Unit 7: Big Fights

Getting sunburnt skin is annoying, painful, and can be tedious. We all know that people get sunburned quite often. Something that many people may not realize though is that sunburn can be very dangerous. UV damage can even lead to skin cancer. According to the Skin Cancer Foundation, over 5.4 million cases of some type of skin cancer are reported annually in the US. In 2016 alone, it is expected that approximately 10,130 will die from melanoma – a type of skin cancer – in the United States. [1, 2]

There are many ways to help prevent overexposure to UV radiation. Some examples are wearing UV protective clothing, seeking shaded areas, and – probably the most common – applying sunscreen to exposed skin. However, taking these preventative measures can be tedious; one may not always want to change their clothes or rub sunscreen on their bodies every time they wish to be in the sun. These measures also may not always be an option. People don’t always have access to proper clothing, shade, and sunscreen, so what should they do then? Not be in sunlight? This answer surely isn’t fair and can also be dangerous because we need the sun to produce vitamin D. Without vitamin D synthesis we would not be able to survive.

You may have heard before that “Dark people don’t burn.” Although this is false, it does have some degree of truth to it. The Fitzpatrick scale is a numeric classification scale for the color of humans’ skin. The scale stretches from I to VI, with I being the lightest skin tone and VI being the darkest tone. According to the scale, a type I skin tone almost always burns and is extremely susceptible to skin cancer, while a type VI almost never or never burns and although not as susceptible, are still at risk of skin cancer.

Although all six of the skin types are at risk of UV damage, it is obvious that type VI people are in a much better position. As strange as it is, it would be possible to genetically engineer humans so that their cells produce a darker form of melanin such as a type VI. However, there are a few obstacles and problems with doing this.

 

Unlike some other traits, skin tone isn’t only affected by one gene, but many. [3]  The TYR gene has instructions for producing an enzyme called tyrosinase which is located in cells called melanocytes. Melanocytes are cells that then produce melanin. However, other genes – especially the SLC24A5 gene [4] affect the type of melanin that one produces. This makes genetically engineering humans to have a darker form of melanin more difficult because we can’t just change one gene; we’d have to change several in just the right order.

Another problem with doing this is the social, religious, and possibly even governmental turmoil that would arise from changing skin tones. As silly as it sounds, it would be a big problem. Many circles dislike and even despise dark toned people. Modifying a light skinned person or embryo that will be light skinned to have dark skin will probably cause certain people to be very angry. It is impossible to say what would happen if such a modification happened because human emotions and biases are so unpredictable. Racists might not say anything or might protest, riot, and fight. The genetically engineered and their offspring could be at great risk of being segregated, hurt, and even killed. The scientists who perform these operations could face similar consequences. Even the law makers or anyone else remotely involved with such a thing could be face negative consequences. In the end, genetically engineering humans to produce darker melanin may not be the easiest, best, or most effective option.

 

Plants live an easy life. They never worry about what other plants think of them; they don’t have cults like the KKK killing off and tormenting plants because of their natural born and unchosen pigments. Come to think of it, they don’t even have to worry about getting sunburn! They don’t have to think about changing their clothes or applying sunscreen when they’re in the sun either

As it turns out, most plants do apply sunscreen. Well, they don’t necessarily apply it; they produce it themselves. That’s right, plants produce a natural sun protective shield that goes into action whenever they need it.

Plants contain something called UVR8. [5] UVR8 is a UV-B photoreceptor that changes gene expressions and sends messages depending on how much UV exposure it receives. When the UVR8 photoreceptor senses a large amount of UV-B hitting the plant, it sends a message to start producing and releasing a type of UV protective molecules called sinapate esters. A common sinapate ester in plants is sinapoyl malate (C15H16O9). When sinapoyl malate is released, it protects the plant from UV-B.

According to Genome.jp, sinapoyl malate [6] comes from an enzyme called sinapoyl transferase[7]. The gene that provides instructions for sinapoyl transferase is gene SNG1. [8, 9]

 

My proposition is that we genetically engineer a human embryo to produce sinapoyl malate. This can be done by taking a sample of a plant that contains the SNG1 gene and removing the SNG1 gene using restriction enzymes. Once this is done, we will then move the SNG1 gene into one of the first cells of a developing human and “paste” it into the embryo’s DNA using enzymes called DNA ligases which join DNA parts together.

Let’s say we were to modify two separate human embryos and have them reproduce with each other after sexual maturity. We could extract two separate SNG1 genes from the same plant and insert them into the embryos. Let’s also say that S is the dominant allele that allows for sinapoyl malate production and s is the recessive allele that does not allow for sinapoyl malate production. Because no plant can or could ever survive without sinapoyl malate, it is impossible for a plant to live with alleles ss. This is because they would die off due to inadequate protection from the sun. This means that there are only enough recessive alleles to create SS and Ss genes, so all offspring will be able to produce sinapoyl malate. Because we’re using the same genes, this will also be true for the modified humans and their offspring, making it a 100% chance that the trait will always be present in the phenotype of offspring. All generations of the modified humans will have sinapoyl malate production.

 

Because we’ve never tried this before, there’s no saying what sinapoyl malate production will do to humans other than protect them from UV-B. It is probably fair to say that sinapoyl malate production will change the texture of human skin. It could also cause weakened sensations such as feeling of touch. For all we know, a new molecule in our body may also cause irritation to our skin or change its color. It is really impossible to say what other unforeseen consequences could come from this genetic modification, making it a very big risk for whichever humans are put through it.

Next, there are two big societal, religious, and moral conflicts. The first is that many people are against genetic engineering. Whether we were doing this or doing something as simple as changing the color of an apple, some people would strongly disagree with it. This can be for a number of reasons: genetic engineering may go against religious beliefs for reasons of “playing God.” A disposition to genetic engineering could also be due to a lack of understanding of the sciences and processes. All of this is to say that no matter what the reason is for, some people will refuse to accept genetic engineering and this will be the case forever.

The next big conflict is one that we have gone through already. Because we have never done this modification before, we have no way to tell if it will end terribly or not. Our genetically modified humans could die the moment they’re conceived. Worse yet, they could survive but be in constant pain, sick, or unhealthy. We know almost certainly that this modification will provide protection from UV-B, but there are countless other unforeseen consequences that could arise. Because of this, many people will disagree with this modification. Even if someone was 100% on-board with genetic modification, they might still disagree with this because of the unknown and possibly horrible outcomes, and they wouldn’t be in the wrong for having this standpoint.

Because of all these things it would also be a huge legal mess. It would have to be approved by any government in which this modification would take place. If in the US, there would be contracts, release forms, insurance, and a whole mess of other legal thresholds before the modification could happen.

In conclusion, it is conceptually possible to genetically modify a human embryo in the early stages in a way that will cause it to produce sinapoyl malate, thus protecting the skin from UV-B damage and greatly reducing the risk of sunburn and some skin cancers. However, the societal, religious, educational, and moral ramifications of doing so could and would probably be very negative from some circles. If we were to modify humans in this way, it could be a major success, a total flop, or anything in between.  

 

 

Yo modifico personas para ellos no recibirse la quemadura de sol. Ellos comportarse y parecerse igual a personas normal, pero no quemadura. El piel de ellos puede tocar diferente que otros personas porque lo tiene sinapoyl malate. La piel puede una color diferente tambien. El proceso es mas o meno facil porque es muy estudiaba para las gentes de ciencias. Pero en el fin, mis personas modifican son igual a otros.

 

 

 

[1] What are the key statistics about melanoma skin cancer? (n.d.). Retrieved April 17, 2016, from https://www.cancer.org/cancer/skincancer-melanoma/detailedguide/melanoma-skin-cancer-key-statistics

[2] National Cancer Institute. Cancer Trends Progress Report: UV Exposure and Sun Protective Practices. Bethesda, MD: National Institutes of Health, U.S. Department of Health and Human Services.

[3] American Society for Biochemistry and Molecular Biology. (2008, February 27). How Skin Color Is Determined. ScienceDaily. Retrieved April 17, 2016 from www.sciencedaily.com/releases/2008/02/080222155212.htm

[4] SLC24A5. (2016, April 12). Retrieved April 17, 2016, from https://ghr.nlm.nih.gov/gene/SLC24A5

[5] Christie, J. M., Arvai, A. S., Baxter, K. J., Heilmann, M., Pratt, A. J., O’Hara, A., . . . Getzoff, E. D. (2012, March 23). Plant UVR8 Photoreceptor Senses UV-B by Tryptophan-Mediated Disruption of Cross-Dimer Salt Bridges. Retrieved April 17, 2016, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505452/

[6] KEGG COMPOUND: C02887. (n.d.). Retrieved April 17, 2016, from https://www.genome.jp/dbget-bin/www_bget?C02887

[7] KEGG ENZYME: 2.3.1.92. (n.d.). Retrieved April 17, 2016, from https://www.genome.jp/dbget-bin/www_bget?ec:2.3.1.92

[8] KEGG T00041: AT2G22990. (n.d.). Retrieved April 17, 2016, from https://www.genome.jp/dbget-bin/www_bget?ath:AT2G22990

[9] SGD. (n.d.). Retrieved April 17, 2016, from https://www.yeastgenome.org/locus/S000003429/overview

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