring is significant in preventing coiled tail formation. The GOPC-deficient spermatozoa provide a valuable model not only for head but also for tail anomalies.
authors.affiliation: Department of Anatomy and Developmental Biology, Graduate School of Medicine, Chiba University, Chiba, Japan. fstoyota@faculty.chiba-u.jp
authors.forename: Fumie
authors.initials: F
authors.lastname: Suzuki-Toyota
authors.forename: Chizuru
authors.initials: C
authors.lastname: Ito
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Toyama
authors.forename: Mamiko
authors.initials: M
authors.lastname: Maekawa
authors.forename: Ryoji
authors.initials: R
authors.lastname: Yao
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Noda
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Toshimori
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics*; D002467:Cell Nucleus / Q000378:metabolism / Q000648:ultrastructure; D004822:Epididymis / Q000648:ultrastructure*; D000077614:Golgi Matrix Proteins; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018345:Mice, Knockout; D018613:Microscopy, Confocal; D008928:Mitochondria / Q000378:metabolism / Q000648:ultrastructure; D008954:Models, Biological; D013079:Sperm Maturation; D013082:Sperm Tail / Q000648:ultrastructure*; D013087:Spermatids / Q000648:ultrastructure*; D013091:Spermatogenesis; D013094:Spermatozoa / Q000002:abnormalities / Q000648:ultrastructure*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; D000077614:Golgi Matrix Proteins; C435484:Gopc protein, mouse; D047908:Intracellular Signaling Peptides and Proteins