I was sixteen the first time I felt insecure about my huge nose. After scrolling through Instagram for thirty minutes, I realized that my nose was too big; my eyes, too small; and my eyebrows, too thick. Of course, it’s common to realize everything that’s “wrong” with your face after looking at Kylie Jenner’s instagram for ten minutes. Unsurprisingly, five minutes after my daily Instagram session, my insecurities led me to scream from the top of my lungs: “Ughhh! Genes are not fair!” However, I won’t feel bad about it. We’ve all been there at least once.
Pop culture has made it seem as if genes only define how you look. Obviously, this would be very shallow, for genes have many functions. However, it is not far from the truth, as studies have shown that phenotypes, how you look on the outside, are closely related to and can be predicted from genotypes, your genetic background. Studies assessing the effects of modifying individual genes in model organisms such as Drosophila melanogaster (informally, fruit flies) have allowed thousands of genes to be associated with phenotypes (1).
To analyze population genomics and quantitative traits, the Drosophila melanogaster Genetic Reference Panel (DGRP) was created (2). Compared to previous populations of recombinant inbred lines (RILs) gathered from limited samples of genetic variation, the DRGP consists of 192 inbred strains gathered from a single population (2). This would enable a favorable scenario for genetic mapping, for there is a large amount of genetic variation, a lack of population structure (organization), and a rapid decay of the difference between observed and expected allelic frequencies (3, 4).
By studying the genomics of Drosophila flies, researchers discovered that there is a genotype-by-diet interaction that drives metabolic phenotype variation (5). A study that quantifies the effect of dietary perturbation on metabolic traits in 146 inbred lines (nearly identical individuals) of Drosophila melanogaster shows that a Drosophila’s genotype and surroundings play a major role in defining its phenotype (5). The study demonstrates that “for several metabolic traits, genotype-by-diet interactions account for more variance (between 12 and 17%) than diet alone (1-2%), and in some cases have as large an effect as genetics alone (11-23%)” (5). In simpler terms, while diet contributes to metabolic phenotypes in D. melanogaster, it does so in a way that is highly genotype dependent (5).
Now, you might be wondering: What do flies have to do with humans? Well, by analyzing the genome of model organisms like the Drosophila melanogaster, we can discover the function of many genes encoded by the human genome (6). Analyzing the genome of model organisms will allow us to classify approximately 70,000 individual genes encoded by the human genome into much smaller multicomponent, core processes of known biochemical function (6). In fact, for decades, the D. melanogaster has been one of the most popular model organisms, for it has allowed us to uncover the function of many genes while being low cost, and possessing a rapid generation time (reproducibility) and excellent genetic tools (7).
However, although model organisms like the Drosophila melanogaster have given us an insight into the human genome, we still are missing a lot of information. We still don’t know the function of many genes and can’t predict the effect of modifying the activity of an uncharacterized gene (1). In addition, it is hard to predict what genes are likely to be involved in a phenotypic variant, for multigene traits and environmental factors contribute to its expression (1).
Thus, while saying “You are cute genes” (like Kendall Jenner once did in Keeping Up With The Kardashians) might be true to some extent, as it has been scientifically proven that your genetic background affects how you look on the outside, we still have to figure out what a lot of genes do. Hopefully, in the decades to come, by analyzing the genome of model organisms, such as D. melanogaster, we will be able to figure out what most genes do.
References:
- Benfey, P. N., & Mitchell-Olds, T. (2008). From Genotype to Phenotype: Systems Biology Meets Natural Variation. Science, 320(5875), 495–497. https://doi.org/10.1126/science.1153716
- Mackay, T., Richards, S., Stone, E. et al. The Drosophila melanogaster Genetic Reference Panel. Nature 482, 173–178 (2012). https://doi.org/10.1038/nature10811
- Mackay TFC, Huang W. Charting the genotype-phenotype map: lessons from the Drosophila melanogaster Genetic Reference Panel. Wiley Interdiscip Rev Dev Biol. 2018;7(1):10.1002/wdev.289. doi:10.1002/wdev.289
- Awais Khan, M. (2019, November 14). Estimation of Linkage Disequilibrium Decay. Plant Breeding and Genomics. https://plant-breeding-genomics.extension.org/estimation-of-linkage-disequilibrium-decay/.
- Reed LK, Williams S, Springston M, et al. Genotype-by-diet interactions drive metabolic phenotype variation in Drosophila melanogaster. Genetics. 2010;185(3):1009-1019. doi:10.1534/genetics.109.113571
- Miklos, G. L. G., & Rubin, G. M. (1996). The Role of the Genome Project in Determining Gene Function: Insights from Model Organisms. Cell, 86(4), 521–529. https://doi.org/10.1016/s0092-8674(00)80126-9
- Tolwinski, N. S. (2017). Introduction: Drosophila—a model system for developmental biology. Journal of Developmental Biology, 5(3), 9. https://doi.org/10.3390/jdb5030009