Under the leadership of IKAWA Masahito , Associate professor, Animal Resource Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, and OKABE Masaru , Professor, Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University, a group of researchers have clarified that protein disulfide isomerase homolog (PDILT)-deficient mice were male infertile.

There are about 20 types of protein disulfide isomerase enzymes that catalyze s-s bonds necessary for folding of a protein into the correct higher-order structure and PDILT is a testis-specific factor. The group created PDILT-deficient mice by genetic engineering and found they were male infertile.

PDILT is necessary to form a higher-order structure of sperm fertilizing protein, ADAM3,  and ADAM3 disappeared from the sperm of PDILT-deficient mice. The mobility of ADAM3-deficient sperm was normal, but the sperm didn't migrate from the uterus into the oviduct and fertilization didn't take place. However, if the sperm were artificially injected into the oviduct, fertilization, pregnancy, and delivery took place. In other words, while not directly involved in the level of fertility of the male mouse, ADAM3 played a crucial role in spermatozoa maturation and quality control.

The group concluded from their research that "testis-specific quality control for nascent proteins in the endoplasmic reticulum is crucial in equipping spermatozoa with their fertilizing ability" and in furthering understanding male fertility and infertility -- greater understanding of which would assist in the development of improved strategies for contraception and treatment of male infertility.

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• Research Institute for Microbial Diseases