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Updated: May 20, 2026
Analysis of Epididymal Protein Synthesis and Secretion
Published on: August 25, 2018
cSrc is necessary for epididymal development and is incorporated into sperm during epididymal transit
Dario Krapf1, Ye Chun Ruan, Eva V Wertheimer
1Department of Veterinary and Animal Science, University of Massachusetts, Amherst, MA 01003, USA.
Abstract:
Changes that occur to mammalian sperm upon epididymal transit and maturation render these cells capable of moving progressively and capacitating. Signaling events leading to mammalian sperm capacitation depend on the modulation of proteins by phosphorylation and dephosphorylation cascades. Recent experiments have demonstrated that the Src family of kinases plays an important role in the regulation of these events. However, sperm from cSrc null mice display normal tyrosine phosphorylation associated with capacitation. We report here that, despite normal phosphorylation, sperm from cSrc null mice display a severe reduction in forward motility, and are unable to fertilize in vitro. Histological analysis of seminiferous tubules in the testes, caput and corpus epididymis do not reveal obvious defects. However, the cauda epididymis is significantly smaller, and expression of key transport proteins in the epithelial cells lining this region is reduced in cSrc null mice compared to wild type littermates. Although previously, we and others have shown the presence of cSrc in mature sperm from cauda epididymis, a closer evaluation indicates that this tyrosine kinase is not present in sperm from the caput epididymis, suggesting that this protein is acquired by sperm later during epididymal maturation. Consistent with this observation, cSrc is enriched in vesicles released by the epididymal epithelium known as epididymosomes. Altogether, these observations indicate that cSrc is essential for cauda epididymal development and suggest an essential role of this kinase in epididymal sperm maturation involving cSrc extracellular trafficking.
Insights
The Src family kinase (SFK) c-Src is crucial for sperm maturation and male fertility. Mice lacking c-Src show impaired sperm motility and reduced epididymis size, indicating c-Src
Area of Science:
- Reproductive Biology
- Molecular and Cellular Biology
- Biochemistry
Background:
- Mammalian sperm undergo epididymal transit and maturation to achieve motility and fertilization capability.
- Sperm capacitation involves protein phosphorylation and dephosphorylation cascades, with the Src family of kinases (SFKs) implicated in these signaling events.
- Previous studies suggested a role for c-Src in sperm capacitation, but its precise function remained unclear.
Purpose of the Study:
- To investigate the role of the Src family kinase c-Src in mammalian sperm maturation and epididymal function.
- To determine the impact of c-Src deficiency on sperm motility, fertilization, and epididymal development.
Main Methods:
- Analysis of sperm from c-Src null mice and wild-type littermates.
- Assessment of sperm motility and in vitro fertilization capacity.
- Histological examination of testes and epididymis.
- Evaluation of protein expression in epididymal epithelial cells.
- Investigation of c-Src localization in sperm and epididymosomes.
Main Results:
- Sperm from c-Src null mice exhibited significantly reduced forward motility and failed in vitro fertilization, despite normal tyrosine phosphorylation patterns.
- Histological analysis revealed a smaller cauda epididymis in c-Src null mice, with decreased expression of key transport proteins.
- c-Src was found to be present in mature sperm from the cauda epididymis but not the caput epididymis, and was enriched in epididymosomes.
Conclusions:
- c-Src is essential for the proper development of the cauda epididymis.
- This tyrosine kinase plays a critical role in epididymal sperm maturation, likely through extracellular trafficking via epididymosomes.
- c-Src is indispensable for achieving functional sperm motility and fertilization capacity in mammals.
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