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How do environments talk to genes?

Nature Neuroscience volume 16, pages 2–4 (2013)Cite this article

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A report elucidates the widely recognized, but poorly understood, concept of gene-environment interaction, finding a molecular mechanism in the case of post-traumatic stress disorder: demethylation of a glucocorticoid response element in the stress response regulator FKBP5 that depends on both the risk allele and childhood trauma.

The term gene-environment interaction was coined by epidemiologists who found cases in which the lifetime risk of suffering from a disease for someone who carries a risk allele is influenced by early exposure to particular environments. A classic example in neurobehavior was the discovery that the association of a polymorphism in the promoter region of the serotonin transporter gene (SLC6A4, also known as 5-HTT) with depression is influenced by stressful life events1. But although the idea of gene-environment interaction emerged as a quantitative description of epidemiological observations, the concrete biochemical meaning of such an interaction has remained elusive. How do environments interact with genes? Is there a molecular chain of events linking environment and gene, or is the interaction just a statistical construct? In this issue of Nature Neuroscience, Klengel et al.2 show that the risk allele of the stress response regulator FKBP5 is preferentially demethylated in children exposed to trauma. This demethylation, which persists into adulthood, enhances expression of FKBP5, resulting in a higher risk of developing post-traumatic stress disorder (PTSD).

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Figure 1: A model mechanism for gene-environment interaction.

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  1. Moshe Szyf is in the Department of Pharmacology and Therapeutics, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.,

    Moshe Szyf

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  1. Moshe Szyf
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Correspondence to Moshe Szyf.

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Szyf, M. How do environments talk to genes?. Nat Neurosci 16, 2–4 (2013). https://doi.org/10.1038/nn.3286

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