Early inception of Puberty in Females Elucidated

Early inception of Puberty in Females Elucidated

In an article entitled, “Epigenetic control of female puberty,” published on 27th January 2013 issue of Nature Neuroscience (doi:10.1038/nn.3319), the lead author Alejandro Lomniczi with nine other associates affiliated to four research groups have presented evidence that a silencing epigenetic mechanism operating in the hypothalamus plays a significant role in timing the initiation of female puberty. This mechanism prevents the premature awakening of genes that otherwise become activated at the normal time of puberty, such as the Kiss1 (Kisspeptin) gene which is essential for puberty to occur. To conduct this research, scientists studied female rats, which like their human counterparts, go through puberty as part of their early aging process. They identified two complementary epigenetic modes of gene silencing. One mode (known as DNA methylation) results from a chemical, reversible modification of DNA regions controlling gene activity and the other one results from structural modifications affecting the ability of histones to interact with these gene-controlling regions. Such modifications result in histone marks associated with either gene silencing or gene activation. Their results show that the pubertal increase in Kiss1 expression is accompanied by the acquisition of epigenetic modifications associated with gene activation, recruitment of activating histones and loss of repressive histones. Their studies further show that these silencing epigenetic marks do not function in a vacuum but instead work in sync with a group of repressive proteins (known as the Polycomb (PcG) group). The repressive influence of PcG genes is lifted at puberty via an epigenetic mechanism involving acquisition of silencing marks (DNA methylation, repressive histones) and loss of activating histone marks from PcG regulatory regions. When the pubertal loss of PcG repression is prevented by delivering two PcG genes to the hypothalamus using a virus as a delivery vehicle, puberty is delayed and reproductive cyclicity is compromised. Altogether, these results support the novel concept that epigenetic mechanisms are integral components of the neuroendocrine process controlling mammalian puberty. These results also suggest that an epigenetic mechanism of transcriptional repression plays a significant role in timing the initiation of mammalian puberty, and that the PcG group of transcriptional silencers is a major contributor to this repressive mechanism. These repressors appear to target downstream genes involved in the stimulatory control of GnRH (Gonadotropin-Releasing Hormone) secretion at puberty. [summarized by Samsad Razzaque, a graduate student at the Plant Biotechnology lab. DU]

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