Fertilization Defects in Sperm from Mice Lacking Fertilin β

TLDR

Fertilization defects arise in sperm lacking the ADAM‑family protein fertilin β, a membrane protein implicated in sperm–egg interactions. Sperm lacking fertilin β show impaired adhesion, fusion, migration, and zona binding, yet egg activation remains normal, indicating fertilin’s direct role in sperm–egg membrane interaction and possibly in zona binding or oviduct migration. Mice lacking fertilin β produce sperm deficient in membrane adhesion, fusion, oviduct migration, and zona pellucida binding.

Abstract

Fertilization Defects in Sperm from Mice Lacking Fertilin β Fertilization Defects in Sperm from Mice Lacking Fertilin β Fertilizer, a member of the ADAM family, is found on the plasma membrane of mammalian sperm. Sperm from mice lacking fertilin β were shown to be deficient in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida. Egg activation was unaffected. The results are consistent with a direct role of fertilin in sperm-egg plasma membrane interaction. Fertilil could also have a direct role in sperm-zona binding or oviduct migration; alternatively, the effects on these functions could result from the absence of fertilin activity during spermatogenesis.