Puberty is programmed through a multifactorial gene network which works to activate the pulsatile secretion of the gonadotropin releasing hormone (GnRH), and subsequently elevate circulating levels of the pituitary gonadotropins that stimulate gonadal activity. Although this developmental transition normally occurs at a limited age-range in individuals of the same genetic background and environment, pubertal onset can occur prematurely or be delayed following changes in ambient conditions, or due to genetic variations or mutations, many of which have remained elusive due to their location in distal regulatory elements. Growing evidence is pointing to a pivotal role for the epigenome in regulating key genes in the reproductive hypothalamus and pituitary at this time, which might mediate some of the plasticity of pubertal timing. This review will address epigenetic mechanisms which have been demonstrated in the KNDy neurons that increase the output of pulsatile GnRH, and those involved in activation of the GnRH gene and its receptor, and describes how GnRH utilizes epigenetic mechanisms to stimulate transcription of the pituitary gonadotropin genes in the context of the chromatin landscape.

青春期是通过多因素基因网络进行编程的，该网络可激活促性腺激素释放激素（GnRH）的搏动性分泌，并随后提高刺激性腺活动的垂体促性腺激素的循环水平。尽管这种发育过渡通常发生在具有相同遗传背景和环境的个体的有限年龄范围内，但是青春期发病可能会过早发生，或者由于环境条件的变化或由于遗传变异或突变而延迟，其中许多原因仍然难以捉摸由于它们位于远端调节元件中。越来越多的证据表明，表观基因组在此时调节生殖下丘脑和垂体中关键基因的关键作用，这可能会介导青春期的可塑性。