In a report that appears today in the journal Genes & Development, Dr. JoAnne S. Richards, professor of molecular and cellular biology at BCM, and Dr. Allison E. Falender, who recently completed graduate work in Richards' lab, said that mice who lack TAF4b are fertile at first, but by 11 weeks of age become infertile and lack the precursor cells for the production of sperm.
"The fact that these animals are initially fertile indicates that the testes have the capacity to produce sperm," said Richards. "That they become infertile is related to the progressive loss of maturing germ cells in the testis."
The animals lack sperm because of defects inherent to the cells that serve as progenitors of sperm - cells that are usually found in the adult testis.
"This is the first paper to show that in the period of growth just after birth, events occur that impact fertility in the adult," said Richards. "The proliferation of germ cells is essential for fertility."
She said further study may indicate whether the loss of TAF4b also has an effect on the fertility of human men.
Falender became aware of the issue when she went to evaluate overcrowding in the mouse colony. She found that all pairs of animals that were no longer breeding had a male mouse that lacked TAF4b. When she compared the testes of these animals to those of normal mice, she found that the organs were much smaller in the mice that lacked the factor.
"That's the fun of science - the unexpected that takes you somewhere exciting," said Richards.
Others who participated in the research include Drs. Kirk C. Lo and Dolores J. Lamb, both of BCM; Richard N. Freiman of Brown University; Kenneth G. Geles and Robert Tijian of University of California, Berkeley; KeumSil Hwang and Patricia L. Morris of The Rockefeller University in New York.
Funding for this research came from the National Institutes of Health and the American Foundation for Urologic Disease.