The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Control of Cognition and Adaptive Behavior by the GLP/G9a Epigenetic Suppressor Complex
Open accessAbstract
The genetic basis of cognition and behavioral adaptation to the environment remains poorly understood. Here we demonstrate that the histone methyltransferase complex GLP/G9a controls cognition and adaptive responses in a region-specific fashion in the adult brain. Using conditional mutagenesis in mice, we show that postnatal, neuron-specific deficiency of GLP/G9a leads to derepression of numerous nonneuronal and neuron progenitor genes in adult neurons. This transcriptional alteration is associated with complex behavioral abnormalities, including defects in learning, motivation, and environmental adaptation. The behavioral changes triggered by GLP/G9a deficiency are similar to key symptoms of the human 9q34 mental retardation syndrome that is associated with structural alterations of the GLP/EHMT1 gene. The likely causal role of GLP/G9a in mental retardation in mice and humans suggests a key role for the GLP/G9a-controlled histone H3K9 dimethylation in regulation of brain function through maintenance of the transcriptional homeostasis in adult neurons.
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“Researchers have reported that postnatal knockout of G9a reduced the anxiety phenotype in mice, while mutation or deletion of one copy of the GLP gene in humans leads to Kleefstra syndrome, characterized by social behavior impairment, impulsivity, aggression, and mental retardation (Schaefer et al., 2009).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Schaefer et al., 2009
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“The HMT complex G9a/G9a-like protein (GLP), composed of the HMT euchromatic histone-lysine N-methyltransferase 2 (EHMT2) or G9a and G9a-like protein (GLP or EHMT1), has been shown to be involved in the monomethylation and dimethylation of H3K9 (Schaefer et al., 2009).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Schaefer et al., 2009
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Researchers have reported that postnatal knockout of G9a reduced the anxiety phenotype in mice, while mutation or deletion of one copy of the GLP gene in humans leads to Kleefstra syndrome, characterized by social behavior impairment, impulsivity, aggression, and mental retardation (Schaefer et al., 2009).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Schaefer et al., 2009
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Thus, G9a/GLP seems to exert temporal effects on developmental histone methylation.”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Schaefer et al., 2009
Experimental — accuracy not yet measuredIn the citing paper
“No statistical methods were used to pre-determine sample sizes but our sample sizes are similar to those reported in previous publications19,31,95,99,108.”
From Epigenetic regulation of brain region-specific microglia clearance activity (2018) · cites this paper as [95]
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Citations
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Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitionsPreprint
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Partitioning and Plasticity of Repressive Histone Methylation States in Mammalian Chromatin
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Targeting Epigenetic Enzymes for Treatment of Autism Spectrum Disorders
Yan, Z. (2024) · Springer eBooks · doi:10.1007/978-3-031-32035-4_176-1
EHMT1 mediates cellular motility in embryonal rhabdomyosarcoma by activating SOX8 expression
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Targeting Epigenetic Enzymes for Treatment of Autism Spectrum Disorders
Yan, Z. (2025) · Springer eBooks · doi:10.1007/978-3-031-73368-0_176
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SET Domain Genes in Neurodevelopmental Disorders
Ohguri, A., Nakagawa, T., Nakagawa, M., & Hosoi, T. (2026) · Genes · doi:10.3390/genes17101313
“Postnatal neuron-specific deletion of Ehmt1 and Ehmt2 causes learning, motivational, and adaptive-behavior abnormalities associated with widespread derepression of genes normally characteristic of non-neuronal cells and neuronal progenitors [111].”
BindingDB (2015) · UC San Diego · doi:10.7270/q2n58nws
BindingDB (2026) · UC San Diego · doi:10.7270/q2gh9ptk
BindingDB (2014) · UC San Diego · doi:10.7270/q2nz892t
BindingDB (2012) · UC San Diego · doi:10.7270/q237793p
BindingDB (2020) · UC San Diego · doi:10.7270/q2x350zg
BindingDB Entry 50045685: Selective inhibitors of protein methyltransferases.
BindingDB (2016) · UC San Diego · doi:10.7270/q28k7bs2
BindingDB (2024) · UC San Diego · doi:10.7270/q25d8x66
Metadata
- Authors
- Schaefer, A., Sampath, S. C., Intrator, A., Min, A., Gertler, T. S., Surmeier, D. J., Tarakhovsky, A., & Greengard, P.
- Affiliations
- Rockefeller University (US)
- Northwestern University (US)
- Corresponding author
- Tarakhovsky, Alexander
- Greengard, Paul
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 64
- Issue
- 5
- Pages
- 678-691
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2814156
- OpenAlex
- W2065364505
- Cited by
- 317
- References
- 57
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 14 · 2023: 11 · 2022: 12 · 2021: 17 · 2020: 16 · 2019: 20 · 2018: 16 · 2017: 24 · 2016: 23 · 2015: 27 · 2014: 28 · 2013: 24 · 2012: 24
- FWCI
- 9.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG09464, P01AG009464)
- National Institute of Mental Health (MH-074866, F30MH082522, MH082522, P50MH074866)
- National Institute on Drug Abuse (R03DA025962, DA025962)
- National Institute of General Medical Sciences (GM 07739, R01GM112811, T32GM007739)
- National Institute of Allergy and Infectious Diseases (AI068058, R01AI068058)
- National Institute of Neurological Disorders and Stroke (P01NS013742)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- EHMT1, histone methyltransferase, epigenetic regulation, cognition, learning and memory, motivation, environmental adaptation, adult neurons
- MeSH terms
- Enhancer of Zeste Homolog 2 Protein, Adaptation, Physiological, Central Nervous System Stimulants, Animals, Animals, Newborn, Behavior, Animal, Benzazepines, Body Weight, Caffeine, Cognition, Cognition Disorders, Conditioning, Classical, Exploratory Behavior, Fear, Food Preferences, Mice, Inbred DBA, Mice, Transgenic, Motor Activity, Histone-Lysine N-Methyltransferase, Mutagenesis, Dopamine Agonists, Maze Learning, Epigenesis, Genetic, Green Fluorescent Proteins, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Polycomb Repressive Complex 2
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