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Updated: Oct 1, 2026

A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model
Published on: February 6, 2018
A testicular germ cell-associated serine-threonine kinase, MAK, is dispensable for sperm formation
Yoichi Shinkai1, Hideo Satoh, Naoki Takeda
1Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan. yshinkai@virus.kyoto-u.ac.jp
Abstract:
A member of the mitogen-activated protein kinase superfamily, MAK, has been proposed to have an important role in spermatogenesis, since Mak gene expression is highly restricted to testicular germ cells. To assess the biological function of MAK, we have established MAK-deficient (Mak(-/-)) mice. Mak(-/-) mice developed normally, and no gross abnormalities were observed. Spermatogenesis of the Mak(-/-) mice was also intact, and most of the mice were fertile. However, Mak(-/-) male-derived litter sizes and their sperm motility in vitro were mildly reduced. These data show that function of MAK is not essential for spermatogenesis and male fertility.
Insights
Mitogen-activated protein kinase (MAPK) superfamily member MAK is not essential for male fertility. MAK-deficient mice showed normal development and intact spermatogenesis, with only mild reductions in litter size and sperm motility.
Area of Science:
- Reproductive biology
- Molecular genetics
- Biochemistry
Background:
- Mitogen-activated protein kinase (MAPK) superfamily member MAK has restricted gene expression in testicular germ cells.
- MAK's proposed role in spermatogenesis necessitates functional investigation.
Purpose of the Study:
- To determine the biological function of MAK in male reproduction.
- To assess the necessity of MAK for spermatogenesis and male fertility.
Main Methods:
- Generation of MAK-deficient (Mak(-/-)) mice.
- Phenotypic analysis of Mak(-/-) mice, including development, spermatogenesis, fertility, litter size, and sperm motility.
Main Results:
- Mak(-/-) mice exhibited normal development without gross abnormalities.
- Spermatogenesis remained intact in MAK-deficient mice, with most individuals being fertile.
- A mild reduction in litter size and in vitro sperm motility was observed in Mak(-/-) males.
Conclusions:
- MAK function is not essential for the completion of spermatogenesis.
- MAK is not indispensable for male fertility, although it may play a modulatory role.
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