Human sperm cells travel up to 6 meters in their transit from testes to penis, and most of that journey occurs in the epididymis, a tightly coiled tube that primes the cells for their ultimate task: fertilization. In a paper released this week in the Proceedings of the National Academy of Sciences, researchers at the University of Illinois report that they have discovered a gene and related mechanism essential to the embryonic development of the epididymis.
The findings are the result of a serendipitous discovery, said professor of veterinary biosciences Humphrey Hung-Chang Yao. His graduate student, Jessica Tomaszewski, was examining the testes of mouse embryos when she noticed something odd: In one specimen the normally convoluted coil of the epididymis was instead a stunted, straight tube.
The lack of coiling had serious implications for the fertility of the mouse, Yao said.
If you take sperm directly from the testis and put it into the female reproductive tract, it wont swim. It wont be able to fertilize the egg, he said. Going through the epididymis changes the biochemical properties of the sperm and helps it develop the energy-generating machinery that allows it to swim. So without this structure, under normal circumstances a male cannot be fertile.
The researchers first thought that the abnormality was due to a lack of the male hormone, testosterone. Decades of research had shown that the development and maintenance of male reproductive structures depend on an increase in testosterone levels that begins in the latter half of the life of an embryo.
But all the normal indicators of adequate testosterone levels (its production and other physiological characteristics) were present in the mutant embryos.
Tomaszewski looked at younger mouse embryos from the same parents, to see how early in their development the abnormality appeared. She found the earliest evidence of a lack of proper c
Contact: Diana Yates
University of Illinois at Urbana-Champaign