Erasing m6A-dependent transcription signature of stress-sensitive genes triggers antidepressant actions
Open accessAbstract
Emerging evidence has shown that stress responsivity and psychiatric diseases are associated with alterations in N6-methyladenosine (m6A) mRNA epigenetic modifications. Fat mass and obesity-associated protein (FTO) is an m6A demethylase that has been linked to increased body mass and obesity. Here, we show that tricyclic antidepressants (TCAs) with weight-gain side effects, such as imipramine and amitriptyline, directly increased FTO expression and activated its epigenetic function in the ventral tegmental area (VTA). VTA-specific genetic disruption of FTO increased stress vulnerability and abolished the antidepressant activity of TCAs, whereas erasing m6A modification in the VTA by FTO overexpression or cycloleucine led to significant antidepressant activity. Mechanistically, both transcriptome sequencing and quantitative PCR revealed that overexpression of FTO in the VTA decreased the transcription of stress-related neuropeptides, such as cocaine- and amphetamine-regulated transcript peptide and urocortin, in the social defeat model, which was mimicked by imipramine, suggesting an m6A-dependent transcription mechanism of stress-related neuropeptides may underlie the responses to antidepressant. Collectively, our results demonstrate that inhibiting m6A-dependent transcription of stress-related genes may work as a novel antidepressant strategy and highlight a previously unrecognized activator of FTO-dependent epigenetic function that may be used for the treatment of other neurological diseases.
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Tricyclic antidepressants increase FTO expression and activate its epigenetic function in the VTA.
“Tricyclic antidepressants increase FTO expression and activate its epigenetic function in the VTA; eliminating m6A modification in the VTA is postulated to cause an antidepressant effect.372”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [372]
Eliminating m6A modification in the VTA is postulated to cause an antidepressant effect.
“eliminating m6A modification in the VTA is postulated to cause an antidepressant effect.372”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [372]
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“372 Moreover, activation of FTO in the hippocampus relieves depression-like behaviors and reduces the density of dendritic spines and the number of branches in mice induced by chronic restraint stress, improving the synaptic plasticity.”
BackgroundNiu, J., Wang, B., Wang, T., & Zhou, T. (2022) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32892 · Cited by 23 · see citing works
- Authors
- Wu, P.-F., Han, Q.-Q., Chen, F.-F., Shen, T.-T., Li, Y.-H., Cao, Y., Chen, J.-G., & Wang, F.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Corresponding author
- Wang, Fang
- Venue
- Neurobiology of Stress
- Publisher
- Elsevier BV
- Published
- 2021-11
- Volume
- 15
- Pages
- 100390
- ISSN
- 2352-2895 (ISSN-L)
- PMC
- PMC8430387
- OpenAlex
- W3198508678
- Cited by
- 32
- References
- 73
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 5 · 2023: 7 · 2022: 7
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neurobiology of Stress (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA modifications and cancer
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- N6-methyladenosine, m6A RNA methylation, FTO, tricyclic antidepressants, antidepressant mechanism, ventral tegmental area, stress vulnerability, social defeat, cocaine- and amphetamine-regulated transcript, urocortin, imipramine, amitriptyline, cycloleucine
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