title: Mutant phenotype analysis suggests potential roles for C-type natriuretic peptide receptor (NPR-B) in male mouse fertility.
abstract: BACKGROUND
  C-type natriuretic peptide (CNP) signaling through its receptor natriuretic peptide receptor B (NPR-B) is a key molecule for mammalian reproduction, and known to play important roles in female fertility. However, the function of these peptides in mouse male reproduction remains largely unknown. To determine the role of CNP/NPR-B signaling in male reproduction we investigated phenotype of Npr2-deficient short-limbed-dwarfism (Npr2(slw/slw)) mice, which have been shown to have gastrointestinal (GI) abnormalities.
  
  
  RESULTS
  In homozygous Npr2(slw/slw) mice, spermatogenesis is developmentally delayed at both 2 and 4 weeks of age, with vacuolation and degenerating apoptotic germ cells being observed at 3 weeks age. However, the adult Npr2(slw/slw) mice exhibited apparently normal spermatogenesis, albeit with some aberrant spermatids, suggesting that developmental delay was overcome. In addition, the adult Npr2(slw/slw) mice showed abnormal penile morphology (paraphimosis).
  
  
  CONCLUSIONS
  The potential role of CNP signaling via the NPR-B receptor in male fertility appears to be mediated not through germ-cell development, but may be through maintenance of normal penile function.
authors.affiliation: Molecular Imaging Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba-shi, Chiba 263-8555, Japan. chizuru.f.sogawa@gmail.com.
authors.forename: Chizuru
authors.initials: C
authors.lastname: Sogawa
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Fujiwara
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tsukamoto
authors.forename: Yuka
authors.initials: Y
authors.lastname: Ishida
authors.forename: Yukie
authors.initials: Y
authors.lastname: Yoshii
authors.forename: Takako
authors.initials: T
authors.lastname: Furukawa
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Kunieda
authors.forename: Tsuneo
authors.initials: T
authors.lastname: Saga
mesh_terms: D000818:Animals; D017209:Apoptosis; D003433:Crosses, Genetic; D007172:Erectile Dysfunction / Q000209:etiology*; D006720:Homozygote; D007248:Infertility, Male / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D009154:Mutation; D010263:Paraphimosis / Q000209:etiology*; D010410:Penile Erection; D010413:Penis / Q000378:metabolism* / Q000503:physiopathology; D017461:Receptors, Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism*; D013087:Spermatids / Q000378:metabolism / Q000473:pathology; D013091:Spermatogenesis; D013094:Spermatozoa / Q000378:metabolism / Q000473:pathology; D013733:Testicular Diseases / Q000209:etiology; D014617:Vacuoles
chemical_list: D017461:Receptors, Atrial Natriuretic Factor; C073616:atrial natriuretic factor receptor C