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Review
. 2021 Jan 22:11:601868.
doi: 10.3389/fgene.2020.601868. eCollection 2020.

Genetic and Epigenetic Consequence of Early-Life Social Stress on Depression: Role of Serotonin-Associated Genes

Tomoko Soga  1 , Chuin Hau Teo  1 , Ishwar Parhar  1
Affiliations
Review

Genetic and Epigenetic Consequence of Early-Life Social Stress on Depression: Role of Serotonin-Associated Genes

Tomoko Soga et al. Front Genet. .

Abstract

Early-life adversity caused by poor social bonding and deprived maternal care is known to affect mental wellbeing and physical health. It is a form of chronic social stress that persists because of a negative environment, and the consequences are long-lasting on mental health. The presence of social stress during early life can have an epigenetic effect on the body, possibly resulting in many complex mental disorders, including depression in later life. Here, we review the evidence for early-life social stress-induced epigenetic changes that modulate juvenile and adult social behavior (depression and anxiety). This review has a particular emphasis on the interaction between early-life social stress and genetic variation of serotonin associate genes including the serotonin transporter gene (5-HTT; also known as SLC6A4), which are key molecules involved in depression.

Keywords: 5-HT receptor; depression; epigenetic modification; serotonin; social stress.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
DNA methylation of CpG islands in the genetic code silences expression of a gene after early-life social stress exposure. Methylation occurs by a methyltransferase (DNMT3) transferring a methyl group to cytosine, and when occurring on a transposable element has the effect of repressing gene transcription related to that element. 5-HTRs, 5-HT receptors; SERT, serotonin transporter; TPH2, tryptophan hydroxylase 2; MAO-A, monoamine oxidase A.
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References

    1. Abdolmaleky H. M., Nohesara S., Ghadirivasfi M., Lambert A. W., Ahmadkhaniha H., Ozturk S., et al. (2014). DNA hypermethylation of serotonin transporter gene promoter in drug naïve patients with schizophrenia. Schizophr. Res. 152, 373–380. 10.1016/j.schres.2013.12.007, PMID: - DOI - PMC - PubMed
    1. Albert P. R., Le Francois B., Vahid-Ansari F. (2019). Genetic, epigenetic and posttranscriptional mechanisms for treatment of major depression: the 5-HT1A receptor gene as a paradigm. J. Psychiatry Neurosci. 44, 164–176. 10.1503/jpn.180209, PMID: - DOI - PMC - PubMed
    1. Anguelova M., Benkelfat C., Turecki G. (2003). A systematic review of association studies investigating genes coding for serotonin receptors and the serotonin transporter: I. affective disorders. Mol. Psychiatry 8, 574–591. 10.1038/sj.mp.4001328, PMID: - DOI - PubMed
    1. Bendre M., Granholm L., Drennan R., Meyer A., Yan L., Nilsson K. W., et al. (2019). Early life stress and voluntary alcohol consumption in relation to Maoa methylation in male rats. Alcohol 79, 7–16. 10.1016/j.alcohol.2018.11.001, PMID: - DOI - PubMed
    1. Benedetti F., Radaelli D., Poletti S., Locatelli C., Dallaspezia S., Lorenzi C., et al. (2011). Association of the C(−1019)G 5-HT1A promoter polymorphism with exposure to stressors preceding hospitalization for bipolar depression. J. Affect. Disord. 132, 297–300. 10.1016/j.jad.2011.02.024, PMID: - DOI - PubMed

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