Required for normal acrosome reaction and for normal male fertility (PubMed:12110578, PubMed:15161660, PubMed:15007175). Can bind Cu(2+) (By similarity). Detected in testis (PubMed:10842180, PubMed:12110578, PubMed:15161660). Detected within seminiferous tubules, on round and elongated spermatids (at protein level) (PubMed:12110578). Not detected in brain (at protein level) (PubMed:10842180, PubMed:15161660). Detected in testis, and at low levels in heart (PubMed:10525406, PubMed:12110578). Expression in brain is very low and barely detectable (PubMed:10525406). Expressed during embryogenesis. A short helical region is required and sufficient for Cu(2+) binding. N-glycosylated (PubMed:10525406, PubMed:10842180). N-glycosylated at two distinct sites (PubMed:10842180). O-glycosylated. Mice are born at the expected Mendelian rate and appear grossly normal and healthy. Females are fertile, but males are almost completely sterile, in spite of normal mating behavior (PubMed:12110578, PubMed:15161660). Two independent studies conclude that male sterility is due to impaired acrosome reaction, but describe contradictory effects on spermatogenesis, possibly due to the use of different mouse strains (PubMed:12110578, PubMed:15161660). Spermatogenesis is normal, with normal sperm counts, normal sperm motility, and no malformation of the sperm head or tail (PubMed:15161660). Late stages of spermiogenesis are impaired, leading to reduced numbers of mature spermatozoa in seminiferous tubules; mutant sperm present morphological abnormalities of the flagellum and sperm head, and decreased motility (PubMed:12110578). Mutant sperm are able to fertilize oocytes in vitro, but many of the resulting embryos die before the morula stage (PubMed:15161660). Mutant sperm cells have elevated levels of DNA damage and DNA strand breaks, and this may be the cause for embryonic lethality (PubMed:15161660). Mice deficient for both Prnd and Prnp have the same phenotype as mice lacking Prnd; they are born at the expected Mendelian rate and appear grossly normal and healthy (PubMed:15161660, PubMed:15007175). Females are fertile, but males deficient for both Prnd and Prnp are sterile, in spite of normal mating behavior (PubMed:15161660, PubMed:15007175). Again, findings about spermatogenesis are contradictory: spermatogenesis is normal, with normal sperm counts, normal sperm motility, and no malformation of the sperm head or tail (PubMed:15161660). Sperm cells display various malformations (PubMed:15007175). Male sterility is due to impaired acrosome reaction (PubMed:15161660). Mutant sperm are able to fertilize oocytes in vitro, but many of the resulting embryos die before the morula stage (PubMed:15161660). Mutant sperm cells have elevated levels of DNA damage and DNA strand breaks, and this may be the cause for embryonic lethality (PubMed:15161660). Aging mice deficient for both Prnd and Prnp do not display loss of cerebellar Purkinje cells or develop ataxia, and do not develop neurological defects (PubMed:15007175). Loss of cerebellar Purkinje cells and ataxia has been observed in mice with mutations that cause Prnd overexpression in the brain, suggesting that aberrant overexpression of Prnd causes neurotoxicity. Belongs to the prion family.