Scientists from Monash University have uncovered a new understanding of how male puberty begins.
The key to their findings lies with a protein known as SMAD3 and the rate at which it is produced. Researchers, Associate Professor Kate Loveland and Dr Catherine Itman from the Faculty of Medicine, Nursing and Health Sciences have discovered through laboratory testing that half as much SMAD3 protein results in faster maturation than the norm, and an inability to create SMAD3 results in abnormal responses to testosterone.
"SMAD3 is a protein that translates signals from the environment outside the cell to the nucleus, where it switches genes on or off," Dr Itman said. "We have been investigating how SMAD3 influences the growth of testis cells and their ability to respond to testosterone".
Puberty begins when the body starts to produce large amounts of the hormone testosterone. Early, or precocious, puberty involves the onset of puberty before eight years of age and affects around 1 in 10,000 boys. On the other hand, puberty is delayed when testis cells cannot respond normally to testosterone. Altered timing of puberty has implications in adulthood, with precocious puberty linked to reduced adult height and delayed puberty associated with reduced bone density.
Testosterone acts through specialized cells in the testis called Sertoli cells. Before puberty, Sertoli cells multiply, allowing the testis to grow. At puberty, Sertoli cells must stop growing so they can support sperm precursor cells to develop into sperm.
Professor Loveland, Dr Itman and their colleagues have been investigating how Sertoli cells switch from a multiplying state, making the testis big enough to make sperm, to a mature state that sustains sperm production.
"We have discovered that this is not an "on-off" switch. Rather, it is the amount of the SMAD3 protein in the Sertoli cell that is different in the immature, multiplyin
|Contact: Karen Sutherland|