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Genomics Web Page

Image courtesy of Psychcentral.


What is psychogenomics?

How does your DNA make you feel? This probably seems like absurd question, given that is it unlikely you can feel your DNA replicating or your transcription factors busy at work. But it is not an absurd question given all the recent data afforded to us by the Human Genome Project. More and more data is amassing that indicates a persons genome has a profound impact on their psychology, and therefor has a strong impact on their behavior, decision making, thoughts, and emotions.
You might feel uncomfortable or perhaps relieved by the notion that a humans psychological health and composition is determined the moment their genome comes into existence. But alas, this is not the case. Your DNA, the entirety of which comprises your genome, is still very much malleable to its environment. We often hear this in regards to other types of inherited characteristics, and this is very much the case in regards to psychogenomics.The nature versus nurture argument is alive and well in the field of psychogenomics! (Robinson 2004). It is the goal of psychogenomics to use the information provided by whole genome sequencing to gain a better understanding of this complicated relationship of environment and genome, with the hope of gaining a better understanding of human psychology, whether it be what we characterize as normal or as diseased (i.e. alcoholism, schizophrenia, depression).

Behavioral Genetics

This field of psychogenomics stems from behavioral genetics, which was founded by Sir Francis Galton (the cousin of Charles Darwin) in the late 1800’s. He was interested in understanding intelligence and whether genetics or environment influence had a greater effect on an individual’s intellectual development. Relying on twin studies he was able to determine that genetics had a greater effect on level of intelligence than upbringing (Simmons 2008). This data opened the door to studies investigating all things related to human psychology and behaviors. Often these topics are around parts of human behavior many had always considered under their control (intelligence, mating behavior, motivation) but have been to shown to really be product of our genomes.

Behavioral genetics and psychogenomics differ in their approach to understanding the relation between behavior and our DNA. Where geneticists look at a specific gene and its inheritance, genomics takes a more broader view. It works backwards, examining the genome as a whole, both functional and nonfunctional segments of DNA, searching for clues to understand gene expression and its regulation far beyond just whether a gene just exists or not. This often involves looking for variation in Single Nucleotide Polymorphisms (SNPs). SNPs are an excellent producer of variation in genetic code found between individuals. SNPs are an example of how gene expression is more complicated than the one gene, one trait experience many of us might be used to. SNPs lay within or near genes and have the ability to regulate gene functioning. A single change of nucleotide in a sequence can therefor can have significant role in producing genetic differences between individuals.
You might be wondering what psychogenomics covers. It is a broad area as it often overlaps with areas of behavior, these are include but are not limited to:

Now we will review three examples where comparing of whole genomes through genomics lead to the discovery of important factors that create variations in psychology and behavior. They will demonstrate to you how genomics and behavior intersect to form psychogenomics.


Mating Behavior in Voles

Figure 2. In the praire vole (b) expression is seen in the diagonal band while in the montan vole (a) it is located in the lateral sterna. When comparing injection of cerebral spinal fluid to AVP (c) the praire vole only shows the monogamous behavior whereas the montain vole does not. Figure courtesy of

Image courtesy of Nature Education.

The vole is a small mouse like mammal that has a very interesting mating behavior that differs from many other mammals and even within their own genus. Voles, specifically prairie moles (Microtus ochrogaster), are monogamous while montane voles (Microtus montanus) are not. And this is not due to true love between the voles; it is actually a product of a polymorphism in the promoter of the V1a receptor gene. When a male mates with a female, AVP is released in his brain and binds to the V1a receptor. Both voles have this receptor, but it is patter of expression in the brain that alters their mating and paternal behavior. By upping expression of the V1a receptor in the promiscuous non-paternal vole (C. montanus) the vole exhibits monogamous and paternal behavior. However, when this is done in the montane vole, there is no change in behavior. Uping the hormone with no reaction supports the assertion that the differences in the receptort. It is thought that polymorphisms in the promoter gene for the receptor alter the location of receptor expression.(Robinson, 2004). Though most mammals have this gene, it is the difference in expression by way of the promoter of this gene that makes such remarkable alterations to the motivation and behavior of the vole.


Schizophrenia is a highly heritable disease that is often difficult to diagnose and treat. Treatment involves both therapy and pharmaceutical intervention and must continue lifelong. Understanding the heredity of the disease has been of great importance since it was determined that schizophrenia is definitely genetically related, though how is much more complicated. It is not one a one gene one disease type of illness, but is much more involved in its genetic origin. By comparing genomes of schizophrenic patients to non-schizophrenic patients, it was determined that 15% of the individuals shared mutations across a large stretch of genes that are related to brain development, energy metabolism, and synaptic function. Variation of these micro deletions and micro duplications (forming these mutations) are existed between the individuals’ genomes. In 2008 Walsh, T. et al found significant variation in genome structure might be related age of onset and when compared to the control and later onset patients. The use of genome comparisons allowed researchers to move toward understanding a disease that breaks the laws that many think diseases follows, meaning that Schizophrenia is not the result of a single gene, but rather many unique mutations across the genome that differ from patient to patient. (Simmons, 2008).



Addiction is a disease that has the ability to take over a human’s brain and dictate their every behavior. It has been shown that genetics may be responsible for 40-60% of an individuals’ propensity to become an addict to drugs and alcohol. Genomics is going to be of great interest in this field because of the ability to look at the entirety of DNA. Prior research as indicated that when dealing with neuropsychiatric disorders the gene or genes involved are often not those ever imagined to be responsible. Whole genome sequencing allows comparisons of genomes to be done between addicts and non-addicts to look for changes in DNA expression during and after exposure to the addictive property. It can also be helpful in understanding what changes in expression cause relapse and withdrawal (Nestler, Eric J. & David Landsman 2001)


Where is psychogenomics going?

The ultimate goal of understanding behavior, both the normal and abnormal, is to be able to treat and prevent disease. The brain is one of the great mysteries still left for us to unravel, and perhaps the use of genomics might be the tool we need to do so. Given the complexity of the brain, and the interactions that our genome has with the environment, it is likely that this area of Biology will continue to defy common rules and conceptions we have held. 



Nestler, Eric J. & David Landsman. Learning about addiction from the genome. Nature 409: 834-835 (2001).

Robison, Gene E. Beyond Nature and Nurture. Science 304: 397-399 (2004).

Simmons, Danielle. Behavioral Genomics. Nature Education 1: 54 (2008).
Walsh et al. Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia. Science 320: 539-543 (2008).


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