Frequent Misconceptions About Genetics and Evolution in Pop Culture

Lately, the consolidation of the entertainment industry has gotten me thinking about all the ways in which genetics and evolution have historically been misrepresented in popular culture. With the popularization of nerd culture, we now see many old misconceptions long present in speculative fiction suddenly reaching a much wider audience. Whether or not you have any personal interest in the Marvel Cinematic Universe, the Star Wars Universe, or myriad other fictional universes is irrelevant – these intellectual properties have become embedded in the zeitgeist, and for the average consumer there is no escape. A child growing up today will encounter myriad fictional interpretations of biological principles, some quite closely related to reality, and some wildly divergent.

Many of the common misconceptions regarding genetics in fiction arise from ones that scientists themselves often held for years or decades. However, even after a general consensus is expunged from the scientific community, it may linger in the collective popular culture consciousness for many more years. Here I wanted to start a series where I explore some of the most common ways in which pop culture gets genetics and evolution wrong. Along the way we can look at how different pieces of fiction are either ignorant of the current scientific consensus, or how they address or circumvent it. We’ll touch on topics such as:

• Genes that influence traits
• Mutation
• The purpose of evolution
• The direction of evolution

Before proceeding, I want to make one thing clear: this is all just for illustrative and educational purposes. Speculative fiction is interesting to us because of all the ways in which its settings don’t match with our world. To illustrate just how boring reality can be, here’s a more plausible retelling of the origins (or lack thereof) of the Incredible Hulk:

In the desert, mild mannered physicist Bruce Banner saves a teenager who unwittingly wanders onto the test site of a nuclear bomb. In the process, his body is exposed to high levels of gamma radiation. Nothing happens. Thirty year later, he develops leukemia which may nor may not have been caused by his previous radiation exposure.

This is not the type of story that will cause comic books to leap off of the shelves into the hands of children – or adults for that matter. This is why science fiction should not necessarily attempt to be scientifically sound. Everyone needs some escapism now and then, after all. Now, without further ado, we can proceed on to our first major misconception:

Part 1: The Gene for X

Here’s something that you’ve probably seen dozens of times across many forms of media: the headline “Scientists discover gene for X.” In fact, you may have seen it so many times that you’ve subconsciously begun to expect that every trait or disease is controlled by a gene. These sorts of headlines typically arise from genome-wide association studies (GWAS), which, as we previously examined, seek to associate the phenotypic variation we see for a trait in a population with underlying genetic variation.

The problem with GWAS studies is that they are easily misinterpreted. While it is true that a well-designed GWAS study can often uncover genes influencing trait X, what is often not reported on is that variation in each of these genes may explain only a very tiny portion (think a few percent or less) of the phenotypic variation that is observed in the population. What’s more, even if we add up all the variation explained by all the significant genes identified in a GWAS study conducted on a very large sample, we still typically only explain a fraction of the variation that we know is due to genetics (i.e. the heritable portion of the phenotypic variation). The cause of this phenomenon is still being debated, and it is fittingly referred to as the missing heritability problem. A recent study examining human disease risk predicted by multiple GWAS studies for multiple diseases found that, on average, the heritability explained by SNPs is quite low.

To be clear here, there are many examples of genetic diseases that are caused by mutations in one or a few genes. Currently, the U.S. National Library of Medicine lists over 1,300 diseases with a  genetic basis. For example, sickle cell anemia is caused by mutations within the HBB gene encoding the two β-globin subunits of hemoglobin. Individuals who are homozygous for mutations of HBB (that is, carry it from both of their parents), will have a malformed version of hemoglobin, which in turn leads to malformed (sickle-shaped) red blood cells which get stuck in small capillaries, limiting blood and oxygen availability to certain tissues.

However, there are just as many if not more examples of traits which have far more complex genetic underpinnings. In a previous post, we talked about quantitative traits – those which are controlled by many different genes. An example would be human body weight. If this trait were controlled by a single gene, we would expect that all adult humans would have just a handful of different possible body weights. However, clearly this is not the case. An adult’s body weight can be any value over a range of several hundred pounds. What’s more, an individual’s body weight can obviously change over time. This brings us to another characteristic of quantitative traits – they are influenced by the environment to varying degrees. Many times there simply is no gene for trait X. Rather, it is more accurate to say that many traits are influenced by hundreds to thousands of genes, and their interactions with each other, and with the organism’s environment.

Although we now generally know better than to try and find single genes underlying complex traits, this doesn’t stop research from being readily misinterpreted. Take, for instance, the recent GWAS study of sexual orientation which definitively stated that there is no single “gay gene” underlying same-sex sexual behavior, and the controversy that erupted when this studies’ data was immediately misused to create a “How Gay Are You?” app. During the Human Genome Project, many scientists expressed optimism that human traits would be “solved” to one extent or another – that we would finally have the key to unlocking the genetic puzzle underlying many of our characteristics and ailments. Twenty years and thousands of GWAS studies later, it is okay to admit that we remain humbled in light of the baffling complexity of the genetics influencing who we are.

Returning to the “gene for X” trope in fiction, it all begins to seem a bit silly talking about a gene for genius-level intellect, or telekinesis, or superhuman strength (actually there is a rare mutation for that one), when there doesn’t appear to be any particular gene underlying many of the traits that make us who we are. To see how far the gene for X trope can diverge from reality, we can look to the subject of transgenic organisms. Genetically-modified crop plants have been grown in parts of the world for several decades. These are typically produced by introducing one gene that does one specific thing into a plant from another organism – usually making the plant immune to a particular herbicide. But what if we could take this transgenic mixing and matching much further? That is where we cross into the realm of science fiction.

An Egregious Example

The 2015 blockbluster Jurassic World shares much of the implausible science of Jurassic Park, but without the work that Michael Crichton put in to give the latter its well-crafted illusion of authenticity. In it, theme park scientists, no longer content to merely resurrect extinct dinosaur species, create a new species of their own. The resulting Indominus rex is made through a process that would be the envy of any real life synthetic biologist. Take some T. rex big n’ scary genes, mix in some Velociraptor claw genes, add a dash of crocodile toothy grin genes. Get rid of all those pesky feather genes. Whisk until batter is smooth. (As an interesting aside, the “raptors” in Jurassic Park were originally modeled after the related, but distinct, Deinonychus antirrhopus. Both are in the family Dromaeosauridae, but Velociraptor and Deinonychus are separate genera within this family).

The Indominus rex displays many remarkable characteristics and abilities, which seem to be inherited from a general blending of the various species that make up its genome. The height of this wildly successful cookie baking experiment comes when the I. rex encounters a group of Velociraptors, and begins to hold a casual conversation with them (in roaring/screeching dinosaur speak). We should keep in mind that the I. rex was raised in isolation in its own pen, so this would be akin to a human being raised in solitary confinement encountering another human and immediately striking up a conversation about the weather. Evidently the raptor language genes (?) that the I. rex carries are quite potent – the biological equivalent of a universal translator.

It shouldn’t come as a surprise to anyone that this is all far from reality. It is true that a sort-of synthetic organism was recently created by the J. Craig Venter Institute. However, it is a monumental leap to go from engineering a bacterium to engineering a multi-ton dinosaur. There is also the question of why we should be in such a rush to create new species when we are rapidly eliminating the ones that already exist. Our dreams of creating a “clever girl” that could one day outsmart Robert Muldoon at his own game will have to wait a little longer. In the meantime, if you want to see dinosaurs in real life, you can always get a pair of binoculars, walk out into the woods, and go bird watching.