Sperm Protein May Hold Clues For Fertility And Contraceptives
- Date:
- September 21, 1998
- Source:
- University Of California, Davis
- Summary:
- A protein found on the surface of the sperm of all mammals appears crucial for the union of the sperm and egg, as well as for movement of the sperm into the animal's oviduct, announce researchers at the University of California, Davis.
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A protein found on the surface of the sperm of all mammals appears crucial for the union of the sperm and egg, as well as for movement of the sperm into the animal's oviduct, announce researchers at the University of California, Davis.
The discovery, which has direct implications for human fertility research as well as development of male contraceptives, is reported in the Sept. 18 issue of the journal Science.
"We suspected that sperm lacking the protein known as fertilin-beta would not be able to penetrate the egg, but we were quite surprised that these sperm even failed to bind with the egg's outer coating and rarely were able to travel from the uterus to the oviduct," said researcher Chunghee Cho. He is a molecular biologist and postdoctoral fellow from Korea working in the laboratory of UC Davis fertility researchers Diana Myles and Paul Primakoff.
The researchers studied the activity of sperm in mice lacking the gene for fertilin-beta, which belongs to a family of proteins found on the surface of cells and is believed to be important in cell binding.
Sperm from the mutant mice looked and moved normally, but most of them failed to attach to the egg. These sperm fused with the plasma membrane, which encases the egg, at just half the rate of sperm from normal mice.
Cho and colleagues anticipated this binding failure at the plasma membrane, but were surprised that the defective sperm were not even binding with the zona pellucida, the thick transparent wall that forms the outermost covering of the egg.
Furthermore, the sperm lacking fertilin-beta seemed unable to migrate from the uterus into the oviduct where the eggs are housed. The researchers speculate that this may be because the mutant sperm were unable to temporarily cling to the lining of the juncture of the uterus and oviduct as they normally would before proceeding into the oviduct.
The fertility rate of the male mice lacking fertilin-beta was 98 percent less than that of the normal male mice in the study.
"We are hopeful that a better understanding of fertilin-beta and related proteins in mice and non-humans will lead to the development of new male contraceptive drugs or vaccines as well as to future treatments for male infertility in humans," Cho said.
These findings were presented at a recent meeting of the International Congress of Spermatology. The study, conducted in collaboration with researchers at the National Institute of Environmental Health Science, was funded by the National Institutes of Health.
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Materials provided by University Of California, Davis. Note: Content may be edited for style and length.
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