Retinol dehydrogenase 10 is indispensible for spermatogenesis in juvenile males

Ming-Han Tong; Qi-En Yang; Jeffrey C Davis; Michael D Griswold

doi:10.1073/pnas.1214883110

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Retinol dehydrogenase 10 is indispensible for spermatogenesis in juvenile males

Journal article

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Retinol dehydrogenase 10 is indispensible for spermatogenesis in juvenile males

Ming-Han Tong, Qi-En Yang, Jeffrey C Davis and Michael D Griswold

Proceedings of the National Academy of Sciences - PNAS, Vol.110(2), pp.543-548

01/08/2013

DOI: https://doi.org/10.1073/pnas.1214883110

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https://hdl.handle.net/2376/113301

PMCID: PMC3545805

PMID: 23267101

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Abstract

Galactosides

Immunohistochemistry

In Situ Nick-End Labeling

Sertoli Cells - metabolism

Testis - metabolism

Alcohol Oxidoreductases - metabolism

Male

DNA Primers - genetics

Reverse Transcriptase Polymerase Chain Reaction

Mice, Knockout

Vitamin A - metabolism

Spermatogenesis - physiology

Animals

Histological Techniques

Tretinoin - metabolism

Mice

Indoles

Real-Time Polymerase Chain Reaction

Alcohol Oxidoreductases - deficiency

Retinoic acid (RA), an active vitamin A derivative, is essential for mammalian spermatogenesis. Genetic studies have revealed that oxidation of vitamin A to retinal by retinol dehydrogenase 10 (RDH10) is critical for embryonic RA biosynthesis. However, physiological roles of RDH10 in postnatal RA synthesis remain unclear, given that Rdh10 loss-of-function mutations lead to early embryonic lethality. We conducted in vivo genetic studies of Rdh10 in postnatal mouse testes and found that an RDH10 deficiency in Sertoli cells, but not in germ cells, results in a mild germ cell depletion phenotype. A deficiency of RDH10 in both Sertoli and germ cells in juvenile mice results in a blockage of spermatogonial differentiation, similar to that seen in vitamin A-deficient animals. This defect in spermatogenesis arises from a complete deficiency in juvenile testicular RA synthesis and can be rescued by retinoid administration. Thus, in juvenile mice, the primary, but not exclusive, source of RA in the testes is Sertoli cells. In contrast, adult Rdh10-deficient mice exhibit phenotypically normal spermatogenesis, indicating that during development a change occurs in either the cellular source of RA or the retinaldehyde dehydrogenase involved in RA synthesis.

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Details

Title: Retinol dehydrogenase 10 is indispensible for spermatogenesis in juvenile males
Creators: Ming-Han Tong - School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USA. minghan@wsu.edu
Qi-En Yang
Jeffrey C Davis
Michael D Griswold
Publication Details: Proceedings of the National Academy of Sciences - PNAS, Vol.110(2), pp.543-548
Academic Unit: Molecular Biosciences, School of
Publisher: United States
Grant note: HD06777 / NICHD NIH HHS R37 HD010808 / NICHD NIH HHS R01 HD010808 / NICHD NIH HHS HD10808 / NICHD NIH HHS
Identifiers: 99900547839501842
Language: English
Resource Type: Journal article