Shenk explains how Mendel’s pea-plant experiment set himself up for the understanding that genes are the sole determinants of heredity (21). This is because all of the plants were exposed to the same exact environment, so this eliminates any environmental impact (184). Shenk then goes on to use a dice metaphor to further explain this idea. Explain this metaphor and use it to delineate how environmental factors impact heredity. What are the flaws to this metaphor? How does the metaphor actually harm Shenk’s point? What would be a better metaphor for the point Shenk is trying to make?
Michaela Margolis (mmargolis989@gmail.com)
Mendelian genetics were long the accepted explanation for inheritance: “parents pass on discrete heritable units-genes- that retain their separate identities in offspring” (Campbell 262). A mother passes a gene on to her child, as does the father, and by doing a basic Punnett square, we can figure out the likelihood that the child will turn out with a certain trait. However, in recent times, the discovery of various Non-Mendelian inheritance mechanisms has upset this theory: epigenetics, multiple- allele inheritance, polymorphism, etc.
ReplyDeleteMendel created his theory by observing pea plants. By carefully maintaining them in constant conditions and strictly regulating reproduction, (pea plants can self-fertilize, but Mendel enforced cross-pollination by removing immature stamens), (http://anthro.palomar.edu/mendel/mendel_1.htm) Mendel was able to isolate certain traits (or so he thought), and come to the conclusion that traits are inherited independently and that genes have preset information that is simply expressed as coded- a blueprint. However, this pea plant model cannot be applied to humans; the pea plants were observed under tightly controlled conditions, and this thus “eliminates any visible environmental impact on heredity” (Shenk 184). Knowing what we now know about epigenetics and how “the genome provides the possibilities, [but] the environment determines which genes become activated”, and using Shenk’s model of GxE, we cannot ignore environmental impact (http://www.school.eb.com/eb/article-288098?query=epigenetics&ct=). “Each human child is his/her own unique genetic entity conceived in his/her own distinct environment” and to ignore environment is to ignore many forces that affect gene expression (Shenk 130).
Shenk goes on to further take down Mendelian genetics by comparing his idea of genes offering a fixed inheritable entity (and our subsequent use of Punnett Squares) to throwing dice: this misunderstanding stems from scientists’ use of the word “probabilistic”, to describe how “having a version of a gene” – such as a mutation, perhaps, which can lead to selective advantages for survival and reproduction and thus be passed down and even contribute to evolution over thousands of years – “may change the odds, making you more or less likely to have a trait…but the actual outcome depends on a tangle of other circumstances” (Shenk 185). Many people, upon reading this, become confused and see the word “probabilistic” and assume that this means each allele has a certain chance of being expressed; however, what it really means is that certain slightly different versions of genes that we have may alter our likelihood of having a trait slightly, but there is no fixed probability, because environmental factors can’t be quantified. “A genotype generally is not associated with a rigidly defined phenotype, but rather with a range of phenotypic possibilities due to environmental influences. This phenotypic range is called the norm of reaction for a genotype” (Campbell 275). The norm of reaction can be varied by a number of factors- nutrition, climate, experience. These factors clearly cannot be plugged into a formula to calculate the probability that this factor here will cause this phenotype, while this factor there will cause that phenotype, unlike the neatness of dice and probability.
A much better metaphor for genetic expression is Shenk’s switchboard metaphor. Rather than viewing genes as fixed blueprints, we can see them as a control panel with various knobs and switches that can be adjusted and set to varying levels of intensity, based on environmental factors: just as loudness in a room or static can cause a sound technician to adjust the panel accordingly, environmental factors from gestation to birth to maturation shape genetic expression accordingly. There is no way to say, precisely, the chance that the sound will turn out a certain way, because we don’t know the conditions in the recording studio that day; likewise, we can’t say how a person will turn out purely based on their inherited genetic code. “Rather than giving us hard-wired instructions on how a trait must be expressed, this process of gene-environment interaction drives a unique developmental path for every unique individual” (Shenk 19). Mendel’s pea plants provided a useful start, and he deserves the title of Father of Genetics, but just as children turn out differently than the genetic code passed down to them from their parents, our understanding of genetics today is quite different based on gained experience and new information.
ReplyDeleteVivian Wang (vivian.wang9895@gmail.com)