Gene–environment interaction

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Gene–environment interaction (or genotype–environment interaction or G×E) is the phenotypic effect of interactions between genes and the environment.

Gene–environment interaction is exploited by plant and animal breeders to benefit agriculture. For example, plants can be bred to have tolerance for specific environments, such as high or low water availability. The way that trait expression varies across a range of environments for a given genotype is called its norm of reaction.

In genetic epidemiology it is frequently observed that diseases cluster in families, but family members may not inherit disease as such. Often, they inherit sensitivity to the effects of various environmental risk factors. Individuals may be differently affected by exposure to the same environment in medically significant ways. For example, sunlight exposure has a much stronger influence on skin cancer risk in fair-skinned humans than in individuals with an inherited tendency to darker skin.[1]

Naive nature versus nurture debates assume that variation in a given trait is primarily due to either genetic variability or exposure to environmental experiences. The current scientific view is that neither genetics nor environment are solely responsible for producing individual variation, and that virtually all traits show gene–environment interaction.[2][3][4] Evidence of statistical interaction between genetic and environmental risk factors is often used as evidence for the existence of an underlying mechanistic interaction.


There are two different conceptions of gene–environment interaction. Tabery[5] has labeled them biometric and developmental interaction, while Sesardic[6] uses the terms statistical and commonsense interaction.

The biometric (or statistical) conception has its origins in research programs that seek to measure the relative proportions of genetic and environmental contributions to phenotypic variation within populations. Biometric gene–environment interaction has particular currency in population genetics and behavioral genetics.[5] Any interaction results in the breakdown of the additivity of the main effects of heredity and environment, but whether such interaction is present in particular settings is an empirical question. Biometric interaction is relevant in the context of research on individual differences rather than in the context of the development of a particular organism.[7]

Developmental gene–environment interaction is a concept more commonly used by developmental geneticists and developmental psychobiologists. Developmental interaction is not seen merely as a statistical phenomenon. Whether statistical interaction is present or not, developmental interaction is in any case manifested in the causal interaction of genes and environments in producing an individual's phenotype.[7]


In some combinations of environments and genotypic ranges, heritability can be 100% even while group differences are completely environmental. For heritability to be 100%, random variation in expression must not occur.
  1. A classic example of gene–environment interaction is Cooper and Zubek's experiment on maze-running ability in rats. They produced a remarkable difference in maze running ability in two selected lines after seven generations of selecting "bright" and "dull" lines by breeding the best and worst maze running rats with others of similar abilities. The difference between these lines was clearly genetic since offspring of the two lines, raised under identical typical lab conditions, performed differently. This difference disappeared in a single generation, if those rats were raised in an enriched environment with more objects to explore and more social interaction.[8] This result suggests that maze running ability is the product of a gene-by-environment interaction; the genetic effect is only seen under some environmental conditions. However, Cooper and Zubek warned against overinterpreting the results due to a potentially problematic ceiling effect in the maze running task used. Sesardic has noted that the study has never been replicated.[9]
  2. Seven genetically distinct yarrow plants were collected and three cuttings taken from each plant. One cutting of each genotype was planted at low, medium, and high elevations, respectively. When the plants matured, no one genotype grew best at all altitudes, and at each altitude the seven genotypes fared differently. For example, one genotype grew the tallest at the medium elevation but attained only middling height at the other two elevations. The best growers at low and high elevation grew poorly at medium elevation. The medium altitude produced the worst overall results, but still yielded one tall and two medium-tall samples. Altitude had an effect on each genotype, but not to the same degree nor in the same way.[10]
  3. Phenylketonuria (PKU) is a human genetic condition caused by mutations to a gene coding for a particular liver enzyme. In the absence of this enzyme, an amino acid known as phenylalanine does not get converted into the next amino acid in a biochemical pathway, and therefore too much phenylalanine passes into the blood and other tissues. This disturbs brain development leading to mental retardation and other problems. PKU affects approximately 1 out of every 15,000 infants in the U.S. However, most affected infants do not grow up impaired because of a standard screening program used in the U.S. and other industrialized societies. Newborns found to have high levels of phenylalanine in their blood can be put on a special, phenylalanine-free diet. If they are put on this diet right away and stay on it, these children avoid the severe effects of PKU.[11]
  4. A functional polymorphism in the monoamine oxidase A (MAOA) gene promoter can moderate the association between early life trauma and increased risk for violence and antisocial behavior. Low MAOA activity is a significant risk factor for aggressive and antisocial behavior in adults who report victimization as children. Persons who were abused as children but have a genotype conferring high levels of MAOA expression are less likely to develop symptoms of antisocial behavior.[12] These findings must be interpreted with caution, however, because gene association studies on complex traits are notorious for being very difficult to confirm.[13]

Medical significance[edit]

  • Doctors are interested in knowing whether disease can be prevented by reducing exposure to environmental risks. Gene–environment interaction means that some people carry genetic factors that confer susceptibility or resistance to a certain disorder in a particular environment. It has been argued that there may be significant public health benefits in using genetic information to stratify the allocation of environmental interventions that prevent disease,[14] although this viewpoint is not universally held.[15]
  • Pharmacogenetics is the study of genetic variation that causes different people to respond to the same drugs in different ways. The clinical importance of pharmacogenetics comes from the possibility that drug treatment can be made safer and more effective when the patient's genotype is known. Pharmacogenetic studies can be considered studies of gene–environment interaction, with drug treatment as the environmental variable.

Timing of environmental effects[edit]

The popular description of an animal being "born that way" does not necessarily discriminate genetic from environmental effects. In viviparous animals, such as humans, environmental influences may act during either pre- or post-natal development; similarly environmental influences may act before and after hatching to affect development in oviparous animals. Environmental influences in utero may be as strong and lasting as genetic or post-natal environmental influence. There is increasing study of environmental influences affecting genetic factors directly but nonheritably; see the Epigenetics article for a detailed discussion.

See also[edit]


  1. ^ Green A; Trichopoulos D (2002). Skin cancer. In Textbook of Cancer Epidemiology (eds Adami, H., Hunter, D. & Trichopoulos, D.) pp. 281–300. Oxford: Oxford University Press. 
  2. ^ Ridley, M. (2003) Nature via Nurture: Genes, Experience, & What Makes Us Human. Harper Collins. ISBN 0-00-200663-4
  3. ^ Rutter, Michael. (2006) Genes and Behavior: Nature-Nurture Interplay Explained Oxford, UK: Blackwell Publishers
  4. ^ Cuhna, Flavio and James J. Heckman Investing in Our Young People, in A. J. Reynolds, A. Rolnick, M. M. Englund, & J. Temple, eds., Cost-effective Early Childhood Programs in the First Decade: A Human Capital Integration, Chapter 18, pp. 381-414, 2010, New York: Cambridge University Press
  5. ^ a b Tabery, J. (2007). Biometric and developmental gene-environment interactions: Looking back, moving forward. Development and Psychopathology, 19, 961–976.
  6. ^ Sesardic, N. (2005). Making sense of heritability. Cambridge: Cambridge University Press, p. 48.
  7. ^ a b Tabery, James and Griffiths, Paul E. (2010). Historical and Philosophical Perspectives on Behavioral Genetics and Developmental Science”, in Hood, Halpern, Greenberg, and Lerner (Eds.), Handbook of Developmental Science, Behavior, and Genetics. Wiley-Blackwell, pp. 41-60.
  8. ^ Cooper RM & Zubek JP (1958). "Effects of enriched and restricted early environments on the learning ability of bright and dull rats". Canadian Journal of Psychology 12 (3): 159–164. PMID 13573245. 
  9. ^ Sesardic, N. (2005). Making sense of heritability. Cambridge: Cambridge University Press, pp. 66–67.
  10. ^ Clausen J, Keck D, Hiesey WM (1948). "Experimental studies on the nature of species. III. Environmental responses of climatic races of Achillea, Carnegie Inst Washington Publ 581". pp. 1–129. 
  11. ^ AAAS publication on Behavioral Genetics
  12. ^ Caspi A, et al. (2002). "Role of genotype in the cycle of violence in maltreated children". Science 297 (5582): 851–854. doi:10.1126/science.1072290. PMID 12161658. 
  13. ^ Munafò M, et al. (2009). "Gene x Environment Interactions at the Serotonin Transporter Locus". Biol Psychiatry 65: 211–219. doi:10.1016/j.biopsych.2008.06.009. PMID 18691701. 
  14. ^ Khoury MJ, Davis R, Gwinn M, Lindegren ML & Yoon P (2005). "Do we need genomic research for the prevention of common diseases with environmental causes?". Am J Epidemiol 161 (9): 799–805. doi:10.1093/aje/kwi113. PMID 15840611. 
  15. ^ Willet W (2002). "Balancing lifestyle and genomic research for disease prevention". Science 269 (5568): 695–698. doi:10.1126/science.1071055. PMID 11976443.