All Phenotypes Nectin2<tm1Smu> MGI Mouse

teratozoospermia ( J:85634 )

• all mutant spermatozoa exhibit a variety of severely malformed heads and midpieces; no single common type of defect is observed

abnormal sperm midpiece morphology ( J:85634 )

• the midpiece of the sperm tail is frequently rough or appears to be much thinner than the principal piece

• however, no undulation of, or any other changes affecting, the principal piece of the tail are observed

abnormal sperm mitochondrial sheath morphology ( J:85634 )

• the mitochondrial sheath is either totally absent or disorganized

abnormal sperm head morphology ( J:85634 )

• all mutant spermatozoa display some degree of head malformation, ranging from mild to severe phenotypes

• the sperm head is often curled back onto the midpiece

• a diverse range of misshapen heads is observed, including a forward-oriented aberrantly shaped head

abnormal ectoplasmic specialization morphology ( J:85634 )

• localization of poliovirus receptor-related 3 (nectin-3) at the Sertoli-spermatid junction is perturbed, presumably leading to abnormal sperm head and midpiece morphology

• espin, an actin-bundling protein specifically expressed at Sertoli cell ectoplasmic specializations, is virtually absent at Sertoli-spermatid junctions

male infertility ( J:85634 )

• male, but not female, homozygotes are infertile

• however, testicular size and epididymal sperm counts remain relatively normal

impaired fertilization ( J:85634 )

• male homozygotes exhibit failure of in vivo fertilization, as assessed by in vitro culture of sperm-exposed oviductal oocytes after overnight mating

impaired binding of sperm to zona pellucida ( J:85634 )

• in vitro, mutant spermatozoa display a 6-fold reduction in their capacity to bind to zona-intact mouse oocytes recovered from ovulated CD1 females

abnormal sperm physiology ( J:85634 )

• although mutant spermatozoa are viable and motile, upon longer incubation (12-24 hrs), in vitro motility and viability declines faster than those of controls, suggesting impaired spermatozoan energy metabolism or fewer mitochondria

impaired sperm migration in female genital tract ( J:85634 )

• homozygous mutant spermatozoa are ~4-fold less efficient in reaching the oviducts relative to heterozygous controls

impaired acrosome reaction ( J:85634 )

• unexpectedly, mutant sperm bind to the oolemma normally but fail to penetrate zona-free hamster oocytes, as shown by a 75-fold and 32-fold reduction of decondensing sperm nuclei in the ooplasm after 45 and 90 min of incubation, respectively