Sperm are produced in the testicles through a three-step process called spermatogenesis.
During the final stage, known as spermiogenesis, a lot of changes take place, including the packaging of DNA into the sperm head and the formation of the sperm tail, which propels the sperm cell toward the egg.
The study conducted using mouse model showed that mice lacking a protein called meiosis expressed gene 1, or MEIG1, were sterile as a result of impaired spermiogenesis - the process that encompasses changes in the sperm head and the formation of the tail.
The team also found that MEIG1 associates with the Parkin co-regulated gene protein, or PACRG protein, and that testicular PACRG protein is reduced in MEIG1-deficient mice.
PACRG is thought to play a key role in assembly of the sperm tail, and the reproductive phenotype of PACRG -deficient mice mirrors that of the MEIG1-mutant mice.
"We discovered that MEIG1 is essential for male fertility. Moreover, our findings reveal a critical role for the MEIG1/PACRG partnership in the function of a structure that is unique to sperm, the manchette. The absence of a normal manchette in mice lacking MEIG1 totally disrupts the maturation process of sperm," said Dr Jerome F. Strauss III, dean in the VCU School of Medicine.
"In addition to having an impact on fertility, the discovery identifies a new target for drug discovery for a much needed reversible male method of contraception," he added.
The study is published in the Early Edition of the Proceedings of the National Academy of Sciences.