DALLAS - November 24, 1998 - Discovery of a mutation that prevents sperm maturation could lead to treatments for male sterility and development of new male contraceptives, UT Southwestern Medical Center at Dallas scientists reported in today's issue of Proceedings of the National Academy of Sciences.
Dubbed morc, or microrchidia, a medical term for abnormally small testes, the mutation in an unidentified gene is expressed only in males during the earliest stages of sperm production, said investigators from the labs of Dr. Mark Watson, assistant professor of pathology, and Dr. Andrew Zinn, assistant professor of internal medicine. The research mice, genetically engineered to have the mutation, are normal at birth and attempt to begin production of sperm at puberty. But their attempts fail, leading researchers to conclude that the morc gene performs a primary regulatory function in male meiosis, the process that produces sperm.
"This uncovers a new point in the regulation of sperm production," said Zinn, who is an investigator in the Eugene McDermott Center for Human Growth and Development. "A difference in this mutation compared with other mouse reproductive mutations is that it is selective for spermatogenesis (sperm production) and does not seem to affect oogenesis (egg formation in females).
The researchers began investigating the effects of this mutation when a former member of the team, Dr. Randall Moreadith, was experimenting to produce a mouse with certain genetic features. The first transgenic animal he made was sterile. The scientists launched an investigation to find out why these first rodents could not reproduce.
The researchers found no abnormalities in the mice except that they were
infertile; the animals looked and behaved normally, including their mating
instincts. Although they formed precursor cells for normal sperm production at
birth, by about 10 days old -- puberty in a mouse -- the cells began
Contact: Susan Steeves
UT Southwestern Medical Center