Rewriting the Genetic Code

Catalyst VOlume 10

DNA, or deoxyribonucleic acid, is at the root of all life as we know it. Using just four component nucleotide bases, DNA contains all the information needed to build any protein. To make a protein, DNA is transcribed into mRNA, which is in turn “translated” into a protein by molecules called ribosomes. More specifically, the mRNA is “read” by ribosomes in groups of three base pairs called codons, each of which codes for one of 20 possible amino acids. The set of rules that determines which codon codes for which amino acid is called the genetic code, and it is common to almost all known organisms--everything, from bacteria to humankind, shares the same protein expression schema. It is this common code that allows synthetic biologists to insert one organism’s genes into another to create transgenic organisms; generally, a gene will be expressed the same way no matter what organism possesses it. Interestingly, some scientists are attempting to alter this biological norm: rather than modifying genes, they are attempting to modify the genetic code itself in order to create genetically recoded organisms, or GROs.

This modification is possible due to the redundancy of the genetic code. Because there are 64 possible unique codons and only 20 amino acids found in nature, many amino acids are specified by more than one codon. Theoretically, then, researchers should be able to swap every instance of a particular codon with a synonymous one without harming a cell, then repurpose the eliminated codon.¹ This was proven possible in a 2013 paper by Lajoie et al. published in Science; in it, a team of scientists working with E. coli cells substituted all instances of the codon UAG, which signals cells to stop translation of a protein, with the functionally equivalent sequence UAA. They then deleted release factor 1 (RF1), the protein that gives UAG its stop function. Finally, they reassigned the function of UAG to code for a non-standard amino acid (NSAA) of their choice.¹

In a more recent paper, Ostrov et al. took this recoding even further by excising seven codons from the E. coli genome, reducing it to 57 codons. Because there are 62,214 instances of these codons in the E. coli genome, researchers couldn’t directly excise them from the E. coli DNA with typical gene-editing strategies. Instead, they resorted to synthesizing long stretches of the modified genome, inserting them into the bacteria, and testing to make sure the modifications were not lethal. At time of publishing, they had completed testing of 63% of the recoded genes and found that most of their changes had not significantly impaired the bacteria’s fitness, indicating that such large changes to the genetic code are feasible.²

Should Ostrov’s team succeed in their recoding, there are a number of possible applications for the resulting GRO. One would be the creation of virus-resistant cells.^1,2,3 Viral DNA injected into recoded bacteria would be improperly translated if it contained the repurposed codons due to the modified protein expression machinery the GRO possesses. Such resistance was demonstrated by Lajoie in an experiment in which he infected E. coli modified to have no UAG codons with two types of viruses: a T7 virus that contained UAG codons in critical genes, and a T4 virus that did not. As expected, the modified cells showed resistance to T7, but were infected normally by T4. The researchers concluded that more extensive genetic code modifications would probably make the bacteria immune to viral infection entirely.² Using such organisms in lieu of unmodified ones in bacteria-dependent processes like cheese- and yogurt-making, biogas manufacturing, and hormone production would reduce the cost of those processes by eliminating the hassle and expense associated with viral infection.^3,4 It should be noted that while GROs would theoretically be resistant to infection, they would also be unable to “infect” anything themselves. If GRO genes were to be taken up by other organisms, they would also be improperly translated as well, making horizontal gene transfer impossible. This means that GROs are “safe” in the sense that they would not be able to spread their genes to organisms in the wild like other GMOs can.⁵

GROs could also be used to make novel proteins. The eliminated codons could be repurposed to code for amino acids not found in nature, or non-standard amino acids (NSAAs). It is possible to use GRO’s to produce a range of proteins with expanded chemical properties, free from the limits imposed by strictly using the 20 standard amino acids.^2,3 These proteins could then be used in medical or industrial applications. For example, the biopharmaceutical company Ambrx develops proteins with NSAAs for use as medicine to treat cancer and other diseases.⁶

While GRO’s can do incredible things, they are not without their drawbacks. Proteins produced by the modified cells could turn out to be toxic, and if these GROs manage to escape from the lab into the wild, they could flourish due to their resistance to viral infection.^2,3 To prevent this scenario from happening, Ostrov’s team has devised a failsafe. In previous experiments, the researchers modified bacteria so that two essential genes, named adk and tyrS, depended on NSAAs to function. Because NSAAs aren’t found in the wild, this modification effectively confines the bacteria within the lab, and it is difficult for the organisms to thwart this containment strategy spontaneously. Ostrov et al. intend to implement this failsafe in their 57-codon E. coli.²

Genetic recoding is an exciting development in synthetic biology, one that offers a new paradigm for genetic modification. Though the field is still young and the sheer amount of DNA changes needed to recode organisms poses significant challenges to the creation of GROs, genetic recoding has the potential to yield tremendously useful organisms.

References

1. Lajoie, M. J., et al. Science 2013, 342, 357-360.
2. Ostrov, N., et al. Science 2016, 353, 819-822.
3. Bohannon, J. Biologists are close to reinventing the genetic code of life. Science, Aug. 18, 2016. http://www.sciencemag.org/news/2016/08/biologists-are-close-reinventing-genetic-code-life (accessed Sept. 29, 2016).
4. Diep, F. What are genetically recoded organisms?. Popular Science, Oct. 15, 2013. http://www.popsci.com/article/science/what-are-genetically-recoded-organisms (accessed Sept. 29, 2016)
5. Commercial and industrial applications of microorganisms. http://www.contentextra.com/lifesciences/files/topicguides/9781447935674_LS_TG2_2.pdf (accessed Nov. 1 2016)
6. Ambrx. http://ambrx.com/about/ (accessed Oct. 6, 2016)

CRISPR: The Double-Edged Sword of Genetic Engineering

Catalyst Volume 10

The phrase “genetic engineering” often brings to mind a mad scientist manipulating mutant genes or a Frankenstein-like creation emerging from a test tube. Brought to the forefront by heated debates over genetically modified crops, genetic engineering has long been viewed as a difficult, risky process fraught with errors.¹

The intentional use of CRISPRs, short for clustered regularly interspaced sport palindromic repeats, turned the world of genetic engineering on its head. Pioneered by Jennifer Doudna of Berkeley² in 2012 and praised as the “Model T” of genetic engineering,³ CRISPR as a tool is both transforming what it means to edit genes and raising difficult ethical and moral questions about genetic engineering as a discipline.

CRISPR itself is no new discovery. The repeats are sequences used by bacteria and microorganisms to protect against viral infections. Upon invasion by a virus, CRISPR identifies the DNA segments from the invading virus, processes them into “spacers,” or short palindromic repeats of DNA, and inserts them back into the bacterial genome.⁴ When the bacterial DNA undergoes transcription, the resulting RNA is a single-chain molecule that acts as a guide to destroy viral material. In a way, the RNA functions as a blacklist for the bacterial cell: re-invasion attempts by the same virus are quickly identified using the DNA record and subsequently stopped. That same blacklist enables CRISPR to be a powerful engineering tool. The spacers act as easily identifiable flags in the genome, allowing for high precision when manipulating individual nucleotide sequences in genes.⁵ The old biotechnology system can be perceived as a confused traveler holding an inaccurate map, with a general location and vague person to meet. By the same analogy, CRISPR provides a mugshot of the person to meet and the precise coordinates of where to find them. Scientists have taken advantage of this precision and now use modified proteins, such as Cas-9, to activate gene expression as opposed to cutting the DNA,⁶ an innovative style of genetic engineering. Traditional genetic engineering can be a shot in the dark, but with the accuracy of CRISPR, mutations are very rare.⁷ For the first time, scientists are able to pinpoint the exact location of genes, cut the desired sequence, and leave no damage. Another benefit of CRISPR is the reincorporation of genes that have become lost, either by breeding or evolution, bringing back extinct qualities. For example, scientists have succeeded in introducing mammoth genes into living elephant cells.^8,9 Even better, CRISPR is very inexpensive, costing around $75 to edit a gene at Baylor College of Medicine,¹⁰ and accessible to anyone with biological expertise, starting with graduate students.¹¹ The term “Model T of genetic engineering” could hardly be more appropriate.

CRISPR stretches the boundaries of bioengineering. One enterprising team from China led by oncologist Dr. Lu You has already begun trials on humans. They plan on injecting cells modified using the CRISPR-Cas9 system into patients with metastatic non-small cell lung cancer--patients who otherwise have little hope of survival.¹² To prevent attacks on healthy cells, extracted critical immune mediators called T cells will be edited with the CRISPR-Cas9 system. CRISPR will identify and “snip” out a gene that encodes PD-1, a protein that acts as a check on the T-cell’s capacity to launch an immune response. Essentially, Lu’s team is creating super-T-cells, ones that have no mercy for any suspicious activity. This operation is very risky. CRISPR’s mechanisms are not thoroughly understood, and mistakes with gene editing could have drastic consequences.¹¹ In addition, the super T cells could attack in an autoimmune reaction, leading to degradation of critical organs. In an attempt to prevent such a response, Lu’s team will extract T-cells from the tumor itself, as those T-cells would likely have already specialized in attacking cancer cells. To ensure patient safety, the team will examine the effects of three different dosage regimens on ten patients, watching closely for side effects and responsiveness.

Trials involving such cutting-edge technology raise many questions. With ease of use and accessibility, CRISPR has the potential to become a tool worthy of science fiction horror. Several ethics groups have raised concerns over the inappropriate use of CRISPR: they worry that the technology could be used by amateurs and thus yield dangerous results. In spite of these concerns, China greenlit direct editing of human embryos, creating international uproar and a moratorium on further human embryo testing.¹³ But such editing could lead to new breakthroughs: CRISPR could reveal how genes regulate early embryonic development, leading to a better understanding of infertility and miscarriages.¹⁴

This double-edged nature defines CRISPR-Cas9’s increasing relevance at the helm of bioengineering. The momentum behind CRISPR and its seemingly endless applications continue to broach long-unanswered questions in biology, disease treatment, and genetic engineering. Still, with that momentum comes caution: with CRISPR’s discoveries come increasingly blurred ethical distinctions.

References

1. Union of Concerned Scientists. http://www.ucsusa.org/food_and_agriculture/our-failing-food-system/genetic-engineering/risks-of-genetic-engineering.html#.WBvf3DKZPox (accessed Sept. 30, 2016).
2. Doudna, J. Nature [Online] 2015, 7583, 469-471. http://www.nature.com/news/genome-editing-revolution-my-whirlwind-year-with-crispr-1.19063 (accessed Oct. 5, 2016).
3. Mariscal, C.; Petropanagos, A. Monash Bioeth. Rev. [Online] 2016, 102, 1-16. http://link.springer.com/article/10.1007%2Fs40592-016-0062-2 (accessed Oct. 5, 2016).
4. Broad Institute. https://www.broadinstitute.org/what-broad/areas-focus/project-spotlight/questions-and-answers-about-crispr (accessed Sept. 30, 2016).
5. Pak, E. CRISPR: A game-changing genetic engineering technique. Harvard Medical School, July 31, 2015. http://sitn.hms.harvard.edu/flash/2014/crispr-a-game-changing-genetic-engineering-technique/ (accessed Sept. 30, 2016)
6. Hendel, A. et al. Nature Biotech. 2015, 33, 985-989.
7. Kleinstiver, B. et al. Nature. 2016, 529, 490-495.
8. Shapiro, B. Genome Biology. [Online] 2015, 228. N.p. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632474/ (accessed Nov. 1, 2016).
9. Reardon, S. Nature. [Online] 2016, 7593, 160-163. http://www.nature.com/news/welcome-to-the-crispr-zoo-1.19537 (accessed Nov. 1, 2016).
10. Baylor College of Medicine. https://www.bcm.edu/research/advanced-technology-core-labs/lab-listing/mouse-embryonic-stem-cell-core/services/crispr-service-schedule (accessed Sept. 30, 2016).
11. Ledford, H. Nature. [Online] 2015, 7554, 20-24. http://www.nature.com/news/crispr-the-disruptor-1.17673 (accessed Oct. 11, 2016).
12. Cyranoski, D. Nature. [Online] 2016, 7613, 476-477. http://www.nature.com/news/chinese-scientists-to-pioneer-first-human-crispr-trial-1.20302 (accessed Sept. 30, 2016).
13. Kolata, G. Chinese Scientists Edit Genes of Human Embryos, Raising Concerns. The New York Times, April 23, 2015. http://www.nytimes.com/2015/04/24/health/chinese-scientists-edit-genes-of-human-embryos-raising-concerns.html?_r=0 (accessed Oct. 2, 2016).
14. Stein, R. Breaking Taboo, Swedish Scientist Seeks To Edit DNA of Healthy Human Embryos. NPR, Sept. 22, 2016. http://www.npr.org/sections/health-shots/2016/09/22/494591738/breaking-taboo-swedish-scientist-seeks-to-edit-dna-of-healthy-human-embryos (accessed Sept. 22, 2016).

Telomeres: Ways to Prolong Life

Catalyst Volume 10

Two hundred years ago, the average life expectancy oscillated between 30 and 40 years, as it had for centuries before. Medical knowledge was fairly limited to superstition and folk cures, and the science behind what actually caused disease and death was lacking. Since then, the average lifespan of human beings has skyrocketed due to scientific advancements in health care, such as an understanding of bacteria and infections. Today, new discoveries are being made in cellular biology which, in theory, could lead us to the next revolutionary leap in life span. Most promising among these recent discoveries is the manipulation of telomeres in order to slow the aging process, and the use of telomerase to identify cancerous cells.

Before understanding how telomeres can be utilized to increase the average lifespan of humans, it is essential to understand what a telomere is. When cells divide, their DNA must be copied so that all of the cells share an identical DNA sequence. However, the DNA cannot be copied all the way to the end of the strand, resulting in the loss of some DNA at the end of the sequence with every single replication.¹ To prevent valuable genetic code from being cut off during cell division, our DNA contains telomeres, a meaningless combination of nucleotides at the end of our chromosomal sequences that can be cut off without consequences to the meaningful part of the DNA. Repeated cell replication causes these protective telomeres to become shorter and shorter, until valuable genetic code is eventually cut off, causing the cell to malfunction and ultimately die.¹ The enzyme telomerase functions in cells to rebuild these constantly degrading telomeres, but its activity is relatively low in normal cells as compared to cancer cells.²

The applications of telomerase manipulation have only come up fairly recently, with the discovery of the functionality of both telomeres and telomerase in the mid 80’s by Nobel Prize winners Elizabeth Blackburn, Carol Grieder, and Jack Sjozak.³ Blackburn discovered a sequence at the end of chromosomes that was repeated several times, but could not determine what the purpose of this sequence was. At the same time, Sjozak was observing the degradation of minichromosomes, chromatin-like structures which replicated during cell division when introduced to a yeast cell. Together, they combined their work by isolating Blackburn’s repeating DNA sequences, attaching them to Sjozak’s minichromosomes, and then placing the minichromosomes back inside yeast cells. With the new addition to their DNA sequence, the minichromosomes did not degrade as they had before, thus proving that the purpose of the repeating DNA sequence, dubbed the telomere, was to protect the chromosome and delay cellular aging.

Because of the relationship between telomeres and cellular aging, many scientists theorize that cell longevity could be enhanced by finding a way to control telomere degradation and keep protective caps on the end of cell DNA indefinitely.¹ Were this to be accomplished, the cells would be able to divide an infinite number of times before they started to lose valuable genetic code, which would theoretically extend the life of the organism as a whole.

In addition, studies into telomeres have revealed new ways of combatting cancer. Although there are many subtypes of cancer, all variations of cancer involve the uncontrollable, rapid division of cells. Despite this rapid division, the telomeres of cancer cells do not shorten like those of a normal cell upon division, otherwise this rapid division would be impossible. Cancer cells are likely able to maintain their telomeres due to their higher levels of telomerase.³ This knowledge allows scientists to use telomerase levels as an indicator of cancerous cells, and then proceed to target these cells. Vaccines that target telomerase production have the potential to be the newest weapon in combatting cancer.² Cancerous cells continue to proliferate at an uncontrollable rate even when telomerase production is interrupted. However, without the telomerase to protect their telomeres from degradation, these cells eventually die.

As the scientific community advances its ability to control telomeres, it comes closer to controlling the process of cellular reproduction, one of the many factors associated with human aging and cancerous cells. With knowledge in these areas continuing to develop, the possibility of completely eradicating cancer and slowing the aging process is becoming more and more realistic.

References

1. Genetic Science Learning Center. Learn.Genetics. http://learn.genetics.utah.edu (accessed Oct. 5, 2016).
2. Shay, J. W.; Woodring W. E.  NRD. [Online] 2016, 5. http://www.nature.com/nrd/journal/v5/n7/full/nrd2081.html (accessed Oct. 16, 2016).
3. The 2009 Nobel Prize in Physiology or Medicine - Press Release. The Nobel Prize. https://www.nobelprize.org/nobel_prizes/medicine/laureates/2009/press.html (accessed Oct. 4, 2016).

Surviving Without the Sixth Sense

Catalyst Volume 10

Though references to the “sixth sense” often bring images of paranormal phenomena to mind, the scientific world has bestowed this title to our innate awareness of our own bodies in space. Proprioception, the official name of this sense, is what allows us to play sports and navigate in the dark. Like our other five senses, our capability for spatial awareness has become so automatic that we hardly ever think about it. But scientists at the National Institute of Health (NIH) have made some breakthroughs about a genetic disorder that causes people to lack this sense, leading to skeletal abnormalities, balance difficulties, and even the inability to discern some forms of touch.¹

The gene PIEZO2 has been associated with the body’s ability to sense touch and coordinate physical actions and movement. While there is not a substantial amount of research about this gene, previous studies on mice show that it is instrumental in proprioception.² Furthermore, NIH researchers have recently attributed a specific phenotype to a mutation in PIEZO2, opening a potential avenue to unlock its secrets.

Pediatric neurologist Carsten G. Bönnermann, the senior investigator at the NIH National Institute of Neurological Disorders and Stroke, had been studying two patients with remarkably similar cases when he met Alexander Chesler at a lecture. Chesler, an investigator at the NIH National Center for Complementary and Integrative Health, joined Bönnermann in performing a series of genetic and practical tests to investigate the disorder.¹

The subjects examined were an 8-year-old girl and an 18-year-old woman from different backgrounds and geographical areas. Even though these patients were not related, they both exhibited a set of similar and highly uncommon phenotypes. For example, each presented with scoliosis - unusual sideways spinal curvature - accompanied by fingers, feet, and hips that could bend at atypical angles. In addition to these physical symptoms, the patients experienced difficulty walking, substantial lack of coordination, and unusual responses to physical touch.¹These symptoms are the result of PIEZO2 mutations that block the gene’s normal activity or production. Using full genome sequencing, researchers found that both patients have at least one recessively-inherited nonsense variant in the coding region of PIEZO2.¹ But because these patients represent the first well-documented cases of specific proprioceptive disorders, there is not an abundance of research about the gene itself. Available previous studies convey that PIEZO2 encodes a mechanosensitive protein - that is, it generates electrical nerve signals in response to detected changes in factors such as cell shape.² This function is responsible for many of our physical capabilities, including spatial awareness, balance, hearing, and touch. In fact, PIEZO2 has even been found to be expressed in neurons that control mechanosensory responses, such as perception of light touch, in mice. Past studies found that removing the gene in mouse models caused intolerable limb defects.² Since this gene is highly homogenous in humans and in mice (the two versions are 95% similar), many researchers assumed that humans could not live without the gene either. According to Bönnermann and Chesler, however, it is clear that this PIEZO2 mutation does not cause a similar fate in humans.

Along with laboratory work, Bönnermann and Chesler employed techniques to further investigate the tangible effects of the mutations. Utilizing a control group for comparison, the researchers presented patients with a set of tests that examined their movement and sensory abilities. The results were startling, to say the least. The patients revealed almost a total lack of proprioception when blindfolded. They stumbled and fell while walking and could not determine which way their joints were moving without looking. In addition, both failed to successfully move a finger from their noses to a target. The absence of certain sensory abilities is also astonishing - both patients could not feel the vibrations of a tuning fork pressed against their skin, could not differentiate between ends of a caliper pressed against their palms, and could not sense a soft brush across their palms and bottom of their feet. Furthermore, when this same soft brush was swept across hairy skin, both of the patients claimed that the sensation was prickly. This particular result revealed that the subjects were generally missing brain activation in the region linked to physical sensation, yet they appeared to have an emotional response to the brushing across hairy skin; these specific brain patterns directly contrasted with those of the control group participants. Additional tests performed on the two women revealed that the patients’ detection of pain, itching, and temperature was normal when compared to the control group findings, and that they possessed nervous system capabilities and cognitive functions appropriate for their ages.¹

Because the patients are still able to function in daily life, it is apparent that the nervous system has alternate pathways that allow them to use sight to largely compensate for their lack of proprioception.^3,4 Through further research, scientists can tap into these alternate pathways when designing therapies for similar patients. Additionally, the common physical features of both patients shed light on the fact that PIEZO2 gene mutations could contribute to the observed genetic musculoskeletal disorders.³ This suggests that proprioception itself is necessary for normal musculoskeletal development; it is possible that abnormalities developed over time as a result of patients’ postural responses and compensations to their deficiencies.⁴

In an era when our lives depend so heavily on our abilities to maneuver our bodies and coordinate movements, the idea of lacking proprioception is especially concerning. Bönnermann and Chesler’s discoveries open new doors for further investigation of PIEZO2’s role in the nervous system and musculoskeletal development. These discoveries can also aid in better understanding a variety of other neurological disorders. But, there is still much unknown about the full effects of the PIEZO2 mutation. For example, we do not know if musculoskeletal abnormalities injure the spinal cord, if the gene mutation poses additional consequences for the elderly, or if women are more susceptible to the disorder than are men. Furthermore, it is very likely that there are numerous other patients around the world who present similar symptoms to the 8-year-old girl and 18-year-old woman observed by Bönnermann and Chesler. While researchers work towards gaining a better understanding of the disease and developing specific therapies, these patients must focus on other coping mechanisms, such as reliance on vision, to accomplish even the most basic daily activities. Because contrary to popular perception, the sixth sense is not an ability to see ghosts; it is so much more.

References

1. Chesler, A. T. et al. N Engl J Med. 2016, 375, 1355-1364
2. Woo, S. et al. Nat Neurosci. 2015, 18, 1756-1762
3. “‘Sixth sense’ may be more than just a feeling”. National Institutes of Health, https://www.nih.gov/news-events/news-releases/Sixth-sense-may-be-more-just-feeling (accessed Sept. 22, 2016).
4. Price, Michael. “Researchers discover gene behind ‘sixth sense’ in humans”. Science Magazine, http://www.sciencemag.org/news/2016/09/researchers-discover-gene-behind-sixth-sense-humans (accessed Sept. 22, 2016)

GMO: How Safe is Our Food?

Catalyst Volume 10

For thousands of years, humans have genetically enhanced other living beings through the practice of selective breeding. Sweet corn and seedless watermelons at local grocery stores as well as purebred dogs at the park are all examples of how humans have selectively enhanced desirable traits in other living creatures. In his 1859 book On the Origin of Species, Charles Darwin discussed how selective breeding by humans had been successful in producing change over time. As technology improves, our ability to manipulate plants and other organisms by introducing new genes promises both new innovations and potential risks.

Genetically modified organisms (GMOs) are plants, animals, or microorganisms in which genetic material, such as DNA, has been artificially manipulated to produce a certain advantageous product. This recombinant genetic engineering allows certain chosen genes, even those from unassociated species, to be transplanted from one organism into another.¹ Genetically modified crops are usually utilized to yield an increased level of crop production and to introduce resistance against diseases. Virus resistance makes plants less susceptible to diseases caused by insects and viruses, resulting in higher crop yields.

Genetic enhancement has improved beyond selective breeding as gene transfer technology has become capable of directly altering genomic sequences . Using a “cut and paste” mechanism, a desired gene can be isolated from a target organism via restriction enzymes and then inserted into a bacterial host using DNA ligase. Once the new gene is introduced, the cells with the inserted DNA (known as “recombinant” DNA) can be bred to generate an advanced strain that can be further replicated to produce the desired gene product.¹ Due to this genetic engineering process, researchers have been able to produce synthetic insect-resistant tomatoes, corn, and potatoes. Humans’ ability to modify crops has improved yields and nutrients in a given environment, becoming the keystone of modern agriculture.² Despite these positive developments, skepticism still exists regarding the safety and societal impact of GMOs.

The technological advancement from selective breeding to genetic engineering has opened up a plethora of possibilities for the future of food. As scientific capabilities expand, ethics and ideals surrounding the invasive nature of the production of GMOs have given rise to concerns about safety and long-term impacts. According to the Center for Food Safety, GMO seeds are used in 90 percent of corn, soybeans, and cotton grown in the United States.² Because GMO crops are so prevalent, any negative ecological interactions involving a GMO product could prove devastating for the environment.

While the dangers of genetic modification are being considered, genetic engineering has proven to have benefits to human health and the farming industry. Genetically modified foods maintain a longer shelf life, which allows for the safe transport of surplus foodstuffs to people in countries without access to nutrition-rich foods. Genetic engineering has supplemented staple crops with vital minerals and nutrients, , helping fight worldwide malnutrition. For example, Golden rice is a genetically-modified variant of rice that biosynthesizes beta-carotene, a precursor of vitamin A.³ This type of rice is intended to be produced and consumed in areas with a shortage of dietary vitamin A, which is a deficiency that kills 670,000 children each year. Despite the controversial risks, genetic engineering of crops promises to continually increase the availability and durability of food.

References

1. Learn.Genetics. http://learn.genetics.utah.edu/content/science/gmfoods/ (accessed Sep 20, 2016)
2. Fernandez-Cornejo, Jorge, and Seth James Wechsler. USDA ERS – Adoption of Genetically Engineered Crops in the U.S.: Recent Trends in GE Adoption. USDA ERS – Adoption of Genetically Engineered Crops in the U.S.: Recent Trends in GE Adoption. https://www.ers.usda.gov/data-products/adoption-of-genetically-engineered-crops-in-the-us/recent-trends-in-ge-adoption.aspx (accessed Sep 30,2016)
3. Dan Charles. In A Grain Of Golden Rice, A World Of Controversy Over GMO Foods. http://www.npr.org/sections/thesalt/2013/03/07/173611461/in-a-grain-of-golden-rice-a-world-of-controversy-over-gmo-foods (accessed Sep 24, 2016)