不妊マウスが男性不妊に希望の光をもたらした
1998年11月24日
テキサスの研究者たちは、ある遺伝子の突然変異により、雌には異常を生じないが、雄の精母細胞の分化が損なわれることを発見した。
この遺伝子（morc遺伝子）がヒトにおいて存在するかは不明であるが、ヒトの男性不妊の研究に応用されるだろう。
Sterile mice shed light on male infertility
Tuesday November 24 10:46 AM ET
NEW YORK, Nov 23 (Reuters Health) -- Researchers have discovered a gene mutation that can cause sterility in male mice, but not females. It is not clear if such a mutation, which is found in the microrchidia (morc) gene, exists in humans, but the findings may have applications for human infertility, according to Texas researchers.
``We don't have any proof yet that the defect in this particular gene is defective in humans, but we expect it would be,'' said Dr. Andrew Zinn, an assistant professor of internal medicine at University of Texas Southwestern Medical Center, Dallas, who conducted the study with Dr. Mark Watson and other colleagues.
Mice with a morc mutation appear normal, but they are infertile. Studying them, the researchers found that in these male mice, the cells that should develop into sperm -- germ cells -- start to undergo cell division and then, for unknown reasons, stop.
Eventually, the germ cells degenerate and the testes shrink, according to a report in the November 24th issue of the Proceedings of the National Academy of Sciences.
``Ultimately, you get a mouse that has no germ cells and there are humans with similar problems,'' Zinn said in an interview with Reuters Health. The discovery was made after a cardiac researcher accidentally mutated the gene and found that male mice were sterile, but females with the mutation were unaffected.
The group is currently trying to identify patients with a family history of unexplained infertility that may be due to a recessive mutation in the morc gene, Zinn said. Such a mutation, if it exists in humans, would be a relatively rare cause of infertility, he noted.
``We are beginning to look for these families now, but we haven't found anything,'' he said. However, the finding may lead to a way to stimulate meiosis, the process of cell division that gives rise to sperm.
``If you could give back this gene -- even if the defect wasn't in the gene itself -- it might stimulate meiosis in men who are not undergoing meiosis,'' he said. The finding may also be used to develop a male-specific contraceptive, according to the Texas researcher.
``We think one of the applications we could see would be the development of a contraceptive, so if you could block the gene you would have a very highly specific male contraceptive,'' he explained. ``You would just have to find a drug that blocks the gene.''
The finding may also help research into testicular cancer. ''One theory of human testicular tumors is that germ cells are blocked in sperm production,'' Zinn explained in a university statement. ``This blockage during cell differentiation could cause them to become malignant, a mechanism that is common in leukemia and lymphoma.''
SOURCE: Proceedings of the National Academy of Sciences 1998;95:14361-14366.