The Evidence
In Footnote 24, David Shenk cites Patrick Bateson noting that "even in the case of eye color," Mendelian inheritance does not always accurately predict the outcome (188). Continuing, Shenk cites work by McKusick, declaring that "although not common, 2 blue-eyed parents can produce children with brown eyes," then uses information from Sturm and Frudakis to mention that "eye color is inherited as a polygenic, not as a monegenic, trait" (188). Shenk also cites a study by Duffy et al. that determines a single gene to be the major factor affecting eye color (188). If an individual possessed secondary genes that contradicted the major factor and somehow managed to silence the major factor, could the individual change his/her eye color in the middle of his life? (or at any point in his/her life?) Can you think of any other examples of apparently Mendelian-inherited traits that are actually polygenic? Consider the limitations and possibilities of the "dynamic development" and "gene-environment interaction" theories presented by David Shenk. Also, considering the effects of alternative splicing and other cell differentiation processes, how would other body mechanisms respond to these changes? Relate your response to inheritance (Mendelian and non-Mendelian) discussed in Chapters 14 and 15 of the Campbell textbook and be sure to address the theme of regulation, especially when answering the responses of other parts of the body.
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ReplyDeleteEven though the color of an eye is mainly caused by one gene, there are other loci that affect the individual's phenotype, or "an organism’s appearance or observable traits" (Campbell 267). According to Richard A. Sturm and Tony N. Frudakis, "studies show that the OCA2 gene on chromosome 15 is the major determinant of brown and/or blue eye colour but also indicate that other loci will be involved," showing how eye color is not Mendelian inheritance (http://www.evergreen.edu/upwardbound/docs/eyecolor.pdf). Instead, the eye color reflects polygenic inheritance, "the additive effect of two or more genes on a phenotypic character" (Campbell 274).
DeleteAlthough it seems impossible to so, there have been cases where one's eye color has changed naturally during one’s life, most often the eye turns colors from green to blue. As the aforementioned article states that the color of the iris is caused by the pigments that are in the eye, and that pigments are the color that they reflect, just like how chlorophyll looks green because it reflects instead of absorbs green light, the color of the eye is the dominant pigment in the eye.
The reason why there can be this epigenetic change is due to the theme of regulation, which moderates the changes of a body through homeostasis. As one part of regulation involves switching genes on and off in response to environmental stress, it is possible that the genes that code for some pigments that lead to eye color are no longer expressed in response to the environment factor of lighting, while some others are still expressed, leading to the 'unusual' color. A possible and likely reason why this regulation occurs is that the eye pigments are no longer needed and the pigments production is stopped. Thus, further production of these pigments would be wastes of ATP, and these pigments would serve no point. Although the purpose of eye pigments are not fully clear, it is possible that specific eye colors allow better vision in certain lighting, as the iris's (the colored part of eyes) job involves blocking light, and so regulation of the production of eye pigments could help one's ability to see better in specific lighting. (http://www.newton.dep.anl.gov/askasci/gen01/gen01750.htm) Also, through the theme of continuity and change, a child might have different eye colors due to some genetic mutation which leads into the production of different colored pigments than the parents.
This possibility in change in eye color shows how the GxE interaction can be manipulated to create an different phenotype. As something previously considered to be Mendelian inheritance is shown to be wrong, it might lead to some other question on how far gene-environment interactions can cause a change in one's phenotype. However, there are some limitations to how drastic a phenotype can be changed, as one's genetic code sets the bound, as Shenk says "genes direct the production of proteins" (21). Without the genes to code for some proteins, and also without a proper environment to induce the production of proteins, there is a limit on how much one's phenotype can be. These changes in phenotype might not be well-accepted by other cells that have gone through alternate splicing, but with body coordination, other cells should be able to adjust to this change in phenotype.
PT. 2
DeleteOne other possible polygenic trait is height. As Shenk says "very few ethnic groups are destined to be taller or smaller than any other groups," there seems to be a possibility that the parents' height will not be a good indicator on how tall the offspring will be (27). Instead, height is likely regulated as a result of the environment, as the environment provides food and water that allow the organism to grow. If there is not enough food for humans to grow taller, then just as plant seeds are dormant in an unsuitable environment to grow due to the regulating factors of the hormone abscisic acid (Campbell 832), then it is possible that hormones prevent height growth in a unsuitable environment to grow. Another possible polygenic trait is skin color, which is similar to the color of the eye as it depends on the pigments in the skin, where different genes will code for different pigments. The possibilities for the traits of an offspring from parents are nearly endless when considering the number of environments that could potentially exist.
All above posted by Matthew Yang (matt.y.yang2013@gmail.com)
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