Puberty is a major developmental milestone set in motion by the interaction of genetic factors and environmental cues. The pubertal process is initiated by an increased pulsatile release of gonadotropin releasing hormone (GnRH) from neurosecretory neurons of the hypothalamus. Although single genes have been identified that are essential for puberty to occur, it appears clear now that many genes controlling diverse cellular functions contribute to the process. The polygenic nature of the neuroendocrine complex controlling puberty has prompted two important questions: are these genes functionally connected and, if they are, is their activity subject to a dynamic level of control independent of changes in DNA sequence? In this article we will discuss emerging evidence suggesting that the onset of puberty is controlled at the transcriptional level by interactive gene networks subjected to epigenetic regulation. At least two modes of epigenetic regulation provide coordination and transcriptional plasticity to these networks: changes in DNA methylation and differential association of histone modifications to genomic regions controlling gene activity. Architecturally, puberty-controlling networks are endowed with “activators,” which move the process along by setting in motion key developmental events, and “repressors,” which play a central role in preventing the untimely unfolding of these events.
|Original language||English (US)|
|Number of pages||23|
|Journal||Research and Perspectives in Endocrine Interactions|
|State||Published - Jan 1 2015|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism