Journal of Andrology
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Published-Ahead-of-Print October 29, 2009, DOI:10.2164/jandrol.109.008227

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The Power of Mouse Genetics to Study Spermatogenesis

Alexander Yatsenko , Naoki Iwamori , Tokuko Iwamori , and Martin M Matzuk *

* To whom correspondence should be addressed. E-mail: mmatzuk{at}bcm.tmc.edu.

Approximately 80 million people suffer from infertility worldwide, and nearly half of all infertility cases are attributed to a male factor (Matzuk and Lamb, 2002). Therefore, progress in reproductive genetics becomes crucial for future diagnosis and treatment of infertility. In recent years, enormous progress has been made in this field. More than 400 mutant mouse models with specific reproductive abnormalities have been produced, and numerous human association studies have been discovered. However, the translation of basic science findings to clinical practice remains protracted, with only modest progress in the application of novel findings to clinical genetic testing and cures. To date, the most significant findings in male infertility remain numerical and structural chromosomal abnormalities and Y-chromosome microdeletions in infertile men. Thus, we anticipate that future genetic investigations will focus on infertile men with a normal somatic karyotype, but with various spermatozoal defects like insufficient production of spermatozoa (oligozoospermia), inadequate motility (asthenozoospermia), abnormal morphology (teratozoospermia), or combinations of these defects. Ultimately, basic advances in mammalian non-human reproduction will translate to clinical advances in human reproduction and testing infertile humans, thereby helping to improve diagnostics and health care for infertile patients.


Key words: Infertility • Reproductive Genetics • Spermatogenesis • Testis • human male infertility • mouse model




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