H3K4 tri-methylation in synapsin genes leads to different expression patterns in bipolar disorder and major depression
Open accessAbstract
The synapsin family of neuronal phosphoproteins is composed of three genes (SYN1, SYN2 and SYN3) with alternative splicing resulting in a number of variants with various levels of homology. These genes have been postulated to play significant roles in several neuropsychiatric disorders, including bipolar disorder, schizophrenia and epilepsy. Epigenetic regulatory mechanisms, such as histone modifications in gene regulatory regions, have also been proposed to play a role in a number of psychiatric disorders, including bipolar disorder and major depressive disorder. One of the best characterized histone modifications is histone 3 lysine 4 tri-methylation (H3K4me3), an epigenetic mark shown to be highly enriched at transcriptional start sites and associated with active transcription. In the present study we have quantified the expression of transcript variants of the three synapsin genes and investigated their relationship to H3K4me3 promoter enrichment in post-mortem brain samples. We found that histone modification marks were significantly increased in bipolar disorder and major depression and this effect was correlated with significant increases in gene expression. Our findings suggest that synapsin dysregulation in mood disorders is mediated in part by epigenetic regulatory mechanisms.
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Case/control differences in histone acetylation and methylation have been observed in depression.
“Like with DNAm, case/control differences in depression have been observed.”
From Epigenetics and depression (2019) · cites this paper as [20]
The SYN2 expression section reports greater H3K4me3 enrichment at the SYN1 promoter in the major-depression group, supporting a case/control difference in histone methylation. The Discussion says the study investigated only one epigenetic modification; it does not report a case/control difference in histone acetylation. (LLM, conf=0.88)
Experimental — accuracy not yet measuredEnhancement of H3K4me3 was found in postmortem brain tissue BA10 in MDD, enriched at transcriptional start sites of synapsin 1 and relevant to increased expression of synapsin 1a and synapsin 1b.
“enhancement of H3K4me3 was found in postmortem brain tissue (BA10) in MDD165: the enriched H3K4me3 was found at transcriptional start sites of synapsin 1, relevant to increased expression of synapsin 1a and synapsin 1b.”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [165]
The results section on H3K4me3 enrichment (page not supplied) reports enrichment at the shared SYN1a/SYN1b promoter in MDD, and the expression results report increased expression of both variants in MDD. The tissue was post-mortem BA10. But the paper found no significant correlation between SYN1 expression and H3K4me3 enrichment, so it does not support the implied link between them. (LLM, conf=0.91)
Experimental — accuracy not yet measuredEnrichment of trimethylated H3K4 at the SYN1 promoter was reported in postmortem prefrontal cortex of MDD patients.
“Another study of histone modifications in postmortem prefrontal cortex (PFC) of MDD patients reported enrichment of trimethylated H3K4—a modification generally associated with transcriptional activity—at the SYN1 promoter.”
From Epigenetics and depression (2019) · cites this paper as [20]
Variable H3-K4 methylation of synapsin genes has been shown to give rise to altered expression patterns in bipolar disorder and major depression.
“Variable H3-K4 methylation of synapsin genes has been shown to give rise to altered expression patterns in bipolar disorder and major depression29”
From Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways (2015) · cites this paper as [29]
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“104 Interestingly, enhancement of H3K4me3 was found in postmortem brain tissue (BA10) in MDD 165 : the enriched H3K4me3 was found at transcriptional start sites of synapsin 1, relevant to increased expression of synapsin 1a and synapsin 1b.”
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- Authors
- Cruceanu, C., Alda, M., Nagy, C., Freemantle, E., Rouleau, G. A., & Turecki, G.
- Affiliations
- Douglas Mental Health University Institute (CA)
- Dalhousie University (CA)
- Centre Hospitalier de l’Université de Montréal (CA)
- Corresponding author
- Turecki, Gustavo
- Venue
- International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-05-09
- Volume
- 16
- Issue
- 2
- Pages
- 289-299
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- PMC
- PMC3564952
- OpenAlex
- W2140687548
- Cited by
- 93
- References
- 62
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 9 · 2023: 6 · 2022: 7 · 2021: 10 · 2020: 7 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 7 · 2015: 10 · 2014: 9 · 2013: 2 · 2012: 2
- FWCI
- 5.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (64410)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- synapsin, synapsin I, alternative splicing, splice variants, histone modifications, epigenetic regulation, bipolar disorder, major depressive disorder, mood disorders, postmortem brain, gene expression
- MeSH terms
- Histone Methyltransferases, Adult, Analysis of Variance, Bipolar Disorder, Brain, Major Depressive Disorder, Female, Histones, Humans, Male, Methylation, Middle Aged, Probability, Promoter Regions, Genetic, Histone-Lysine N-Methyltransferase, Statistics as Topic, Gene Expression, Synapsins, Epigenesis, Genetic, Chromatin Immunoprecipitation
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