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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.
Research in the laboratories of Y.S. and Y.A. was supported by Grants in Aid from the Ministry of Education, Science, Culture and Sports of Japan.
We thank M. Shibuya and K. K. Lee for providing anti-MAK Ab and anti-MST Ab, respectively. We are deeply indebted to R. Ogasawara, M. Nohara, and Y. Takeda for their technical support and to B. J. Danzo for editorial assistance in preparing the manuscript.