Epigenetic regulation of female puberty
Open accessAbstract
Substantial progress has been made in recent years toward deciphering the molecular and genetic underpinnings of the pubertal process. The availability of powerful new methods to interrogate the human genome has led to the identification of genes that are essential for puberty to occur. Evidence has also emerged suggesting that the initiation of puberty requires the coordinated activity of gene sets organized into functional networks. At a cellular level, it is currently thought that loss of transsynaptic inhibition, accompanied by an increase in excitatory inputs, results in the pubertal activation of GnRH release. This concept notwithstanding, a mechanism of epigenetic repression targeting genes required for the pubertal activation of GnRH neurons was recently identified as a core component of the molecular machinery underlying the central restraint of puberty. In this chapter we will discuss the potential contribution of various mechanisms of epigenetic regulation to the hypothalamic control of female puberty.
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Increasing evidence implicates epigenetic mechanisms in timing of puberty.
“Increasing evidence implicates epigenetic mechanisms in timing of puberty.114”
From Pubertal development and regulation (2016) · cites this paper as [114]
The availability of powerful new technologies has contributed to expanding knowledge of the regulation of puberty and recognising the role of genetic imprinting in the control of the activation of GnRH secretion at the time of puberty initiation.
“The availability of powerful new technologies has contributed to expanding our knowledge of the regulation of puberty and recognising the role of genetic imprinting in the control of the activation of GnRH secretion at the time of puberty initiation.114”
From Pubertal development and regulation (2016) · cites this paper as [114]
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“Many of the genes that are connected to multiple TRG genes are themselves potential regulators of gene expression, such as KDM3B (also known as JMJD1B), a histone demethylase involved in removal of the repressive H3K9me2 and H3K9me1 histone marks (Kim et al., 2012; Krishnan et al., 2011).”
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Self-citationEpigenetics: The Language of the Cell?
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Self-citationStructure and Function of Histone H3 Lysine 9 Methyltransferases and Demethylases
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- Authors
- Lomniczi, A., Wright, H., & Ojeda, S. R.
- Affiliations
- Oregon National Primate Research Center (US)
- Corresponding author
- Lomniczi, Alejandro
- Ojeda, Sergio R.
- Venue
- Frontiers in Neuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 36
- Pages
- 90-107
- ISSN
- 0091-3022 (ISSN-L)
- PMC
- PMC6824271
- OpenAlex
- W2048700120
- Cited by
- 136
- References
- 239
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 9 · 2023: 12 · 2022: 12 · 2021: 16 · 2020: 9 · 2019: 15 · 2018: 17 · 2017: 11 · 2016: 18 · 2015: 3 · 2013: 1
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Frontiers in Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Keywords
- epigenetic regulation, female puberty, GnRH neurons, excitatory synaptic input, gene regulatory networks
- MeSH terms
- Animals, Female, Humans, Hypothalamus, Gonadotropin-Releasing Hormone, Neurons, Puberty, Sexual Maturation, Epigenesis, Genetic
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