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Int. J. Mol. Sci. 2017, 18(6), 1300; doi:10.3390/ijms18061300

Knockout of Murine Mamld1 Impairs Testicular Growth and Daily Sperm Production but Permits Normal Postnatal Androgen Production and Fertility

1
Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan
2
Faculty of Biomedical Engineering, Toin University of Yokohama, Yokohama 225-8502, Japan
3
Department of Reproductive Biology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan
4
Department of NCCHD Child Health and Development, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8510, Japan
5
Department of Comprehensive Reproductive Medicine, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8510, Japan
6
Department of Pediatric Urology, Jichi Medical University, Children’s Medical Center Tochigi, Tochigi 329-0498, Japan
7
Department of Pediatrics, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan
*
Author to whom correspondence should be addressed.
Received: 16 May 2017 / Revised: 8 June 2017 / Accepted: 15 June 2017 / Published: 19 June 2017
(This article belongs to the Special Issue Cell Growth Regulation)
View Full-Text   |   Download PDF [1638 KB, uploaded 19 June 2017]   |  

Abstract

MAMLD1 has been implicated in testicular function in both human and mouse fetuses. Although three patients with MAMLD1 mutations were reported to have hypergonadotropic hypogonadism in their teens, the functional significance of MAMLD1 in the postnatal testis remains unclear. Here, we analyzed the phenotype of Mamld1 knockout (KO) male mice at reproductive ages. The reproductive organs of KO male mice were morphologically unremarkable, except for relatively small testes. Seminiferous tubule size and number of proliferating spermatogonia/spermatocytes were reduced in the KO testis. Daily sperm production of KO mice was mildly attenuated, whereas total sperm counts in epididymal semen remained normal. Sperm motility and morphology, as well as androgen levels in serum and testicular tissues and the number of pups born from cross-mated wildtype (WT) female mice, were comparable between WT and KO male mice. These results indicate that MAMLD1 contributes to the maintenance of postnatal testicular growth and daily sperm production but is dispensable for androgen biosynthesis and fertility. MAMLD1 likely plays supporting roles in multiple and continuous steps of male reproduction. View Full-Text
Keywords: androgen; knockout mouse; mutation; reproduction; testis androgen; knockout mouse; mutation; reproduction; testis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Miyado, M.; Yoshida, K.; Miyado, K.; Katsumi, M.; Saito, K.; Nakamura, S.; Ogata, T.; Fukami, M. Knockout of Murine Mamld1 Impairs Testicular Growth and Daily Sperm Production but Permits Normal Postnatal Androgen Production and Fertility. Int. J. Mol. Sci. 2017, 18, 1300.

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