A new protein involved in sperm fertility

Mar 2, 2007 10:18 GMT  ·  By

Till a recent research, the luteinizing hormone (LH) receptor was thought to be the only explanation behind the sexual precocity in both boys and girls.

Recently, a mixed team from the Institute of Genetics and Molecular and Cellular Biology (IGBMC, CNRS / Inserm / Universit? Louis Pasteur de Strasbourg)), University of Dallas and the University of Louvain, has discovered a key regulator of male fertility, the SHP protein, discovery that explains many symptoms of infertility disorders in males.

Puberty, the moment fertility installs, is triggered by endocrine alterations genetically programmed from the moment of sexual differentiation in the embryo. It encompasses anatomical alterations: the complete development of primary sexual traits (penis, scrotum and testes) and the emergency of secondary sexual traits (hair growth, breaking of the voice, bone and muscle growth etc). These changes are provoked by hormonal discharges made by the pituitary gland, which synthesizes LH and STH (follicle stimulating hormone).

These hormones induce in the testes the sperm and testosterone production. Testosterone is the hormone that inflicts the development of secondary sexual traits in boys.

Beside LH, the new research identified a new compound involved in the sexual maturation of males, the SHP protein, in studies made on mice. The team investigated two mice types, one with SHP protein and another lacking it, with surprising results. The mice lacking SHP could reproduce about a week earlier, a huge difference as male mice are sexually mature at 7 or 8 weeks.

Males lacking SHP generated more testosterone prematurely, thus matured earlier their primary sexual traits, regardless of the pituitary's activity. But the same protein was found to delay the differentiation of the sperm cells by decreasing the metabolism of retinoic acids. Thus, mutations of SHP could be the cause of some kinds of human sexual precocity cases with unknown causes.

The novel technologies of synthetic ligands could cure these mutations in humans.

This research also redirects investigations aimed at improving the sperm production in men with various degrees of infertility.