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Disruption of mouse CD46 causes an accelerated spontaneous acrosome reaction in sperm
Naokazu Inoue1, Masahito Ikawa, Tomoko Nakanishi
1Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka 537-8511, Japan.
Abstract:
Human membrane cofactor protein (MCP, CD46) is a ubiquitously expressed protein known to protect cells from complement attack. Interestingly, when we examined the expression of mouse CD46, which we recently cloned, the message was found only in testis and the protein was found on the inner acrosomal membrane of sperm. In order to elucidate the function of CD46, we produced mice carrying a null mutation in the CD46 gene by using homologous recombination. Despite the absence of CD46, the mice were healthy and both sexes were fertile. However, to our surprise, the fertilizing ability of males appeared to be facilitated by disruption of the CD46 gene, as the average number of pups born from CD46(-/-) males was significantly greater than that of wild-type males. It was also revealed that the incidence of the spontaneous acrosome reaction doubled in CD46(-/-) sperm compared to that in wild-type sperm. It was assumed that this increase caused the heightened fertilizing ability found in CD46(-/-) sperm. These data suggest that CD46 may have some role in regulating sperm acrosome reaction.
Insights
Mouse CD46 (membrane cofactor protein) normally protects cells. In mice lacking CD46, male fertility increased due to enhanced sperm acrosome reaction, suggesting CD46 regulates this process.
Area of Science:
- Immunology
- Reproductive Biology
- Genetics
Background:
- Human membrane cofactor protein (MCP, CD46) ubiquitously protects cells from complement attack.
- Mouse CD46 expression is restricted to the testis, localized to the inner acrosomal membrane of sperm.
Purpose of the Study:
- To investigate the function of mouse CD46 in vivo.
- To determine the role of CD46 in male fertility and sperm function.
Main Methods:
- Generation of CD46-deficient mice using homologous recombination.
- Assessment of fertility in CD46 knockout and wild-type mice.
- Analysis of sperm acrosome reaction incidence.
Main Results:
- CD46-deficient mice were healthy and fertile.
- Males lacking CD46 exhibited significantly enhanced fertilizing ability, indicated by a greater average number of pups.
- Sperm from CD46-deficient mice showed a doubled incidence of spontaneous acrosome reaction.
Conclusions:
- CD46 is not essential for mouse health or fertility.
- CD46 appears to play a regulatory role in the sperm acrosome reaction.
- Disruption of CD46 enhances male fertilizing capacity, likely via increased acrosome reaction.