Genetics and epigenetics in the psychology classroom: How to teach what your textbook doesn’t
By Jessica Habashi, PhD, Utah State University Brigham City Regional Campus and Kristin H. Whitlock, MEd, Viewmont High School, Bountiful, Utah
Most psychology students come to class with a basic understanding of genetics. They know that how they look, how their bodies function and, to some extent, how they act or what diseases they may develop are determined by their DNA; however, few of them have a clear understanding of what DNA is, where it’s found in the body and how it defines us as individuals. Many introductory psychology textbooks provide an inadequate amount of description in this area; therefore, teachers may shy away from including genetic concepts in their courses for fear they cannot do them justice.
Compounding this problem is the rise of epigenetics (the study of how variation in inherited traits can originate through means other than variations in DNA). For some teachers, epigenetics is too new and may not be in their textbooks; thus, they may think it’s not a subject worth broaching in their classes, lest they be faced with questions they can’t answer. Failure to teach psychology students about both genetics and epigenetics, however, means ignoring the latest research on nature versus nurture and not informing students about the next generation of tests and treatments for mental disorders. The goals of this article are to provide psychology teachers with a basic understanding of genetics and epigenetics, and to provide resources for use in lecture and hands-on activities to increase students’ grasp of these fields.
DNA and genes: The basics
Essential to our understanding of genetics is an understanding of DNA and how it influences our traits. DNA, or deoxyribonucleic acid, is a molecule (a combination of chemical elements held together in a specific way) found in nearly all of the 50 trillion cells in the body. (Only mature red blood cells lack DNA.) Structurally, DNA resembles a twisted ladder (double helix; for review, go to the University of Utah Genetic Science Learning Center DNA to Protein website and click “What is DNA?”). A single DNA molecule is only 2.5 billionths of a meter across, so it’s impossible to view with the naked eye. It’s relatively easy, however, to purify DNA en masse from human cells so that it can be viewed in a test tube. It’s also inexpensive and takes little time to do; thus, it’s a great in-class activity. The DNA Necklace Kit from Carolina Biological Supply Company (#211138) allows students to isolate DNA from their own cheek cells in as few as 45 minutes — and they get to take it home. The DNA in our cells doesn’t exist as a single molecule. Instead, our cells contain multiple DNA molecules (46 in most cells), commonly referred to as chromosomes.
Every chromosome is subdivided into regions called genes. Using our image of DNA as a ladder-shaped molecule, the first five rungs might correspond to one gene, while the next five rungs might correspond to a second gene. DNA molecules, however, are much longer than the tiny compartment inside our cells (called a nucleus) where they are located (for a summary of cell structure, see the National Institute of General Medical Sciences Inside the Cell website): the 46 chromosomes in a single cell would stretch 2 m end-to-end, but a single nucleus is only about 5 millionths of a meter across (Annunziato, 2008; National Institute of General Medical Sciences, p. 11). To get around this, DNA molecules wrap around clusters of proteins called histones. The resulting compaction of the DNA enables it to fit easily inside the nucleus. Understanding DNA, however, means more than considering its structure — we also need to discuss its function.
Proteins: The link between DNA and our traits
There is a clear relationship between genes and traits, and the bridge between these two concepts is protein. Proteins, made of small molecules called amino acids (Figure 1 (PDF, 169KB)), carry out numerous functions in the body. For example, collagen is a protein found in skin, bones and cartilage that helps withstand stretching. Antibodies are immune system proteins that help fight infections. Also, the oxygen we inhale is delivered to the cells of the body by a protein found in our red blood cells known as hemoglobin. Each of the 20,000-25,000 genes included in our genome (the sum total of your DNA) encodes (carries the instructions for producing) a single type of protein (International Human Genome Sequencing Consortium, 2004).
How does a gene carry instructions for making a protein? DNA molecules are polymers composed of small units called nucleotides, which are linked together like the cars in a train, and every three nucleotides in a gene specify a particular amino acid. Expressing a gene (producing the protein it encodes) is a two-step process (Figure 2 (PDF, 169KB)). In the first step, called transcription, cellular proteins create a temporary copy of a gene known as a messenger RNA (or mRNA) molecule. This mRNA molecule moves out of the nucleus and into the fluid-filled interior of the cell known as the cytosol (Figure 3 (PDF, 169KB)). Here, the mRNA molecule will undergo the second step in protein production, called translation. During translation, molecules known as transfer RNA work with small structures called ribosomes to read the mRNA molecule, three nucleotides at a time, to assemble the protein product (Figure 4 (PDF, 169KB)). Use of the term translation is appropriate because as the process proceeds, the instructions for making a protein, which were written in the language of nucleotides during transcription, are switched to the language of amino acids.
Using the one-gene-one-protein model described above, many diseases may be understood as originating with some alteration of our DNA. For example, radiation and certain viruses can damage our DNA such that transcription and translation produce a protein that either doesn’t work well or doesn’t work at all, thereby negatively impacting cellular function. For example, sickle cell anemia (a condition in which the body lacks enough healthy red blood cells) has been shown to be caused by a single nucleotide change in a gene that produces hemoglobin. A visual representation of the changes that occur at the DNA, protein, and cellular levels in sickle cell anemia can be found at Understanding Evolution website.
Though an understanding of genetics and the genome is essential to understanding the workings of the human body, it is an incomplete view of gene expression and heredity (the passing of traits from parents to offspring). For a more comprehensive view, we need to address a second set of instructions that influences how our DNA is handled: the epigenome.
The epigenome: A second means of controlling gene expression
The prefix “epi” means above, while “genome” refers to all of an individual’s genetic information. Thus, the epigenome is information about us that is stored outside of our DNA — just outside of it, as it happens. Specifically, special chemicals called tags can become attached to the nucleotides of our DNA or to our histone proteins, and, depending on the nature of these tags, specific genes can either be silenced (prevented from being expressed as protein) or pushed to become more active (so that the abundance of a particular protein in our cells will rise). An excellent way to introduce your students to this topic is through a directed reading. For an accessible article that covers epigenetics in a variety of contexts (e.g., fruit flies, rats and humans), see “Why Your DNA Isn’t Your Destiny,” by John Cloud.
Tags that shut down, or silence, the expression of a gene include methylgroups. For example, the methylation (attachment of methyl groups) of tumor suppressor genes in cells infected with Epstein-Barr virus inactivates those genes, thereby promoting tumor formation (Kaneda et al., 2012). A second major type of tag, called an acetyl group, may be added to our histone proteins. The addition of acetyl tags (acetylation) weakens DNA-histone binding, making the DNA at that location more available to the proteins that drive transcription (Sapolsky, 2004). For example, garlic has been shown to increase the acetylation (and therefore the activity) of anti-cancer genes (Druesne-Pecollo and Latino-Martel, 2011).
Studies have revealed that changes in the epigenome do not affect our DNA directly. That is, a change in the degree of methylation of a gene will not affect its nucleotides (i.e., instructions). It only affects the degree to which that gene will be translated into protein. Understanding how this occurs requires that we look again at transcription. To create an mRNA molecule, special enzymes in our cells must become attached to a gene at its starting point. When a gene is lightly methylated, these enzymes can access the starting point easily, whereas, in a heavily methylated gene, the DNA is more tightly wound, such that the starting point of the gene is more difficult to access.
An interactive animation to help students visualize how the degree of methylation can alter gene expression (i.e., how much protein is produced) can be found at the University of Utah Genetic Science Learning Center Gene Control website. Increasing the number of epigenetic tags by turning a dial alters how much green fluorescent protein is produced in a cell. This animation is particularly effective because it shows the density of tags on the gene itself, the abundance of mRNA molecules produced from the gene and the amount of protein produced through translation; moreover, the change in gene expression as the number of tags varies is presented as a change in volume. A great take-home assignment for students to get them thinking about the factors in their own environment that may be influencing their epigenome is the “Your Environment, Your Epigenome” worksheet, Students can be assigned a 24-hour period during which to monitor the foods they eat, how much exercise they do and their anxiety levels.
Epigenetics and psychology
Much current literature in epigenetics and psychology consists of studies of rats or mice, and these studies have provided strong evidence of the impact of environment on the epigenome. For example, one study showed that high levels of handling, including licking and grooming, by rat mothers altered the methylation and acetylation patterns in their pups within the first week of life and that these epigenetic changes occurred specifically within the hippocampus and resulted in lower circulating levels of stress hormones (Weaver et al., 2004). They also showed that cross-fostering (i.e., transferring pups from their biological mother to a foster mother with an opposite handling style) caused the pups to acquire an epigenetic pattern that was consistent with the mothering style of the foster mother. Further, the researchers took rats that had been raised with little handling and administered drugs to them that induced the types of epigenetic changes seen in pups with regular handling. Interestingly, the rats that received the drugs exhibited the same features as their adult counterparts who had been handled regularly as pups, including lower stress hormone levels.
The second major surprise of epigenetics is “transgenerational transmission.” A notable demonstration of this concept came from a study of mice raised in an “enriched environment,” meaning one that included high levels of exposure to novel objects (e.g., cardboard boxes and pet toys), interactions with other animals and opportunities for exercise (Arai et al., 2009). Compared to control mice, the enriched mice exhibited enhanced long-term potentiation (LTP), and the offspring of these animals exhibited the same enhancement in LTP — even if they had not been raised in an enriched environment. While this effect was relatively short lived (it did not transfer to the second generation), it showed that changes to the epigenome can be transmitted to offspring.
For biologists, the fact that epigenetic tags can be passed from parent to offspring is startling. After all, Charles Darwin held that populations evolve, but individuals don’t. Thus, epigenetics has raised interest in the work of Jean-Baptiste Lamarck, a French naturalist who proposed his own theory of evolution in 1809 (the year Darwin was born). Lamarck proposed that changes in an organism’s environment would provoke a change in behavior, which would increase or decrease the use of certain body structures, and this change in usage would affect the organism’s anatomy (e.g., increased use would cause that part of the body to enlarge). Lamarck argued that such changes were heritable. Interestingly, Darwin acknowledged that Lamarck’s idea of use/disuse as a driving force in evolution may have some merit, and both men agreed that adaptive changes in organisms can occur in response to environmental pressure over time (University of California Museum of Paleontology, n.d.). While some who do not support evolution have pounced on epigenetics as a way to try to discredit Darwin, epigenetics should not be considered an alternative to evolution. New traits will always be subject to natural selection, whether they arise through epigenetic means or are purely genetic in origin (Zurich, 2009).
Other studies have demonstrated a link between epigenetic tags and mental illness in humans. For example, in a recent study by Melas et al. (2012), genome-wide and local (gene-specific) changes in methylation level were found in the leukocytes (white blood cells) of individuals with schizophrenia compared with normal controls. While the significance of these findings remains to be elucidated (e.g., does the change in methylation in schizophrenics reflect the cause of the disease or is it an outcome of chemical treatment), they may be used to produce a blood test for schizophrenia. In such a test, clinicians would examine the methylation status of an individual’s leukocytes.
Increasing focus is being placed on the potential for epigenetic modification through drug treatment, and recent work has shown that some drugs in use for the treatment of mental illness may affect the epigenome. For example, the anti-depressant Tranylcypromine (brand name Parnate) is a monoamine oxidase (MAO) inhibitor that has been shown to affect a monoamine oxidase as well as a demethylase (an enzyme that decreases gene methylation) (McGowan, Meaney, and Szyf, 2008). Interestingly, lithium, used to treat bipolar disorder, has been shown to target the same demethylase as Tranylcypromine, reinforcing the idea that the epigenome is a reasonable target for drug design (Kubota, Miyake, and Hirasawa, 2012).
Beyond the use of medicines, individuals may be able to exert direct control over their epigenome simply by modifying their diet or exposure to certain chemicals. For example, bisphenol A (BPA), a compound used to make certain plastics, was shown to decrease the methylation of a specific gene in mice, while a supplement of folic acid was shown to prevent that change (Dolinoy, Huang, and Jirtle, 2007). As knowledge of the effects of lifestyle on the human epigenome increases, the way that nutritionists advise their clients could change. For an excellent discussion of nutrition and the epigenome, go to the University of Utah Genetic Science Learning Center Nutrition and the Epigenome website or the Epigenetics? website.
It’s easy to get excited about epigenetics, given the promise of new drugs or changes in lifestyle as a prescription for avoiding or treating certain diseases; however, the influence of genetic factors (such as mutations) in human health should not be minimized. In fact, there is currently no consensus as to whether genetic or epigenetic effects are the major causative factor in mental disorders, including autism spectrum disorders (Eapen, 2011).
Given the link between biology and psychology, it is important for teachers of psychology to incorporate biological principles, including genetics and epigenetics, into their courses. Such topics are indispensable to our understanding of the relationship between nature and nurture. We encourage teachers of psychology to take advantage of the many resources available online and integrate them into their lessons.
Annunziato, A. (2008). DNA packaging: Nucleosomes and chromatin. Nature Education, 1(1).
Arai, J.A., Li, S., Hartley, D.M., & Feig, L.A. (2009). Transgenerational rescue of a genetic defect in long-term potentiation and memory formation by juvenile enrichment. The Journal of Neuroscience, 29(5), 1496 -1502.
Dolinoy, D.C., Huang, D., & Jirtle, R.L. (2007). Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proceedings of the National Academy of Sciences of the United States of America, 104(32), 13056-13061.
Druesne-Pecollo, N., & Latino-Martel, P. (2011). Modulation of histone acetylation by garlic sulfur compounds. Anticancer Agents in Medicinal Chemistry, 11(3), 254-259.
Eapen, V. (2011) Genetic basis of autism: Is there a way forward? Current Opinion in Psychiatry, 24(3), 226-236.
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Kaneda, A., Matsusaka, K., Aburatani, H., & Fukayama, M. (2012). Epstein-Barr virus infection as an epigenetic driver of tumorigenesis. Cancer Research, 72(14), 3445-50.
Kubota, T., Miyake, K., & Hirasawa, T. (2012). Epigenetic understanding of gene-environment interactions in psychiatric disorders: a new concept of clinical genetics. Clinical Epigenetics, 4(1), 1-8.
McGowan, P.O., Meaney, M.J., & Szyf, M. (2008). Diet and the epigenetic (re)programming of phenotypic differences in behavior. Brain Research, 1237, 12-24.
Melas, P.A., Rogdaki, M., Ösby, U., Schalling, M., Lavebratt, C., & Ekström, T.J. (2012). Epigenetic aberrations in leukocytes of patients with schizophrenia: Association of global DNA methylation with antipsychotic drug treatment and disease onset. FASEB Journal, 26(6), 2712-2718.
Sapolsky, R.M. (2004). Mothering style and methylation. Nature Neuroscience, 7(8), 791-792.
Weaver, I.C.G., Cervoni, N., Champagne, F.A., D'Alessio, A.C., Sharma, S., Seckl, J.R., Dymov, S., Szyf, M., & Meaney, M.J. (2004). Epigenetic programming by maternal behavior. Nature Neuroscience, 7, 847-54.
Zurich, E.T.H. (2009, April 13). Epigenetics: DNA isn’t everything. ScienceDaily. Retrieved August 21, 2012, from http://www.sciencedaily.com /releases/2009/04/090412081315.htm
About the authors
Jessica Habashi, PhD, is a biology lecturer at Utah State University’s Brigham City Regional Campus. She teaches courses in human physiology, elementary microbiology, and biology and the citizen. She received her PhD from Yale University.
Kristin H. Whitlock, MEd, teaches Advanced Placement (AP) psychology and sports psychology at Viewmont High School in Bountiful, Utah. She currently serves as the AP Psychology College Board advisor, is a member of the Test Development Committee, and is a question leader at the annual AP psychology readings. She has served as chair of the APA High School Psychology Standards Working Group and served as member-at-large for the Teachers of Psychology in Secondary Schools (TOPSS). Mrs. Whitlock was the recipient of the Moffett Memorial Teaching Award, a Presidential Citation from the APA, and the TOPSS Excellence in Teaching Award.