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Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The initiation of mammalian puberty requires an increased pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. This increase is brought about by changes in transsynaptic and glial-neuronal communication. Coordination of these cellular interactions likely requires the participation of sets of genes hierarchically arranged within functionally connected networks. Using high throughput, genetic, molecular and bioinformatics strategies, in combination with a systems biology approach, three transcriptional regulators of the pubertal process have been identified, and the structure of at least one hypothalamic gene network has been proposed. A genomewide analysis of hypothalamic DNA methylation revealed profound changes in methylation patterns associated with the onset of female puberty. Pharmacological disruption of two epigenetic marks associated with gene silencing (DNA methylation and histone deacetylation) resulted in pubertal failure, instead of advancing the onset of puberty, suggesting that disruption of these two silencing mechanisms leads to activation of repressor genes whose expression would normally decrease at puberty. These observations suggest that the genetic underpinnings of puberty are polygenic rather than specified by a single gene, and that epigenetic mechanisms may provide coordination and transcriptional plasticity to this genetic network.
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PMID:New concepts on the control of the onset of puberty. 1995 55

In recent years the pace of discovering the molecular and genetic underpinnings of the pubertal process has accelerated considerably. Genes required for human puberty to occur have been identified and evidence has been provided suggesting that the initiation of puberty requires coordinated changes in the output of a multiplicity of genes organized into functional networks. Recent evidence suggests that a dual mechanism of epigenetic regulation affecting the transcriptional activity of neurons involved in stimulating gonadotropin-releasing hormone release plays a fundamental role in the timing of puberty. The Polycomb group (PcG) of transcriptional silencers appears to be a major component of the repressive arm of this mechanism. PcG proteins prevent the premature initiation of female puberty by silencing the Kiss1 gene in kisspeptin neurons of the arcuate nucleus (ARC) of the hypothalamus. Because the abundance of histone marks either catalyzed by--or associated with--the Trithorax group (TrxG) of transcriptional activators increases at the time when PcG control subsides, it appears that the TrxG complex is the counteracting partner of PcG-mediated gene silencing. In this chapter, we discuss the concept that a switch from epigenetic repression to activation within ARC kisspeptin neurons is a core mechanism underlying the initiation of female puberty.
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PMID:The Emerging Role of Epigenetics in the Regulation of Female Puberty. 2668 May 69