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Aberrant Distribution of ADAM3 in Sperm from Both Angiotensin-Converting Enzyme (Ace)- and Calmegin (Clgn)-Deficient Mice¹

Genome Information Research Center,⁶ Pharmaceutical Sciences,⁷ Research Institute for Microbial Diseases,⁸ Osaka University, Osaka, 565-0871, Japan

ABSTRACT

Male mice deficient for the calmegin (Clgn) or the angiotensin-converting enzyme (Ace) gene show impaired sperm migration into the oviduct and loss of sperm-zona pellucida binding ability in vitro. Since CLGN is a molecular chaperone for membrane transport of target proteins and ACE is a membrane protein, we looked for ACE on the sperm membranes from Clgn^–/– mice. ACE was present and showed normal activity, indicating that CLGN is not involved in transporting ACE to the sperm membranes. The ablation of the Adam2 and Adam3 genes generated animals whose sperm did not bind the zona pellucida, which led us to examine the presence of ADAM2 and ADAM3 in Clgn^–/– and Ace^–/– sperm. ADAM3 was absent from Clgn^–/– sperm. In the Ace^–/– mice, while ADAM2 was found normally in the sperm, ADAM3 disappeared from the Triton X-114 detergent-enriched phase after phase separation, which suggests that ACE is involved in distributing ADAM3 to a location where it can participate in sperm-zona pellucida binding. This diminished amount of ADAM3 in the Triton X-114 detergent-enriched phase may explain the inability of Clgn^–/– and Ace^–/– sperm to bind to the zona pellucida.

gamete biology, in vitro fertilization, male sexual function, sperm capacitation

² Correspondence: Masaru Okabe, Genome Information Research Center, Osaka University, Yamadaoka 3–1, Suita, Osaka, 565-0871, Japan. FAX: 81 6 6879 8376; okabe{at}gen-info.osaka-u.ac.jp

³ These authors contributed equally to this work.

⁵ On sabbatical leave from the Center for Research on Reproduction and Women's Health, University of Pennsylvania Medical Center, Philadelphia, PA 19104.

⁴ Current address: Graduate School of Life and Environmental Sciences, Tsukuba University, Tsukuba Science City, Ibaraki 305-8572, Japan.

¹ Supported by grants (11234203 and 00531), a grant-in-aid for Scientific Research, and the 21st Century 200 COE program from the Ministry of Education, Culture, Sports, Science, and Technology of Japan, and by NIH HD06274 (S.B.M.).

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