Junk Becomes Us
By Kaitlyn Scacalossi
The author imitated herein is a mystery, though not too much of a mystery. That is to say I know myself, and by knowing myself, it is apparent that the reader would have a guess as good as mine, assuming the reader is familiar with 20th century Italian fiction writers.
Why I, the scientist-turned-narrator, selected this author’s voice will become apparent in time, but first I should warn that the reader must have patience to read a description in this style, which is akin to the exasperated narration of someone explaining the meaning of life while on LSD, getting words out before they disappear, unwinding ideas in writing, telling the whole truth and clarifying when that truth is not yet complete. That’s not to say the reader’s requirement for patience is unique; the writer must also share this patience in order to portray a scientific concept in this fantastical style, particularly when it is the nature of scientists to succinctly state facts. Then, further burdening the scientist-turned-narrator is the underlying thought that the scientific idea described herein is one that did not yet exist in the imitated author’s lifetime: Our cells have DNA, and the vast majority of this DNA was thought to be meaningless, and it was called “junk.” But this “junk DNA,” as it turns out, is not junk at all.
To explain: It has long been known that there is the cell, and within the cell there is the nucleus, and within the nucleus there is DNA. Scientists examine DNA using various tools, but those tools and are imperfect and ever-changing and ever-improving. So scientists and their ever-improving tools, through these stages of improvement, make mistakes. That is not to say that science is untrustworthy or a mistake in itself, only that, like the tools used by scientists, science is itself ever-changing and ever-improving.
Not long ago, scientists, using the best tools they had at the time, could only discern a function for 2% of the human genome. That 2% of the human genome, it seemed, provided the instructions, the code, for cells to make the proteins that carried out the basic functions of life, while the other 98% of the human genome, it seemed, did nothing at all. Or rather, the majority of our genome was able to make an intermediate product called RNA, just as the protein-coding genes did. But for 2% of genes, the intermediate RNA carried the all-important code for making proteins, and for the junk genes, the RNA had no such protein code; it was non-coding and thus utterly useless, or so it seemed.
At the same time, scientists did not know how these 2% of all-important protein-coding genes were regulated or how they could account for our complexity as a species. How is it, for example, possible that humans have the same number, or sometimes even fewer, protein-coding genes than less complex organisms? The answers to such dilemmas were to be found, at least partially, with the other 98% of the genome that does not code for proteins, that was “junk,” but isn’t junk.
Eventually the tools to examine our genes improved, and so too did scientific theories. While it is true that those once called junk-genes do not make proteins, it is false that the product they make, called RNA, is utterly useless. The product that these junk genes make is something scientists call “non-coding RNA,” to clarify that this kind of RNA is not merely an intermediate product on the way to protein; these non-coding RNAs are the final product themselves. Never mind that the vast majority of RNA in a cell is non-coding RNA and only 2% of genes make protein-coding RNA, those 2% were studied first and it is thus the majority that get the modifier “non-coding,” rather than the other way around. These seemingly superfluous words are too not junk; like the long-winded ramblings of author Italo Calvino, they are necessary for proper clarification.
Now, with our new scientific tools, it seems that these “non-coding RNAs,” as we now call them, made by our junk genes, play vital roles in health, disease, and even human complexity. They bind to our genome and control how other genes are expressed, modifying the landscape surrounding important genes with marks that act as signs for openness: “Read more of me – make more of this gene’s product!” or conversely by hiding the genes behind inhibitive marks that prevent them from being read, “Closed today, try again later.” More importantly, the non-coding RNAs that have all of these important functions are often responsive to stimuli – environmental queues that tell these RNAs how to behave. Thus, while our genes may not change, how our genes read does change in part due to these non-coding RNAs, which respond to the environment. Smoking or ingestion of saturated fats, for example, cause increased (and decreased) activity of hundreds of non-coding RNAs that thus regulate thousands of genes related to inflammation. Both for better and for worse, non-coding RNAs are a means to change our inherited genetic landscapes.
Thus, humans may have fewer protein-coding genes than an onion, but we are far more genetically complex than such a simple plant. We have more junk DNA and thus more non-coding RNAs to regulate how our genes are expressed. In fact, while humans have the same number, or sometimes even fewer, protein-coding genes than some less complex organisms, the number of non-coding genomic elements consistently increases with complexity from worms, to flies, to humans. Junk genes, and the non-coding RNAs they produce, make us who we are: incredibly advanced lifeforms whose cognitive complexity allows them to read and write the cascading prose in which you, dear reader, have been most recently immersed.
Kaitlyn Scacalossi is a Ph.D. student at NYU, where she studies the genomics of inflammation. She is not particularly fond of Italo Calvino’s long-winded prose, but does enjoy a challenge.