Role of MeCP2, DNA methylation, and HDACs in regulating synapse function
Open accessAbstract
Over the past several years there has been intense effort to delineate the role of epigenetic factors, including methyl-CpG-binding protein 2, histone deacetylases, and DNA methyltransferases, in synaptic function. Studies from our group as well as others have shown that these key epigenetic mechanisms are critical regulators of synapse formation, maturation, as well as function. Although most studies have identified selective deficits in excitatory neurotransmission, the latest work has also uncovered deficits in inhibitory neurotransmission as well. Despite the rapid pace of advances, the exact synaptic mechanisms and gene targets that mediate these effects on neurotransmission remain unclear. Nevertheless, these findings not only open new avenues for understanding neuronal circuit abnormalities associated with neurodevelopmental disorders but also elucidate potential targets for addressing the pathophysiology of several intractable neuropsychiatric disorders.
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Inhibiting HDACs with Trichostatin A (TSA) resulted in reduced postsynaptic excitatory firing of cortical pyramidal neurons.
“This finding was further supported on inhibiting HDACs with Trichostatin A (TSA), which resulted in reduced postsynaptic excitatory firing of cortical pyramidal neurons, a finding that paralleled MeCP2-null cells in the study by Adachi et al. (2009).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Kavalali et al., 2011
The “MeCP2, HDACs, and synaptic transmission” section reports that HDAC inhibitors including TSA reduced miniature excitatory postsynaptic current (mEPSC) frequency, similarly to MeCP2-null neurons. But those experiments used hippocampal cultures; the paper does not report that TSA reduced postsynaptic excitatory firing in cortical pyramidal neurons. Its table describes reduced firing in cortical slices from MeCP2-null mice, a different condition. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMale Mecp2/Y mice have a fully penetrant phenotype.
“Although female Mecp2/+ mice show phenotypic variance in part due to random X-chromosome inactivation, male Mecp2/Y mice have a fully penetrant phenotype.”
From A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett syndrome (2013) · cites this paper as [5]
The Rett syndrome section (page unavailable) reports that constitutive MeCP2 knockout mice recapitulate some neurological symptoms. The synaptic-transmission table also lists abnormalities in male MeCP2−/y mice, but neither passage establishes that every male mouse develops a phenotype; the claim of full penetrance is unsupported. (LLM, conf=0.78)
Experimental — accuracy not yet measuredMecp2 null males are normal at birth and weaning, but develop limb clasping, tremors, lethargy and abnormal breathing, symptoms that progressively worsen until death at 6-16 weeks of age.
“Null males are normal at birth and weaning, but develop limb clasping, tremors, lethargy and abnormal breathing, symptoms that progressively worsen until death at 6 – 16 weeks of age.”
From A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett syndrome (2013) · cites this paper as [5]
The Rett syndrome section (page unavailable) says constitutive MeCP2 knockout mice develop some neurological symptoms and die early in postnatal development. It does not specify that null males are normal at birth and weaning, list limb clasping, tremors, lethargy or abnormal breathing, or give a death range of 6–16 weeks. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMeCP2 is able to modulate synaptic transmission frequency through transcriptional repression via HDAC recruitment.
“Overall, it appears that MeCP2 is able to modulate synaptic transmission frequency through transcriptional repression via HDAC recruitment (Kavalali et al., 2011).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Kavalali et al., 2011
Mouse models recapitulate many of the symptoms of RTT.
“Mouse models recapitulate many of the symptoms of RTT and their study has provided insight into the physiological basis of disease3–5.”
From A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett syndrome (2013) · cites this paper as [5]
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- Authors
- Kavalali, E. T., Nelson, E. D., & Monteggia, L. M.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Monteggia, Lisa M.
- Venue
- Journal of Neurodevelopmental Disorders
- Published
- 2011-03-02
- Volume
- 3
- Issue
- 3
- Pages
- 250-256
- ISSN
- 1866-1947 (ISSN-L)
- 1866-1955
- PMC
- PMC3261274
- OpenAlex
- W1998017143
- Cited by
- 46
- References
- 62
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 4 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 1 · 2017: 3 · 2016: 1 · 2015: 3 · 2014: 4 · 2013: 4 · 2012: 2
- FWCI
- 2.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Journal of Neurodevelopmental Disorders (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (R01MH081060, R56MH081060, R01MH066198)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- MeCP2, DNA methylation, histone deacetylase, synaptic function, synaptogenesis, synapse maturation, excitatory neurotransmission, inhibitory neurotransmission, epigenetic regulation, neurodevelopmental disorders, neuropsychiatric disorders
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