New concepts on the control of the onset of puberty

Sergio Ojeda, Alejandro Lomniczi, Ursula Sandau, Valerie Matagne

    Research output: Contribution to journalArticlepeer-review


    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.

    Original languageEnglish (US)
    Pages (from-to)44-51
    Number of pages8
    JournalEndocrine Development
    StatePublished - Nov 2009

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Pediatrics, Perinatology, and Child Health
    • Endocrinology
    • Endocrine and Autonomic Systems


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