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BOR - Papers in Press, published online ahead of print October 11, 2006.
Biol Reprod 2006, 10.1095/biolreprod.106.053181
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BIOLOGY OF REPRODUCTION 76, 130–141 (2007)
DOI: 10.1095/biolreprod.106.053181
© 2007 by the Society for the Study of Reproduction, Inc.


research-article

CDH1 Is a Specific Marker for Undifferentiated Spermatogonia in Mouse Testes1

Masutaka Tokuda 3 4, Yuzo Kadokawa 2 3 4, Hiroki Kurahashi 4 5, and Tohru Marunouchi 3 4

Division of Cell Biology, Institute for Comprehensive Medical Science,3 21st Century COE Program, Development Center for Targeted and Minimally Invasive Diagnosis and Treatment,4 Division of Molecular Genetics, Institute for Comprehensive Medical Science,5 Fujita Health University, Toyoake 470-1192, Japan

ABSTRACT

In the mammalian testis, spermatogenesis is initiated from a subset of stem cells belonging to undifferentiated type A spermatogonia. In spite of the biologic significance of undifferentiated type A spermatogonia, little is known about their behavior and properties because of a lack of specific cell surface markers. Here we show that CDH1 (previously known as E-cadherin) is expressed specifically in undifferentiated type A spermatogonia in the mouse testis. Histologic analysis showed that CDH1-positive cells had all the characteristics of undifferentiated type A spermatogonia. Whole-mount immunohistochemistry showed that CDH1-positive cells made clusters mainly comprising one, two, four, or eight cells. They survived after administration of the cytotoxic agent busulfan to mice, and then regenerated seminiferous epithelia. Transplantation experiments showed that only CDH1-positive cells had colonizing activity in the recipient testis. Our data clearly demonstrated that spermatogenic stem cells reside among undifferentiated type A spermatogonia, which express CDH1.

CDH1 (E-cadherin), developmental biology, spermatogenesis, spermatogenic stem cells, testis, undifferentiated spermatogonia


FOOTNOTES

1Supported in part by a grant-in-aid for the 21st Century Center of Excellence Program of Fujita Health University, the Collaboration with Local Communities Project, and a grant-in-aid for Scientific Research on Priority Areas (18051015) from the Ministry of Education, Culture, Sports, Science and Technology, Japan.

Correspondence: 2 Yuzo Kadokawa, Division of Cell Biology, Institute for Comprehensive Medical Science, Fujita Health University, 1–98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi 470-1192, Japan. FAX: 81 562 93 8834; e-mail: ykado{at}fujita-hu.ac.jp




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