Gene–environment and gene–gene interactions are likely to play a key role in the development, prevention and treatment of common diseases.
Keywords: genes; environments; common diseases; statistical genetic models
Gene–Environment Interaction
Sharon LR Kardia, University of Michigan, Ann Arbor, Michigan, USA
Published online: December 2007
DOI: 10.1002/9780470015902.a0005413.pub2
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Figure 1. Adaptation of Wolterek's (1909) original demonstration of a reaction norm. The proportional growth of the head relative to the body size of the Hyalodaphnia is dependent on food availability and the strain (i.e. genotype A, B or C) of Hyalodaphnia.
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Figure 2. Norms of reaction can be categorized based on their shape, that is, linear or nonlinear – and whether they indicate the presence or absence of response to environmental change (i.e. plastic versus nonplastic).
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Figure 3. Application of the norm-of-reaction concept to common chronic disease risk models. At birth, we start with initial biological conditions set by our genotype (e.g. AA or aa) and our fetal environments. Over time, changes in the environment (x-axis) manifest as variation in measures of health (y-axis) such that two people with the same susceptibility genotype can end up with different levels of health (past environmental exposures). Furthermore, given information on the type of norm of reaction (i.e. level of sensitivity) of a particular genotype, predictions can be made as to the amount of change in the phenotype that can occur with future changes to the individual's environment.
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| other National Academies of Science (2006) Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate. | |
| other National Academies of Science (in press) Institute of Medicine Committee on Applications of Toxicogenomic Technologies to Predictive Toxicology. | |
| book Wolf JB, Brodie ED III and Wade MJ (2000) Epistasis and the Evolutionary Process. New York, NY: Oxford University Press. | |
| Web Links | |
| ePath angiotensinogen (serine or cysteine) proteinase inhibitor, clade A (alpha-1 antiproteinase, antitrypsin), member 8) (AGT); LocusID: 183. LocusLink: http://www.ncbi.nlm.nih.gov/LocusLink/LocRpt.cgi?l=183 | |
| ePath angiotensinogen (serine or cysteine) proteinase inhibitor, clade A (alpha-1 antiproteinase, antitrypsin), member 8) (AGT); MIM number: 106150. OMIM: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?106150 | |
